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LncCSMD1 promotes growth and metastasis of xenograft tumors derived from Hep3B HCC cells. (A) In the tumor growth curve, the tumors grow faster in the mice subcutaneously inoculated with Hep3B cells overexpressing lncCSMD1 than in mice with the HCC cells carrying a control vector (left); Images of xenograft tumors derived from Hep3B cells stably overexpressing lncCSMD1 or carrying a control vector (middle); the weights of xenograft tumors in the two groups were compared with histogram (right), in which data were analyzed by sample-paired t test; *P <0.05 (the followings are the same). (B) Representative images of HE staining (left) and Ki67 IHC staining (middle) displayed the pathological configuration and proliferation capacity of HCC xenograft cells; IHC scores for Ki67 were compared in the two groups with histogram (right). (C) Representative images of nude mouse lungs with metastatic foci derived from tail-vein injected Hep3B cells stably overexpressing lncCSMD1 or carrying a control vector (n=5 mice/each group); the metastatic foci ratios (foci to the observed lung area) were compared in the two groups with histogram. (D) Representative images of metastatic foci stained with HE in the lung tissue sections (left); survivals mice tail-vein injected with Hep3B cells stably expressing lncCSMD1 or a control vector were analyzed with Kaplan-Meier curve (right).
Source publication
Emerging evidence suggests that long non-coding RNAs (lncRNA) play critical roles in the development and progression of diverse cancers including hepatocellular carcinoma (HCC), but the underlying molecular mechanisms of lncRNAs that are involved in hepatocarcinogenesis have not been fully explored.
Methods: In this study, we profiled lncRNA expres...
Contexts in source publication
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... assay was conducted in the 3 HCC cells stably overexpressing or less-expressing lncCSMD1. The result showed that more migrated cells were observed in the membrane of wells inoculated with HCC cells stably overexpressing lncCSMD1 ( Figure S3A-B), and wound scratch assay also indicated that the Hep3B cells with lncCSMD1 overexpression migrated faster than the control cells (Figure S3C). When lncCSMD1 was knocked down by shRNA in Hep3B, HepG2 and SMMC7721 cells, HCC cells migrated much less in the transwell membrane when compared with the control HCC cells (Figure S3D). ...
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... assay was conducted in the 3 HCC cells stably overexpressing or less-expressing lncCSMD1. The result showed that more migrated cells were observed in the membrane of wells inoculated with HCC cells stably overexpressing lncCSMD1 ( Figure S3A-B), and wound scratch assay also indicated that the Hep3B cells with lncCSMD1 overexpression migrated faster than the control cells (Figure S3C). When lncCSMD1 was knocked down by shRNA in Hep3B, HepG2 and SMMC7721 cells, HCC cells migrated much less in the transwell membrane when compared with the control HCC cells (Figure S3D). ...
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... result showed that more migrated cells were observed in the membrane of wells inoculated with HCC cells stably overexpressing lncCSMD1 ( Figure S3A-B), and wound scratch assay also indicated that the Hep3B cells with lncCSMD1 overexpression migrated faster than the control cells (Figure S3C). When lncCSMD1 was knocked down by shRNA in Hep3B, HepG2 and SMMC7721 cells, HCC cells migrated much less in the transwell membrane when compared with the control HCC cells (Figure S3D). We then explored the effect of lncCSMD1 on the invasion of HCC cells. ...
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... the 30th day after Hep3B cells were injected subcutaneously, all mice were euthanized, and xenograft tumors were resected, weighed, fixed in 10% buffered formalin and sectioned in a rotary microtome. The tumors from HCC cells stably overexpressing lncCSMD1 grew faster than those from the control HCC cells (Figure 3A left), and the tumor weights were significantly increased in the lncCSMD1 overexpression group compared with the control group ( Figure 3A middle and right). Under a microscope, the xenograft tumors were confirmed to be HCCs in H&E stained slices by experienced pathologist (Figure 3B left), and lncCSMD1 was corroborated to be highly expressed in the xenograft tumor from HCC cells overexpressing lncCSMD1 ( Figure S3E). ...
