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Impaired cell viability and colony formation ability of lung cancer cells after CEP55 knockdown. (A) An MTT assay was used to determine the cell viability in the A549 and 95D cells following transfection with a lentivirus containing sh-2 or sh-NC. (B) Representative images of colonies formed in the A549 and 95D cells with two treatments (sh-2 and sh-NC). (C) Statistical analysis of colony numbers in the A549 and 95D cells. *** P<0.001. CEP55, centrosomal protein 55; NC, negative control.
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Centrosomal protein 55 (CEP55), identified as a centrosome‑associated protein, has been reported to be involved in human malignancies. However, its biological function in human lung cancer remains largely unknown. In the present study, we firstly analyzed the expression of CEP55 in 20 pairs of lung cancer and matched non‑tumor tissues using quantit...
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... lower after five consecutive days in the CEP55-knockdown (sh-2) cells compared with that noted in the non-target scramble control shRNA-transfected cells (sh-NC) in both the A549 and 95D cell lines (Fig. 3A, p<0.001). Furthermore, we determined the colony formation ability of the lung cancer cells after knockdown of CEP55. As shown in Fig. 3B, knockdown of CEP55 obviously reduced the size of the single colonies and the number of colonies formed in the A549 and 95D cells. The number of colonies in the sh-2 group was apparently smaller than that in the sh-NC group in both cell . Expression of CEP55 was stably knocked down in the A549 and 95D cell lines. CEP55 mRNA levels were ...
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Citations
... After phosphorylation, it plays a role in regulating the cell cycle. The overexpression of CEP55 is significantly correlated with the tumor stage, invasion and metastasis of many malignant tumors [47]. Jiang et al. found that CEP55 expression was commonly elevated in NSCLC tissues and overexpression of CEP55 was correlated with unfavorable prognosis in the patients with NSCLC [48]. ...
Non-small cell lung cancer (NSCLC) is the most common histopathological type, and it is purposeful for screening potential prognostic biomarkers for NSCLC. This study aims to identify the lncRNAs and mRNAs related to survival of non-small cell lung cancer (NSCLC). The expression profile data of lung adenocarcinoma and lung squamous cell carcinoma were downloaded in The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) dataset. A total of eight survival related long non-coding RNAs (lncRNAs) and 262 survival related mRNAs were filtered. By gene set enrichment analysis, 17 significantly correlated Gene Ontology signal pathways and 14 Kyoto Encyclopedia of Genes and Genomes signal pathways were screened. Based on the clinical survival and prognosis information of the samples, we screened eight lncRNAs and 193 mRNAs by single factor Cox regression analysis. Further single and multifactor Cox regression analysis were performed, 30 independent prognostication-related mRNAs were obtained. The PPI network was further constructed. We then performed the machine learning algorithms (Least absolute shrinkage and selection operator, Recursive feature elimination, and Random forest) to screen the optimized DEGs combination, and a total of 17 overlapping mRNAs were obtained. Based on the 17 characteristic mRNAs obtained, we firstly built a Nomogram prediction model, and the ROC values of training set and testing set were 0.835 and 0.767, respectively. By overlapping the 17 characteristic mRNAs and PPI network hub genes, three genes were obtained: CDC6, CEP55, TYMS, which were considered as key factors associated with survival of NSCLC. The in vitro experiments were performed to examine the effect of CDC6, CEP55, and TYMS on NSCLC cells. Finally, the lncRNAs-mRNAs networks were constructed.
... CEP55 is a key regulator of physical cytokinesis [26]. The overexpression of CEP55 was earlier linked to the pathogenesis and poor prognosis of lung [27], oral [28], cervical [29], breast cancers [28], and osteosarcoma [30]. In addition, CEP55 knockdown was also found to inhibit tumor cell proliferation [31]. ...
Background:
Previously reported breast invasive carcinoma (BRIC) biomarkers have compromised utility because of their heterogeneity-specific behaviors. The goal of this study was to find BRIC biomarkers that could be used in spite of the heterogeneity barrier.
