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YBX1 had significantly higher expression levels in colorectal cancer tumor tissues than in normal tissues. YBX1 mRNA expression levels in 17 paired clinical samples (A), TCGA database (B, C), and the GEO database (GSE113513 and GSE44076) (D–F).
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Background:
Colorectal cancer is one of the most common malignant digestive tract tumors with a poor prognosis. RNA 5-methylcytosine (m5 C) is an important posttranscriptional widespread modification involved in many biological processes. However, the association between genetic variations of m5 C modification genes and the prognostic value of col...
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Background
Mucosal melanoma is rare and has distinct clinical and genetic features. Even with advances in targeted and immune therapy, the survival of patients with advanced or recurrent mucosal melanomas remains poor. The standard treatment remains controversial and we conducted this real-world study aimed to test continuous intravenous Endostar i...
Citations
... 48 Studies have suggested that genetic variations could regulate cancer prognosis by affecting gene expression levels. 49 In this study, we found irinotecan-based chemotherapy was markedly correlated to decreased PFS and OS of patients with CC/CT genotype of rs4288573. In the stratified analysis of patients treated with irinotecan chemotherapy, we also found that smokers with CC/CT genotype of rs4288573 had lower OS and PFS. ...
Background
Primary cilia are antenna‐like organelles that conduct physical and chemical signals, which affect cell proliferation, migration, and differentiation. Some researchers have reported the correlation between primary cilia‐related genes and prognosis of colorectal cancer (CRC).
Methods
The association between single nucleotide polymorphisms (SNPs) of primary cilia‐related genes and outcome after the first‐line chemotherapy was explored by the Cox regression model. Expression qualitative trait locus (eQTL) analysis was performed to explore the impact of SNPs on gene expression. Tumor Immune Estimation Resource and TISIDB databases were used for investigating the relevance between ODF2L and tumor infiltration immune cells and immunomodulators.
Results
We identified that rs4288473 C allele of ODF2L had poor progression‐free survival (PFS) and overall survival (OS) of CRC patients in the additive model (adjusted HR PFS = 1.39, 95% CI = 1.14–1.70, p = 1.36 × 10 ⁻³ , and adjusted HR OS = 1.31, 95% CI = 1.03–1.65, p = 2.62 × 10 ⁻² ). The stratified analysis indicated that rs4288573 CC/CT genotype was involved with poor prognosis in the irinotecan‐treated subgroup ( P PFS = 1.03 × 10 ⁻² , P OS = 3.29 × 10 ⁻³ ). Besides, ODF2L mRNA expression level was notably up‐regrated in CRC tissues. The C allele of rs4288573 was notably related to higher ODF2L mRNA expression levels based on eQTL analysis. Functionally, knockdown of ODF2L inhibited cell proliferation and decrease the chemoresistance of HCT‐116 and DLD‐1 cells to irinotecan.
Conclusion
Our study indicates that rs4288573 in ODF2L is a potential predictor of the chemotherapy prognosis of CRC.
... Results: Among the five analyzed SNPs, NOL1 rs3764909 and NSUN4 rs10252 variants significantly increased the susceptibility of pediatric ALL, while NSUN3 rs7653521, NSUN5 rs1880948, and NSUN6 rs3740102 variants were not associated with the risk of ALL. Stratification analyses demonstrated that NOL1 rs3764909 C>A exhibited a significant association with increased pediatric ALL risk in subgroups of common B ALL, pre-B ALL, T-cell ALL, low and middle risk, other gene fusion types, non-gene fusion, hypodiploid, normal diploid, primitive lymphocytes in marrow < 5% on week 12, and minimal residual disease (MRD) <0.01% on week 12 after induced therapy; NSUN4 rs10252 G>A was related to increased risk of ALL children in subgroups of age ≥ 120 months, normal white blood cell (WBC) number, middle risk, nongene fusion, MRD ≥ 0.01 on days [15][16][17][18][19], and primitive lymphocytes in marrow < 5% on day 33 after induced therapy. Compared with the reference haplotype Introduction Acute lymphoblastic leukemia (ALL) is the most common malignant tumor in children and adolescents (1)(2)(3). ...
... Chen and Cao et al. performed a case-control study and verified that m5C modification genes were related to survival and chemotherapy efficacy of colorectal cancer. Two SNPs of YBX1 gene, rs10890208 and rs3862218, may predict a reduction by using the Cox regression model to analyze the association between 13 candidate SNPs of m5C modifier gene and overall survival (OS) of colorectal cancer (CRC) after chemotherapy (17). However, the role of SNPs in the m5C methyltransferase gene in ALL risk has not been reported. ...
... There is only one available study on the epidemiological assessment of SNPs in the m5C modification core gene and cancer. In July of this year, a case-control study was performed and revealed that two SNPs of YBX1 gene, rs10890208 and rs3862218, may predict a reduction by using the Cox regression model to analyze the association between 13 candidate SNPs of the m5C modifier gene and OS of CRC after chemotherapy (17). ...