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... the 30th day after Hep3B cells were injected subcutaneously, all mice were euthanized, and xenograft tumors were resected, weighed, fixed in 10% buffered formalin and sectioned in a rotary microtome. The tumors from HCC cells stably overexpressing lncCSMD1 grew faster than those from the control HCC cells (Figure 3A left), and the tumor weights were significantly increased in the lncCSMD1 overexpression group compared with the control group ( Figure 3A middle and right). Under a microscope, the xenograft tumors were confirmed to be HCCs in H&E stained slices by experienced pathologist (Figure 3B left), and lncCSMD1 was corroborated to be highly expressed in the xenograft tumor from HCC cells overexpressing lncCSMD1 ( Figure S3E). ...
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... tumors from HCC cells stably overexpressing lncCSMD1 grew faster than those from the control HCC cells (Figure 3A left), and the tumor weights were significantly increased in the lncCSMD1 overexpression group compared with the control group ( Figure 3A middle and right). Under a microscope, the xenograft tumors were confirmed to be HCCs in H&E stained slices by experienced pathologist (Figure 3B left), and lncCSMD1 was corroborated to be highly expressed in the xenograft tumor from HCC cells overexpressing lncCSMD1 ( Figure S3E). Furthermore, Ki-67 IHC scores were much higher in the tumors with lncCSMD1 overexpression ( Figure 3B middle and right). ...
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... tumors from HCC cells stably overexpressing lncCSMD1 grew faster than those from the control HCC cells (Figure 3A left), and the tumor weights were significantly increased in the lncCSMD1 overexpression group compared with the control group ( Figure 3A middle and right). Under a microscope, the xenograft tumors were confirmed to be HCCs in H&E stained slices by experienced pathologist (Figure 3B left), and lncCSMD1 was corroborated to be highly expressed in the xenograft tumor from HCC cells overexpressing lncCSMD1 ( Figure S3E). Furthermore, Ki-67 IHC scores were much higher in the tumors with lncCSMD1 overexpression ( Figure 3B middle and right). ...
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... a microscope, the xenograft tumors were confirmed to be HCCs in H&E stained slices by experienced pathologist (Figure 3B left), and lncCSMD1 was corroborated to be highly expressed in the xenograft tumor from HCC cells overexpressing lncCSMD1 ( Figure S3E). Furthermore, Ki-67 IHC scores were much higher in the tumors with lncCSMD1 overexpression ( Figure 3B middle and right). ...
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... validate the results that lncCSMD1 promoted migration, invasion and EMT of HCC cells in vitro, we constructed a lung metastasis mouse model by tail-vein injection of Hep3B cells with overexpression of lncCSMD1 or control vector. At the seventh week after injection, all the mice were euthanized, and whole lungs were harvested for computing the number of metastatic foci (Figure 3C). Compared with the control group, the number of metastatic foci in the lung was dramatically increased in the lncCSMD1 overexpression group by counting of metastatic foci under a microscope (Figure 3D left). ...
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... the seventh week after injection, all the mice were euthanized, and whole lungs were harvested for computing the number of metastatic foci (Figure 3C). Compared with the control group, the number of metastatic foci in the lung was dramatically increased in the lncCSMD1 overexpression group by counting of metastatic foci under a microscope (Figure 3D left). More important, survival analysis suggests that mice injected with HCC cells expressing lncCSMD1 have shorter survival time compared with the control mice (Figure 3D right). ...
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... with the control group, the number of metastatic foci in the lung was dramatically increased in the lncCSMD1 overexpression group by counting of metastatic foci under a microscope (Figure 3D left). More important, survival analysis suggests that mice injected with HCC cells expressing lncCSMD1 have shorter survival time compared with the control mice (Figure 3D right). Altogether, lncCSMD1 facilitates tumor growth and metastasis of HCC cells in vivo. ...
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... was confirmed in HepG2 and LO2 cells ( Figure 4A). The RNAs extracted from cytoplasm and nucleus respectively, was measured with qRT-PCR assay, and the result also indicates that lncCSMD1 is mainly located in the nucleus (Figure S3F). These results suggest that lncCSMD1 may be involved in regulation of gene transcription. ...
