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Background: In this study, we sought to investigate the association between N6-methyladenosine (m6A) RNA methylation-modification patterns and patient prognosis in clear cell renal cell carcinoma (ccRCC) and construct a ccRCC molecular signature according to expressions of m6A-related genes. Methods: First, the clinical data and the transcriptomes of 530 patients with ccRCC were downloaded from The Cancer Genome Atlas (TCGA). The expression patterns of m6A-related genes were extracted, and the differences in m6A-modification patterns between normal and tumor renal tissues were analyzed. To explore the prognostic role of m6A-modification patterns a in ccRCC, the molecular subtypes of ccRCC were identified based on the expression patterns of the m6A-related genes, and survival rates in patients with the different subtypes were compared. According to expressions of m6A-related genes and clinical prognosis data, a prognostic molecular signature was constructed using least absolute shrinkage and selector operation (LASSO)-Cox regression analysis. Results: Among the 13 m6A -related genes identified in this study, 8 (YTHDC1, YTHDF2, HNRNPC, METTL14, ZC3H13, FTO, YTHDC2, and YTHDF1) showed significant expression differences between normal and tumor renal tissues. The molecular subtypes of ccRCC identified according to their expression of the 13 m6A-related genes were associated with differential clinical outcomes. Conclusions: Following TCGA data-mining, different molecular subtypes of ccRCC based on m6A RNA methylation patterns were found to have different prognoses. The molecular signature constructed according to the expression patterns of m6A-related genes could predict patient prognosis in ccRCC. We believe m6A RNA methylation modification is a potential therapeutic target and may play a crucial role in ccRCC.
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OBJECTIVE: Previous research showed that ALG3 was associated with several cancers, but the function of ALG3 in bladder cancer (BC) was yet unknown. The purpose of this study was to investigate the relative expression of ALG3 in BC tissues and corresponding normal tissues and the relationship between the relative expression of ALG3 and clinical outcome in bladder cancer patients. METHODS: In this study, the expression of ALG3 in bladder cancer was detected by immunochemistry. In order to determine the cell proliferation and migration ability more accurately, we performed colony forming assay, MTT assay and wound healing migration assay. The role of ALG3 on tumor growth and metastasis was explored by animal model in vivo. RESULTS: ALG3 was expressed higher in bladder cancer than that in the normal tissues (P<0.05). At the same time, we found that there was a positive correlation between ALG3 expression and the prognosis (P<0.05). Moreover, we also discovered that the expression of ALG3 was associated with clinical pathological features (P<0.05). The proliferation and migration abilities of bladder cancer cell line T24 and 5637 were inhibited by silencing ALG3. In addition, the growth of bladder cancer cell line T24 cells were inhibited by silencing ALG3 in vivo. CONCLUSION: Silencing ALG3 plays a critical role in bladder cancer development and growth. It inhibits bladder cancer cells growth in vitro and in vivo.