Methods:
Previously reported BRIC-linked hub genes were obtained from the literature via a search technique. A protein-protein interaction (PPI) network of the extracted hub genes was constructed, visualized, and analyzed to explore the top six real hub genes. Following this, real hub genes' expression profiling was carried out using various TCGA data sources and RNA sequencing (RNA-seq) of BT 20 and HMEC cell lines to uncover the tumor-driver roles of the real hub genes.
Results:
In total, 124 BRIC-linked hub genes were collected from the literature via the search technique. From these collected hub genes, a total of 6 genes, including Centrosomal protein of 55 kDa (CEP55), Kinesin Family Member 2C (KIF2C), kinesin family member 20A (KIF20A), Ribonucleotide Reductase Regulatory Subunit M2 (RRM2), Aurora A Kinase (AURKA), and Protein Regulator of cytokinesis 1 (PRC1) were determined to be the real hub genes. Via expression profiling and validation analyses, we documented the overexpression of CEP55, KIF2C, KIF20A, RRM2, AURKA, and PRC1 real hub genes in BRIC patients with different clinical variables. Further correlational analyses showed diverse associations among real hub genes' expression and other important parameters, including promoter methylation status, genetic alteration, overall survival (OS), relapse-free survival (RFS), tumor purity, CD8+ T, CD4+ T immune cell infiltration, and different mutant genes across BRIC samples. Finally, in this work, we investigated several transcription factors (TFS), microRNAs, and therapeutic medicines related to the real hub genes that have great therapeutic potential.
Conclusion:
In conclusion, we discovered six real hub genes, which may be employed as novel potential biomarkers for BRIC patients with different clinical parameters.
... It has been reported that the up-regulation of CEP55 expression can facilitate cell migration and invasion and that high expression of CEP55 is implicated in poor prognoses of patients with liver cancer (Yang et al. 2020b), anaplastic thyroid cancer (Li et al. 2020), cervical cancer (Qi et al. 2018), and LUAD (Wu et al. 2019). Liu et al. (Liu et al. 2016) found that inhibition of CEP55 expression reduced viability and induced apoptosis of LUAD cells, which was consistent with the results of this study. We also verified the binding between CEP55 and E2F7 by using ChIP and dual-luciferase assays, and confirmed that E2F7 increased the activity of LUAD cells and inhibited apoptosis via activating CEP55 by using cell experiments. ...
Lung adenocarcinoma (LUAD) is a common malignancy. Many studies have shown that LUAD is resistant to gemcitabine chemotherapy, resulting in poor treatment outcomes in patients. We designed this study to reveal influences of hsa-miR-195-5p/E2F7/CEP55 axis on gemcitabine resistance and autophagy of LUAD cells. The expression data of LUAD-related mRNAs were downloaded from TCGA-LUAD database for differential expression analysis. The bioinformatics databases (hTFtarget, starBase and TargetScan) were used to predict the upstream and downstream regulatory molecules of E2F7. Then the binding relationships between E2F7 and regulatory molecules were verified by ChIP and dual-luciferase reporter assay. qRT-PCR and western blot were used to detect the mRNA and protein levels of has-miR-195-5p, E2F7, and CEP55. CCK-8 assay was used to analyze the half-maximal inhibitory concentration (IC50) and cell proliferation ability of LUAD cells after gemcitabine treatment. Apoptosis was detected by flow cytometry. Apoptosis/autophagy markers and LC3 aggregation were detected by western blot and immunofluorescence, respectively. Finally, the mouse transplantation model was constructed to verify the regulation mechanism in vivo. In LUAD cells and tissues, E2F7 and CEP55 were highly expressed, while has-miR-195-5p was relatively less expressed. The ChIP or dual-luciferase assays demonstrated the binding relationships of E2F7 to the CEP55 promoter region and has-miR-195-5p to the 3’-UTR of E2F7. Cell experiments demonstrated that overexpression of hsa-miR-195-5p stimulated LUAD cell apoptosis and inhibited autophagy and gemcitabine resistance, while further overexpression E2F7/CEP55 could reverse the impact by hsa-miR-195-5p overexpression. In vivo experiments identified that hsa-miR-195-5p/E2F7/CEP55 axis constrained the growth of LUAD tumor. Hsa-miR-195-5p promoted apoptosis, repressed proliferation, and autophagy via E2F7/CEP55 and reduced gemcitabine resistance in LUAD, indicating that hsa-miR-195-5p/E2F7/CEP55 may be a novel target for LUAD.