Similar publications
Background long noncoding RNAs (lncRNA) play a role in leukemogenesis, maintenance, development, and therapeutic resistance of AML. While few studies have focused on the prognostic significance of LINC00649 in AML, which we aim to investigate in this present study.
Methods We compared the expression level of LINC00649 between AML patients and healt...
Citations
... Western blotting showed that LINC02321 knockdown significantly downregulated the protein levels of RUVBL2 and LINC02321 overexpression upregulate the protein levels of RUVBL2 in UMUC3 and RT112 cells (Fig. 4C). Usually, the elevated protein level can result from either increased synthesis or an extended half-life [29]. LncRNAs can regulate protein expression by affecting protein degradation [30]. ...
Bladder cancer (BC) has a high incidence and is prone to recurrence. In most instances, the low 5-year survival rate of advanced BC patients results from postoperative recurrence and drug resistance. Long noncoding RNAs (lncRNAs) can participate in numerous biological functions by regulating the expression of genes to affect tumorigenesis. Our previous work had demonstrated that a novel lncRNA, LINC02321, was associated with BC prognosis. In this study, A high expression of LINC02321 was found in BC tissues, which was associated with poor prognosis in patients. LINC02321 promoted both proliferation and G1-G0 progression in BC cells, while also inhibited sensitivity to cisplatin. Mechanistically, LINC02321 can bind to RUVBL2 and regulate the expression levels of RUVBL2 protein by affecting its half-life. RUVBL2 is involved in the DNA damage response. The potential of DNA damage repair pathways to exert chemosensitization has been demonstrated in vivo. The rescue experiment demonstrated that RUVBL2 overexpression can markedly abolish the decreased cell proliferation and the increased sensitivity of BC cells to cisplatin caused by LINC02321 knockdown. The results indicate that LINC02321 functions as an oncogene in BC, and may serve as a novel potential target for controlling BC progression and addressing cisplatin resistance in BC therapy.
... Cell migration assay was measured by using the Transwell method (BD Biosciences, Lexington, UK) described previously [16]. Cells, 5 × 10 4 cells/well, were plated into the upper chambers with serum-free RPMI-1640 medium, and the lower chambers contained RPMI-1640 medium plus 10% FBS. ...
Tripartite motif–containing 29 (TRIM29), also known as the ataxia telangiectasia group D-complementing (ATDC) gene, has been reported to play an oncogenic or tumor suppressive role in developing different tumors. So far, its expression and biological functions in hepatocellular carcinoma (HCC) remain unclear. We investigated TRIM29 expression pattern in human HCC samples using quantitative RT-PCR and immunohistochemistry. Relationships between TRIM29 expression level, clinical prognostic indicators, overall survival (OS), and disease-free survival (DFS) were evaluated by Kaplan–Meier analysis and Cox proportional hazards model. A series of in vitro experiments and a xenograft tumor model were conducted to detect the functions of TRIM29 in HCC cells. RNA sequencing, western blotting, and immunochemical staining were performed to assess the molecular regulation of TRIM29 in HCC. We found that the mRNA and protein levels of TRIM29 were significantly reduced in HCC samples, compared with adjacent noncancerous tissues, and were negatively correlated with poor differentiation of HCC tissues. Survival analysis confirmed that lower TRIM29 expression significantly correlated with shorter OS and DFS of HCC patients. TRIM29 overexpression remarkably inhibited cell proliferation, migration, and EMT in HCC cells, whereas knockdown of TRIM29 reversed these effects. Moreover, deactivation of the PTEN/AKT/mTOR and JAK2/STAT3 pathways might be involved in the tumor suppressive role of TRIM29 in HCC. Our findings indicate that TRIM29 in HCC exerts its tumor suppressive effects through inhibition of the PTEN/AKT/mTOR and JAK2/STAT3 signaling pathways and may be used as a potential biomarker for survival in patients with HCC.