Objective
To explore the functions of the polymorphisms in 5-methylcytosine (m5C) modification-related coding genes on the susceptibility of pediatric acute lymphoblastic leukemia (ALL).
Methods
Case–control study and multinomial logistic regression analysis were performed to construct models to evaluate the susceptibility of pediatric ALL. The relationship between five functional SNPs in m5C modification-coding genes and pediatric ALL risk was analyzed. Genotyping of 808 cases and 1,340 healthy samples from South China was identified using a TaqMan assay; odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the relationship between the five selected SNPs and pediatric ALL susceptibility.
Results
Among the five analyzed SNPs, NOL1 rs3764909 and NSUN4 rs10252 variants significantly increased the susceptibility of pediatric ALL, while NSUN3 rs7653521, NSUN5 rs1880948, and NSUN6 rs3740102 variants were not associated with the risk of ALL. Stratification analyses demonstrated that NOL1 rs3764909 C>A exhibited a significant association with increased pediatric ALL risk in subgroups of common B ALL, pre-B ALL, T-cell ALL, low and middle risk, other gene fusion types, non-gene fusion, hypodiploid, normal diploid, primitive lymphocytes in marrow < 5% on week 12, and minimal residual disease (MRD) <0.01% on week 12 after induced therapy; NSUN4 rs10252 G>A was related to increased risk of ALL children in subgroups of age ≥ 120 months, normal white blood cell (WBC) number, middle risk, non-gene fusion, MRD ≥ 0.01 on days 15–19, and primitive lymphocytes in marrow < 5% on day 33 after induced therapy. Compared with the reference haplotype CAGTA, children who harbored haplotypes CCGTG and ACATA were remarkably related to increased ALL susceptibility. rs3764909 and rs10252 varieties of alleles were not associated with MRD levels after the selected chemotherapeutics.
Conclusions
In conclusion, NOL1 rs3764909 and NSUN4 rs10252 variants were enhanced by pediatric ALL risk and were suggested to be potential biomarkers for pediatric ALL.
It is well known that 5‐methylcytosine (m ⁵ C) is involved in variety of crucial biological processes in cancers. However, its biological roles in lung adenocarcinoma (LAUD) remain to be determined. The LUAD samples were used to assess the clinical value of NOP2/Sun RNA Methyltransferase 2 (NSUN2). Dot blot was used to determine global m ⁵ C levels. ChIP and dual‐luciferase assays were performed to investigate the MYC‐associated zinc finger protein (MAZ)‐binding sites in NSUN2 promoter. RNA‐seq was used to explore the downstream molecular mechanisms of NSUN2. Dual luciferase reporter assay, m ⁵ C‐RIP‐qPCR, and mRNA stability assay were conducted to explore the effect of NSUN2‐depletion on target genes. Cell viability, transwell, and xenograft mouse model were designed to demonstrate the characteristic of NSUN2 in promoting LUAD progression. The m ⁵ C methyltransferase NSUN2 was highly expressed and caused elevated m ⁵ C methylation in LUAD samples. Mechanistically, MAZ positively regulated the transcription of NSUN2 and was related to poor survival of LUAD patients. Silencing NSUN2 decreased the global m ⁵ C levels, suppressed proliferation, migration and invasion, and inhibited activation of PI3K‐AKT signaling in A549 and SPAC‐1 cells. Phosphoinositide‐3‐Kinase Regulatory Subunit 2 (PIK3R2) was upregulated by NSUN2‐mediated m ⁵ C methylation by enhancing its mRNA stabilization and activated the phosphorylation of the PI3K‐AKT signaling. The present study explored the underlying mechanism and biological function of NSUN2‐meditated m ⁵ C RNA methylation in LUAD. NSUN2 was discovered to facilitate the malignancy progression of LUAD through regulating m ⁵ C modifications to stabilize PIK3R2 activating the PI3K‐AKT signaling, suggesting that NSUN2 could be a novel biomarker and promising therapeutic target for LUAD patients.
RNA modification plays an important role in epigenetics at the posttranscriptional level, and 5-methylcytosine (m⁵C) has attracted increasing attention in recent years due to the improvement in RNA m⁵C site detection methods. By influencing transcription, transportation and translation, m⁵C modification of mRNA, tRNA, rRNA, lncRNA and other RNAs has been proven to affect gene expression and metabolism and is associated with a wide range of diseases, including malignant cancers. RNA m⁵C modifications also substantially impact the tumor microenvironment (TME) by targeting different groups of immune cells, including B cells, T cells, macrophages, granulocytes, NK cells, dendritic cells and mast cells. Alterations in immune cell expression, infiltration and activation are highly linked to tumor malignancy and patient prognosis. This review provides a novel and holistic examination of m⁵C-mediated cancer development by examining the exact mechanisms underlying the oncogenicity of m⁵C RNA modification and summarizing the biological effects of m⁵C RNA modification on tumor cells as well as immune cells. Understanding methylation-related tumorigenesis can provide useful insights for the diagnosis as well as the treatment of cancer.