... Bone marrow plasma obviously contains molecules synthesized by BM cells and components from blood, suggesting that the content of BM plasma does not entirely reflect what comes from mononuclear cells. Moreover, mRNA and protein quantities in a given biological entity can be unrelated (63)(64)(65)(66), and cell lysis and/or apoptosis may have occurred during the collection and separation of BM plasma. Another possible explanation is that MDS-RS cases present serious problems of splice machinery (mutation of SF3B1), leading to disrupted mRNA translation, with increases in some mRNAs without proportional changes in protein synthesis. ...
Myelodysplastic syndrome (MDS) is a hematological disorder characterized by abnormal stem cell differentiation and a high risk of acute myeloid leukemia transformation. Treatment options for MDS are still limited, making the identification of molecular signatures for MDS progression a vital task. Thus, we evaluated the proteome of bone marrow plasma from patients (n = 28) diagnosed with MDS with ring sideroblasts (MDS-RS) and MDS with blasts in the bone marrow (MDS-EB) using label-free mass spectrometry. This strategy allowed the identification of 1,194 proteins in the bone marrow plasma samples. Polyubiquitin-C (UBC), moesin (MSN), and Talin-1 (TLN1) showed the highest abundances in MDS-EB, and centrosomal protein of 55 kDa (CEP55) showed the highest relative abundance in the bone marrow plasma of MDS-RS patients. In a follow-up, in the second phase of the study, expressions of UBC, MSN, TLN1, and CEP55 genes were evaluated in bone marrow mononuclear cells from 45 patients by using qPCR. This second cohort included only seven patients from the first study. CEP55, MSN, and UBC expressions were similar in mononuclear cells from MDS-RS and MDS-EB individuals. However, TLN1 gene expression was greater in mononuclear cells from MDS-RS (p = 0.049) as compared to MDS-EB patients. Irrespective of the MDS subtype, CEP55 expression was higher (p = 0.045) in MDS patients with abnormal karyotypes, while MSN, UBC, and TALIN1 transcripts were similar in MDS with normal vs. abnormal karyotypes. In conclusion, proteomic and gene expression approaches brought evidence of altered TLN1 and CEP55 expressions in cellular and non-cellular bone marrow compartments of patients with low-risk (MDS-RS) and high-risk (MDS-EB) MDSs and with normal vs. abnormal karyotypes. As MDS is characterized by disrupted apoptosis and chromosomal alterations, leading to mitotic slippage, TLN1 and CEP55 represent potential markers for MDS prognosis and/or targeted therapy.
... As a member of the centrosome-related protein family, centrosomal protein of 55 kDa (CEP55) first discovered in 2005 that modulates the separation of two daughter cells in the end stage of cytokinesis 9,10 , of which the regulatory effect was detected by more and more subsequent studies and the regulatory mechanism was improved 11,12 . Furthermore, studies of tumors manifested that CEP55 had a direct or indirect relation to many tumors [13][14][15][16][17] . Hence, studying and exploring the role and possible mechanism of CEP55 in ATC might be conducive to the treatment of ATC. ...
Objective:
The purpose of this study was to determine the role of centrosomal protein of 55 kDa (CEP55) in anaplastic thyroid cancer (ATC) and to further explore the mechanism, which might provide a new molecular marker for treatment of ATC.