... For example, lncRNA FGD5-AS1 accelerates the proliferation of pancreatic cancer cells by regulating miR-520a-3p/KIAA1522 axis [10], lncRNA MIR22HG regulates the proliferation and apoptosis of numerous human cancers [11]. In addition, aberrations in lncRNA expression, deletion or mutation are closely associated with HCC development and metastasis, indicating their potential as oncogenes [12]. ...
Background: RNA methylation modifications are important post-translational modifications that are regulated in an epigenetic manner. Recently, N⁶-methyladenosine (m⁶A) RNA modifications have emerged as potential epigenetic markers in tumor biology.
Methods: Gene expression and clinicopathological data of LIHC were obtained from the cancer genome atlas (TCGA) database. The relationship between long non-coding RNAs (lncRNAs) and m⁶A-related genes was determined by gene expression analysis using Perl and R software. Co-expression network of m⁶A-lncRNA was constructed, and the relevant lncRNAs associated with prognosis were identified using univariate Cox regression analysis. These lncRNAs were then divided into two clusters (cluster 1 and cluster 2) to determine the differences in survival, pathoclinical parameters, and immune cell infiltration between the different lncRNA subtypes. The least absolute shrinkage and selection operator (LASSO) was carried out for regression analysis and prognostic model. The HCC patients were randomly divided into a train group and a test group. According to the median risk score of the model, HCC patients were divided into high-risk and low-risk groups. We built models using the train group and confirmed them through the test group. The m⁶A-lncRNAs derived from the models were analyzed for the tumor mutational burden (TMB), immune evasion and immune function using R software. AL355574.1 was identified as an important m⁶A-associated lncRNA and selected for further investigation. Finally, in vitro experiments were conducted to confirm the effect of AL355574.1 on the biological function of HCC and the possible biological mechanisms. Huh7 and HepG2 cells were transfected with AL355574.1 siRNA and cell proliferation ability was measured by CCK-8, EdU and colony formation assays. Wound healing and transwell assays were used to determine the cell migration capacity. The expression levels of MMP-2, MMP-9, E-cadherin, N-cadherin and Akt/mTOR phosphorylation were all determined by Western blotting.
Results: The lncRNAs with significant prognostic value were classified into two subtypes by a consistent clustering analysis. We found that the clinical features, immune cell infiltration and tumor microenvironment (TME) were significantly different between the lncRNA subtypes. Our analysis revealed significant correlations between these different lncRNA subtypes and immune infiltrating and stromal cells. We created the final risk profile using LASSO regression, which notably included three lncRNAs (AL355574.1, AL158166.1, TMCC1-AS1). A prognostic signature consisting of the three lncRNAs was constructed, and the model showed excellent prognostic predictive ability. The overall survival (OS) of the low-risk cohort was significantly higher than that of the high-risk cohort in both the train and test group. Both risk score [hazard ratio (HR)=1.062; P<0.001] and stage (HR=1.647; P< 0.001) were considered independent indicators of HCC prognosis by univariate and multivariate Cox regression analysis. In Huh7 and HepG2 cells, AL355574.1 knockdown inhibited cell proliferation and migration, suppressed the protein expression levels of MMP-2, MMP-9, N-cadherin and Akt/mTOR phosphorylation, but promoted the protein expression levels of E-cadherin.
Conclusions: This study established a predictive model for the OS of HCC patients, and these OS-related m⁶A-lncRNAs, especially AL355574.1 may play a potential role in the progression of HCC. In vitro experiments also showed that AL355574.1 could enhance the expression of MMPs and EMT through the Akt/mTOR signaling pathway, thereby affected the proliferation and migration of HCC. This provides a new perspective on the anticancer molecular mechanism of AL355574.1 in HCC.
... LncRNA SBF2-AS1 modulates TGFBR1-mediated signaling due to sponging miR-140-5p and this promotes HCC progression [103]. Among lncRNAs acting via Myc pathway is CSMD1-1, which is upregulated in HCC and associated with increased cancer cell proliferation, migration, invasion, and metastasis and tumor progression [104]. CSMD1-1 blocks ubiquitin-proteasomal degradation of transcription factor Myc leading to activation of downstream target genes. ...