Patients and methods:
The expression level of CEP55 in clinical cases was tested by fluorescence quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Also, qRT-PCR assay was performed in different TC cell lines. The relationship between CEP55 expression and clinicopathological characteristics was statistically analyzed. Kaplan-Meier curve and Cox's proportional hazards regression model were performed in survival analysis. Further, Western blot assay was used to analyze the protein expression changes in PI3K/Akt pathway.
Results:
The expression level of CEP55 in TC tissues showed a noticeable upgrade, especially in ATC. In vitro, CEP55 expression was also increased in four kinds of TC cells, in which, the highest expression was found in ATC (TA-K) cells. The clinicopathological features, including lymph node metastasis, distant metastasis, and prognostic index were found to be correlated with the expression level of CEP55. Besides, the ATC patients with higher expression of CEP55 had a statistically worse overall survival (OS) time. In univariate analyses and multivariate analyses, the CEP55 level was an independent prognosis index of patients with ATC. In vitro study, CEP55 protein expression level was significantly reduced in si-CEP55-transfected TA-K cells. Notably, the downregulation of CEP55 could suppress the phosphorylation of PI3K and AKT.
Conclusions:
This study found that CEP55 could promote ATC progression, and PI3K/AKT pathway might be the downstream target of its action. These results provided a new therapeutic direction for the treatment of ATC.
... In this study, we found CEP55 was highly expressed in both LUAD and LUSC compared to normal cells, and was more significantly expressed in LUSC. Previously, CEP55 has proven to be a useful biomarker for a variety of cancers, including lung cancer [15,16]. However, its predictive value in the two subtypes of LUAD and LUSC in non-small cell lung cancer has not been reported. ...
Objective
To investigate the value of CEP55 as a diagnostic marker and independent prognostic factor in lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC), and to analyze its co-expression genes and related signaling pathways.
Methods
TCGA database and GEO database were used to analyze the expression of CEP55 in LUAD and LUSC compared with normal tissues. The co-expression genes of CEP55 in LUAD and LUSC were excavated by cBioPortal and enriched by KEGG and GO. Establishing Receiver operating characteristic (ROC) curve to evaluate the value of CEP55 as a diagnostic and prognostic factor. The association between CEP55 expression and the clinicopathological features was evaluated using χ2 tests. ROC curves for diagnosis and prognosis detection were constructed. Prognostic values were analyzed by univariate and multivariate Cox regression models.
Results
Compared with normal lung tissues, CEP55 expression was significantly upregulated in both LUAD and LUSC. ROC curve analysis showed that CEP55 could be used as an effective diagnostic target for LUAD (AUC = 0.969) and LUSC (AUC = 0.994). When CEP55 gene was selected as an independent prognostic factor, high expression of CEP55 was more disadvantageous to OS and RFS of LUAD patients (P<0.05), but no significant difference was found in LUSC patients (P>0.05). The number of co-expression genes of CEP55 in LUAD is more than that in LUSC, and is related to cell cycle, DNA replication and P53 signaling pathway.
Conclusion
CEP55 can be used as a diagnostic marker for LUAD and LUSC, but only as an independent prognostic factor for LUAD rather than LUSC.
... 21 The knockdown of CEP55 markedly inhibited proliferation and induced apoptosis of lung cancer (LC) cells. 22 Furthermore, high expression of CEP55 was associated with advanced T and N staging of LC. 23 Another study found that CEP55 could enhance the proliferation and invasive ability of tumour cells via the AKT signalling pathway in osteosarcoma. 24 The knockdown of the CEP55 gene suppressed the proliferation of glioma cells, whereas CEP55 overexpression induced proliferation of the cells. ...
Objective
To identify genes associated with the clinicopathological features of colorectal cancer (CRC).
Methods
Gene expression profiles were downloaded and preprocessed by GEOquery and affy R packages, respectively. The limma package was applied to identify the differentially expressed genes (DEGs) in CRC. Gene Ontology and Kyoto Gene and Genome Encyclopedia (KEGG) pathway enrichment analyses for the DEGs were carried out using the clusterProfiler package. Protein–protein interaction (PPI) and weighted gene co-expression (WGC) networks were constructed using the STRING database and WGCNA package, respectively.