... For example, statistically significant downregulation of hsa_circ_0004018 (p˂0.001), [63,64,70,74,85,[95][96][97][98][99][100][101][102][103][104], metabolic reprogramming [108,111], epithelial-mesenchymal transition/morphogenesis [81,82,86,89], tumor microenvironment remodeling [88], cell cycle [107], and apoptosis [84,87,103,106]. (B) CircRNAs implicated in cell signaling [132,133], cell cycle [108,118,134,135], transcriptional regulation [136,137,154], metabolic reprogramming [145][146][147], epithelial-mesenchymal transition [139][140][141][142], immune response [144,149,150], and angiogenesis [129,131]. ...
The vast majority of human transcriptome is represented by various types of small RNAs with little or no protein-coding capability referred to as non-coding RNAs (ncRNAs). Functional ncRNAs include microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), which are expressed at very low, but stable and reproducible levels in a variety of cell types. ncRNAs regulate gene expression due to miRNA capability of complementary base pairing with mRNAs, whereas lncRNAs and circRNAs can sponge miRNAs off their target mRNAs to act as competitive endogenous RNAs (ceRNAs). Each miRNA can target multiple mRNAs and a single mRNA can interact with several miRNAs, thereby creating miRNA-mRNA, lncRNA-miRNA-mRNA, and circRNA-miRNA-mRNA regulatory networks. Over the past few years, a variety of differentially expressed miRNAs, lncRNAs, and circRNAs (DEMs, DELs, and DECs, respectively) have been linked to cancer pathogenesis. They can exert both oncogenic and tumor suppressor roles. In this review, we discuss the recent advancements in uncovering the roles of DEMs, DELs, and DECs and their networks in aberrant cell signaling, cell cycle, transcription, angiogenesis, and apoptosis, as well as tumor microenvironment remodeling and metabolic reprogramming during hepatocarcinogenesis. We highlight the potential and challenges in the use of differentially expressed ncRNAs as biomarkers for liver cancer diagnosis and prognosis.
... Furthermore, lncCSMD1 has been shown to act as an oncogene, promoting HCC cell proliferation, migration, invasion, and EMT. As a result, it was speculated that lncCSMD1 could be a novel and reproducible prognostic biomarker for HCC patients, as well as playing an important role in HCC progression [76]. Using the GEO and TCGA databases, a study identified several novel driver genes including CSMD1 associated with HCC and demonstrated that this gene was strongly related to the prognosis of early recurrence and an effective prognostic marker for HCC [77]. ...
... Elucidating the relationship of CSMD1 with the aforementioned diseases in this review may be important in terms of both treatment and diagnosis in the future. Recent studies have revealed a possible role for CSMD1 in immunotherapy for some cancer types [73][74][75][76][77][78][79][80][81][82]. The determination of the factors affecting the expression of CSMD1 and the clarification of the signalling pathways it affects will increase the clinical utility of CSMD1. ...
CUB and Sushi Multiple Domains 1 (CSMD1), a tumour suppressor gene, encodes a large membrane-bound protein including a single transmembrane domain. This transmembrane region has a potential tyrosine phosphorylation site, suggesting that CSMD1 is involved in controlling cellular functions. Although the specific mechanisms of action for CSMD1 have not yet been uncovered, it has been linked to a number of processes including development, complement control, neurodevelopment, and cancer progression. In this review, we summarise CSMD1 functions in the cellular processes involved in the complement system, metastasis, and Epithelial mesenchymal transition (EMT) and also in the diseases schizophrenia, Parkinson’s disease, and cancer. Clarifying the association between CSMD1 and the aforementioned diseases will contribute to the development of new diagnosis and treatment methods for these diseases. Recent studies in certain cancer types, e.g., gastric cancer, oesophageal cancer, and head and neck squamous cell carcinomas, have indicated the involvement of CSMD1 in response to immunotherapy.