Results
A total of 523 DEGs (283 downregulated and 240 upregulated genes) in CRC tissues were identified. These DEGs were mainly enriched in 111 biological processes, 16 cellular components and 40 molecular functions, such as proteinaceous extracellular matrix, extracellular structure organization and chemokine-mediated signalling pathway. PPI and WGC networks showed that four upregulated genes (KIF2C, CDC45, CEP55 and DTL) were key genes. Subgroup analysis based on individual cancer stages and histological subtypes indicated that the expression of these key genes was upregulated in CRC stages I–IV, adenocarcinoma and mucinous adenocarcinoma.
Conclusions
The study provides new insights into understanding the pathogenesis of CRC. These identified genes may act as potential targets for CRC diagnosis and treatment.
... [23][24][25] Centrosomal protein 55 (CEP55) is identified as a coiled-coil centrosomal protein and an important part in some cellular processes, such as cytokinesis, cell growth and transformation. 26-28 CEP55 acts as a tumor promoter in cancers of the lung, breast and pancreas, [29][30][31] and it has been reported to be associated with metastasis in renal cell carcinoma. 32 Kinesin family member 11 (KIF11) acts as an oncogene in meningioma 33 and is also associated with poor outcomes in meningioma, breast and oral cancer. ...
One of the most common sites of extra‐thoracic distant metastasis of nonsmall‐cell lung cancer is the brain. Our study was performed to discover genes associated with postoperative brain metastasis in operable lung adenocarcinoma (LUAD). RNA seq was performed in specimens of primary LUAD from seven patients with brain metastases and 45 patients without recurrence. Immunohistochemical (IHC) assays of the differentially expressed genes were conducted in 272 surgical‐resected LUAD specimens. LASSO Cox regression was used to filter genes related to brain metastasis and construct brain metastasis score (BMS). GSE31210 and GSE50081 were used as validation datasets of the model. Gene Set Enrichment Analysis was performed in patients stratified by risk of brain metastasis in the TCGA database. Through the initial screening, eight genes (CDK1, KPNA2, KIF11, ASPM, CEP55, HJURP, TYMS and TTK) were selected for IHC analyses. The BMS based on protein expression levels of five genes (TYMS, CDK1, HJURP, CEP55 and KIF11) was highly predictive of brain metastasis in our cohort (12‐month AUC: 0.791, 36‐month AUC: 0.766, 60‐month AUC: 0.812). The validation of BMS on overall survival of GSE31210 and GSE50081 also showed excellent predictive value (GSE31210, 12‐month AUC: 0.682, 36‐month AUC: 0.713, 60‐month AUC: 0.762; GSE50081, 12‐month AUC: 0.706, 36‐month AUC: 0.700, 60‐month AUC: 0.724). Further analyses showed high BMS was associated with pathways of cell cycle and DNA repair. A five‐gene predictive model exhibits potential clinical utility for the prediction of postoperative brain metastasis and the individual management of patients with LUAD after radical resection.
... Growing evidence indicates the association between CEP55 upregulation and the development and progression of a variety of malignant tumors, including breast tumors, gastric tumors, and lung tumors [13][14][15]. The knockdown of CEP55 can significantly inhibit the viability and proliferation of a tumor cell and even lead to tumor cell death [16,17]. ...
... It plays a critical role in regulating the physical cytokinesis [20]. CEP55 upregulation was previously reported to promote the migration and invasion of tumor cells and is related to the dismal prognosis for lung cancer [16], breast cancer [21], oral squamous cell carcinoma [22], cervical cancer [23], and osteosarcoma [24]. Such finding was consistent with our findings in liver cancer. ...
Purpose. This study was performed to investigate the association of CEP55 expression with liver cancer and explore potential underlying mechanisms. Materials and Methods. Data obtained from The Cancer Genome Atlas (TCGA) was used to investigate CEP55 expression, its prognostic value, the potential mechanisms of its upregulation, CEP55-related pathways, and its biological functions in liver cancer. Data from Gene Expression Omnibus (GEO) and International Cancer Genome Consortium (ICGC) was used to validate survival analysis. The correlation between CEP55 and tumor-infiltrating immune cells (TIICs) in liver cancer was determined by using Tumor Immune Estimation Resource (TIMER). Results. CEP55 was significantly overexpressed in the liver tumor sample compared to the adjacent normal liver sample. High CEP55 expression was significantly associated with histological grade, advanced stages, histological type, high T classification, and survival status. High CEP55 expression was significantly related to dismal prognosis compared with low CEP55 expression, which was validated by the GSE54236 dataset and ICGC database. Meanwhile, CEP55 was identified as the risk factor to independently predict overall survival (OS) for patients with liver cancer upon multivariate analysis. Enrichment analysis indicated that cell cycle, DNA replication, pathways in cancer, mTOR signaling pathway, and VEGF signaling pathway were significantly enriched in the high CEP55 expression group. In addition, the CEP55 expression was significantly related to the infiltration level of B cells, CD4+ T cells, CD8+ T cells, macrophages, neutrophils, and dendritic cells in hepatocellular carcinoma (HCC). CEP55 methylation level was negatively correlated to its mRNA expression. And patients with CEP55 hypermethylation and low expression can achieve a better prognosis than those with CEP55 hypomethylation and high expression. Conclusion. CEP55 may serve as a candidate treatment target for it is a determinant of prognosis and immune infiltration in liver cancer patients. DNA hypomethylation might contribute to the overexpression of CEP55 in liver cancer.
1. Introduction
Liver cancer ranks the 6th place in terms of global tumor incidence, and it is the 4th leading cause of cancer-related deaths [1]. Hepatocellular carcinoma (HCC), one of the frequently seen primary liver tumors, occupies about 80% of liver cancers, followed by cholangiocarcinoma (CCA), accounting for approximately 15%. Worldwide, the highest liver cancer morbidity is reported in Asia and Africa. Approximately 75% of liver cancer occurs in Asia, and China accounts for more than half of the total cases in the world. Aflatoxin exposure and chronic hepatitis B virus (HBV) infection are two major risk factors reported across most high-incidence countries in Asia and Africa [2]. Although great progresses have been achieved in diagnosing and treating liver tumor over the past few decades, prognosis for liver tumor remains dismal. Liver cancer has become the second most fatal tumor after pancreatic cancer with a 5-year survival rate of 18% [3]. Finding reliable predictors and potential therapeutic targets involved in the occurrence and development of liver cancer is urgently needed.
Centrosome proteins have long been considered to be scaffold proteins that regulate mitotic spindle and microtubule tissue, so they are essential to the cell cycle process [4]. Centrosome protein 55 (CEP55), also referred as FLJ10540 and C10orf3, was initially recognized as a key component of abscission, which is the final stage of cytoplasmic division that is responsible for regulating the physical disjunction of two daughter cells [5]. CEP55 is located in the centrosome during the whole cell cycle, in the mitotic spindle during mitosis, and in the midbody during the process of cytokinesis [6]. Cytokinesis is strictly controlled in the process of cell division and requires the recruitment of multicomponent subunits to the midbody in a CEP55-dependent manner [4, 7, 8]. CEP55 has been identified both as a cancer testis antigen and a tumor-associated antigen [9, 10]. Cancer testis antigens are proteins normally expressed predominantly in the testes but which become more widely expressed in cancer [11]. Recently, some literature reported that CEP55 participated in promoting tumorigenesis and regulating the PI3K/AKT signaling pathway [12, 13]. Growing evidence indicates the association between CEP55 upregulation and the development and progression of a variety of malignant tumors, including breast tumors, gastric tumors, and lung tumors [13–15]. The knockdown of CEP55 can significantly inhibit the viability and proliferation of a tumor cell and even lead to tumor cell death [16, 17].