... Loss of alleles, aberrant methylation levels, and mutations of CSMD1 gene have been implicated in various cancers, including head and neck, breast, lung, liver, colorectal, prostate, and skin cancers, oral squamous cell carcinoma, chronic myeloid leukemia, and recurrent ALL. [20][21][22][23] In this patient, there was no CSMD1 gene mutation at the initial diagnosis of ALL and was detected at the onset of sAML, and the CSMD1 gene mutation in this patient may contribute to the development of sAML. 24 It was speculated that chemotherapy drugs such as idarubicin and cyclophosphamide may lead to the mutation of CSMD1 gene which resulted in the development of sAML. ...
Background
Acute lymphoblastic leukemia (ALL) has the highest incidence among childhood hematologic cancers. Exposure to certain cytotoxic therapies for ALL is correlated with a higher risk of secondary malignancies.
Case
We report a rare case of a 6‐year‐old girl being diagnosed with secondary acute myeloid leukemia (AML) during her maintenance phase of treatment for ALL with TEL‐AML1 fusion gene, approximately 17 months after the primary diagnosis.
Conclusion
This case indicates that we should recognize the increased risk of secondary AML for pediatric ALL patients with TEL‐AML1 fusion gene if multiple alkylating drugs and inhibitors for topoisomerase II are included in induction chemotherapy.
... Accumulating evidence has suggested that long noncoding RNAs (lncRNAs) are a type of RNA transcripts in eukaryotic cells longer than 200 nucleotides defined by a lack of protein-coding potential [7]. More and more studies have revealed the regulation of lncRNAs in a range of biological processes, involving cell growth, apoptosis, migration, and invasion in almost all human cancers, including gastric cancer, hepatocellular carcinoma, and prostate cancer [8][9][10][11]. LncRNA solute carrier organic anion transporter family member 4A1 antisense RNA 1 (SLCO4A1-AS1) was verified to be an oncogene in some cancers [12]. For example, in non-small-cell lung cancer, SLCO4A1-AS1 facilitates cellular processes by mediating the miR-223-3p/ IKKα/NF-κB signaling [13]. ...
In this study, we intended to figure out the biological significance of long non-coding RNAs (lncRNAs) solute carrier organic anion transporter family member 4A1 antisense RNA 1 (SLCO4A1-AS1) in pancreatic cancer (PC). Cell counting kit-8, colony formation, wound healing, transwell, and flow cytometry experiments were performed to reveal how SLCO4A1-AS1 influences PC cell proliferation, migration, invasion, and apoptosis. Thereafter, bioinformatics analysis, RNA immunoprecipitation assay, luciferase reporter assay, and RNA pull-down assay were applied for determining the binding sites and binding capacities between SLCO4A1-AS1 and miR-4673 or kinesin family member 21B (KIF21B) and miR-4673. The results depicted that SLCO4A1-AS1 was upregulated in PC, and SLCO4A1-AS1 knockdown suppressed PC cell growth, migration, invasion, and induced cell apoptosis. Furthermore, SLCO4A1-AS1 was verified to modulate the expression of KIF21B by binding with miR-4673. SLCO4A1-AS1 exerted an oncogenic function in PC. The overexpression of SLCO4A1-AS1 aggravated the malignant behaviors of PC via the upregulation of KIF21B by sponging miR-4673. Our findings revealed a novel molecular mechanism mediated by SLCO4A1-AS1, which might play a significant role in modulating the biological processes of PC.
... The lncRNA CSMD1-1 hyperactivates oncogenic phosphatase and tensin homolog deleted on chromosome ten signaling, thereby enhancing the malignant phenotypes of HCC cells [8]. The lncRNA CSMD1-1 enables HCC malignancy by blocking the ubiquitinproteasome degradation pathway of MYC and increasing MYC expression, which favors HCC progression [9]. Among the multiple mechanisms by which lncRNAs interfere with gene expression, the competing endogenous RNA (ceRNA) mechanism has always been a research hotspot. ...