Though Li et al. [18] previously reported that the overexpression of CEP55 can result in poor prognosis of liver patients, their study is limited to HCC. In this study, we included both HCC and CCA patients from The Cancer Genome Atlas (TCGA) to investigate the prognostic significance of CEP55 expression and DNA methylation of CEP55 in liver cancer. The biological functions and signal pathways associated with CEP55 regulatory mechanism were also explored. In addition, we investigated the correlation between CEP55 and tumor-infiltrating immune cells (TIICs) in liver cancer using Tumor Immune Estimation Resource (TIMER).
2. Materials and Methods
2.1. Data Mining and Collection
A flow chart of our study design is showed in Figure 1. The gene expression profile data, DNA methylation data, and the clinical information of liver cancer patients had been collected from TCGA (https://cancergenome.nih.gov/). The clinical data included age, sex, survival time, survival status, clinical stage, histological grade, TNM classification, and histological type. Additionally, gene expression data of liver cancer patients with survival information was downloaded from the International Cancer Genome Consortium (ICGC) (http://icgc.org/). And GSE54236 dataset was obtained from the Gene Expression Omnibus (GEO) (https://www.ncbi.nlm.nih.gov/geo/). The expression levels of CEP55 in several common cancers were reviewed by using the TIMER database (https://cistrome.shinyapps.io/timer/). The CEP55 protein expression in normal liver samples and liver cancer samples was examined using immunohistochemistry (IHC) data from the Human Protein Atlas (HPA) database (http://www.proteinatlas.org/).
... 5 It has been found that CEP55 is expressed in both normal tissues and tumor cells and coupled with centrosomes and intermediates in the cell cycle which plays a role in regulating cell cycle after phosphorylation. 6,7 In addition, CEP55 overexpression has been shown to be significantly correlated with tumor staging, invasiveness and metastasis of many malignant tumors, 7,8 and can be used as a biomarker for tumor occurrence, progression and prognosis. ...
... 5 It has been found that CEP55 is expressed in both normal tissues and tumor cells and coupled with centrosomes and intermediates in the cell cycle which plays a role in regulating cell cycle after phosphorylation. 6,7 In addition, CEP55 overexpression has been shown to be significantly correlated with tumor staging, invasiveness and metastasis of many malignant tumors, 7,8 and can be used as a biomarker for tumor occurrence, progression and prognosis. ...
Objective
This study aims to explore whether miR-195-5p can inhibit proliferation and induce apoptosis of non-small cell lung cancer (NSCLC) cells by targeting CEP55.
Methods
qRT-PCR was used to measure the expression of miR-195-5p in NSCLC cells. MTT assay, colony formation assay, and flow cytometry were used to detect the role of miR-195-5p in NSCLC cells. Western blot was used to measure the protein expression of CEP55, Bax and Bcl-2 in cells. Dual-Luciferase assay was performed to verify the relationship between miR-195-5p and CEP55.
Results
The expression of miR-195-5p was higher in human normal lung cell lines than in NSCLC cells. MiR-195-5p overexpression inhibited cell proliferation, which could block the cell cycle of A549 cell line in the G0/G1 phase. Moreover, overexpression of miR-195-5p increased cell apoptotic rate of A549 cell lines, with the expression of pro-apoptotic protein Bax up-regulated and that of the anti-apoptotic protein Bcl-2 down-regulated. The Dual-Luciferase assay showed that miR-195-5p could specifically target CEP55. Furthermore, CEP55 was down-regulated in NSCLC cells. Overexpression of CEP55 enhanced the proliferation and colony formation ability of A549 cell line. Overexpression of CEP55 can reverse the inhibitory effect of miR-195-5p.
Conclusion
MiR-195-5p inhibits proliferation and induces apoptosis of NSCLC cells by negatively regulating CEP55.