Statement of Retraction
We, the Editors and Publisher of the journal Bioengineered, have retracted the following article:
Yanjie Mou & Qinguo Sun (2022) The long non-coding RNA ASMTL-AS1 promotes hepatocellular carcinoma progression by sponging miR-1343-3p that suppresses LAMC1 (laminin subunit gamma 1), Bioengineered, 13:1, 746-758, DOI: 10.1080/21655979.2021.2012628
Since publication, significant concerns have been raised about the integrity of the data and reported results in the article. When approached for an explanation, the authors did not provide their original data or any necessary supporting information. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. All authors listed in this publication have been informed. The authors have not responded to notice of this retraction.
We have been informed in our decision-making by our ethical policies and the COPE guidelines.
The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as ‘Retracted’.
... In recent years, lncRNAs has been considered potential prognostic markers and therapectic targets for cancers (Sanchez Calle et al., 2018;Zhang et al., 2021). Liu et al. (2020) found that lncCSMD1-1 is overexpressed in hepatocellular carcinoma (HCC) and interacts with the MYC protein to promote tumor progression, suggesting that it may serve as a prognostic marker for HCC. The lncRNA PiHL (RP11-382A18.2) is upregulated in colorectal cancer (CRC), and its upregulation is an independent predictor of poor CRC prognosis (Deng et al., 2020). ...
The nonfunctioning pituitary adenoma (NFPA) recurrence rate is relatively high after surgical resection. Here, we constructed effective long noncoding RNA (lncRNA) signatures to predict NFPA prognosis. LncRNAs expression microarray sequencing profiles were obtained from 66 NFPAs. Sixty-six patients were randomly separated into a training (n = 33) and test group (n = 33). Univariable Cox regression and a machine learning algorithm was used to filter lncRNAs. Time-dependent receiver operating characteristic (ROC) analysis was performed to improve the prediction signature. Three lncRNAs (LOC101927765, RP11-23N2.4 and RP4-533D7.4) were included in a prognostic signature with high prediction accuracy for tumor recurrence, which had the largest area under ROC curve (AUC) value in the training/test group (AUC = 0.87/0.73). The predictive ability of the signature was validated by Kaplan-Meier survival analysis. A signature-based risk score model divied patients into two risk group, and the recurrence-free survival rates of the groups were significantly different (log-rank p < 0.001). In addition, the ROC analysis showed that the lncRNA signature predictive ability was significantly better than that of age in the training/testing/entire group (AUC = 0.87/0.726/0.798 vs. AUC = 0.683/0.676/0.679). We constructed and verified a three-lncRNA signature predictive of recurrence, suggesting potential therapeutic targets for NFPA.
... 17 An increasing number of literatures suggested that miR-9 to 1 were also involved in tumorigenesis. [18][19][20][21] In different types of cancer cells, miR-9 to 1 can have different effects on apoptosis and proliferation of cancer cells through targeting different mRNA targets. [22][23][24] miR-9 to 1 is found to over-express in human Hodgkin's lymphoma cells, 25 primary brain tumors, 26 cervical cancer, 27 and colorectal cancer. ...
Lung cancer is listed as the most common reason for cancer-related death all over the world despite diagnostic improvements and the development of chemotherapy and targeted therapies. MicroRNAs control both physiological and pathological processes including development and cancer. A microRNA-9 to 1 (miR-9 to 1) overexpression model in lung cancer cell lines was established and miR-9 to 1 was found to significantly suppress the proliferation rate in lung cancer cell lines, colony formation in vitro, and tumorigenicity in nude mice of A549 cells. Ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) was then identified to direct target of miR-9 to 1. The inhibition of UHRF1 by miR-9 to 1 causes G1 arrest and p15, p16, and p21 were re-expressed in miR-9 to 1 group in mRNA level and protein level. Silence of UHRF1 expression in A549 cells resulted in the similar re-expression of p15, p16, p21 which is similar with miR-9 to 1 infection. Therefore, we concluded that UHRF1 is a new target for miR-9 to 1 to suppress cell proliferation by re-expression of tumor suppressors p15, p16, and p21 mediated by UHRF1.
