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Introduction: the predictive value for survival outcomes and mechanisms of the CXCL gene family in kidney Clear Cell Carcinoma (KIRC).Objective: We evaluated the predictive value for survival outcomes and mechanisms of the CXCL gene family in Kidney Clear Cell Carcinoma (KIRC). Methods: Transcriptional and survival data of CXCL genes in KIRC patients were retrieved from Oncomine and GEPIA databases to assess their functions. Mutations’ data were downloaded from the cBioPortal, while immune cell components data were obtained from TIMER databases. Enrichment analysis was performed using the STRING database. In vitro assays were performed to validate our findings. Results: A total of 8 CXCL (CXCL2/5/9/10/11/12/13/16) genes were found to be differentially expressed in KIRC tissues. Among them, only CXCL2 and CXCL5 had survival values. In vitro assays revealed that upregulated CXCL2 promotes renal cancer cell proliferation, migration and invasion. Additionally, CXCL2 exhibited an effect on three KIRC immune cell components (B cells, CD4 T cells, and Neutrophils). After evaluating the miRNA sequences upstream of CXCL2, it was established that hsa-miR-532-5p/CXCL2 pathways are potentially involved in the regulatory mechanisms. Finally, we established a prospective signature (CXCL1/5/13) for improved survival outcomes among KIRC patients.Conclusion: Among KIRC patients, 8 CXCL genes were differentially expressed, however, only CXCL2 and CXCL5 exhibited a significant survival value. Upregulated CXCL2 promotes renal cancer cell progression.

Objective. Regarding the imperfect mechanism of occurrence and development of prostate adenocarcinoma (PRAD), this study investigated mRNA-modified FUS/NRF2 signalling to inhibit ferroptosis and promote prostate adenocarcinoma growth. Methods. Bioinformatics analysis was used to obtain the expression of FUS and its mRNA modification in PRAD. The expression of FUS in prostate cells (CRPC) and the level of m6A methylation modification, ferroptosis (P53 and GPX4), apoptosis (Caspase3), ferroptosis (P53 and GPX4), and apoptosis (Caspase3) in CRPC after ferroptosis inducer Erastin, ferroptosis inhibitor, and FUS knockdown were detected. Autophagy (LC3B), oxidative stress (GSH and ROS), and expression of NRF2/HO-1 pathway are indicators. Results. FUS was highly expressed in PRAD and phenomenally reduced the survival rate of patients. After knocking down FUS, the level of m6A methylation was significantly reduced, and the expressions of ferroptosis markers P53 and GPX4 were phenomenally reduced, while the levels of apoptosis and autophagy markers Caspase3 and LC3B remained unchanged. Upregulated and NRF2/HO-1 pathway indicators were upregulated. It shows that m6A methylation modification is reduced when FUS is the low expression, inhibits the expression of P53 and GPX4, downregulates GSH, upregulates ROS, activates the NRF2/HO-1 pathway, and promotes ferroptosis to inhibit the occurrence of RPAD. Conclusions. The increase of m6A methylation modification can increase the expression of FUS, thereby promoting the expression of P53 and GPX4, upregulating GSH, downregulating ROS, inhibiting the NRF2/HO-1 pathway, inhibiting ferroptosis, and promoting the growth of PRAD.

Purpose. Recent research has indicated that the calcium-binding protein S100A16 promotes carcinogenesis and tumor growth in several forms of cancer. The objective of this study was to examine the relationship between S100A16 and renal cell cancer. Methods. By using The Cancer Genome Atlas (TCGA) database, the differentially expressed gene S100A16 was identified, and its appearance and link to the prognosis of persons with renal cancer were confirmed. Cox regression was used in multivariate analysis, and a nomogram was developed for internal validation. The correlation between S100A16 and immune cells was analyzed in the TIMER database. Moreover, the potential mechanism of action was investigated utilizing GO and KEGG enrichment analyses. Proliferation, migration, and angiogenesis were investigated in vitro, and the involvement of S100A16 in the undesirable biological events of renal cell carcinoma (RCC) was further explored. Results. S100A16 was the differentially expressed molecule identified through database screening. Malignant tissues showed higher S100A16 expression than noncancerous tissues, and S100A16 expression was mostly localized in the cytoplasm. According to the TCGA and KM-plotter datasets, patients with RCC and low S100A16 expression had superior OS, PFI, and DSS. The C-index of the nomogram was 0.754 (0.726–0.782), and the accuracy of the prediction model was high. The TIMER database shows that the expression of S100A16 is associated with immune infiltration and may play an important role in promoting tumor cell immune escape in the RCC tumor microenvironment. S100A16 may influence the biological processes of RCC via the VEGF/VEGFR2 signaling route and PI3K-Akt signaling pathway and through P53 alteration and cell cycle according to the gene enrichment technique. In vitro cytological experiments demonstrated that S100A16 knockdown can inhibit the proliferation and migration of renal cancer cells and the expression levels of VEGF, VEGFR2, and phosphorylated AKT within renal cancer cells, thereby inhibiting angiogenesis in renal cancer cells and resulting in a poor prognosis of RCC. Conclusion. A decrease in S100A16 expression may dramatically increase the OS, PFI, and DSS of patients with RCC and may thus be used as a biomarker for predicting RCC. It may be associated with the immune infiltration of RCC and play a crucial role in the immune evasion of tumor cells within the RCC microenvironment. Intervention of s100a16 can promote the progression and angiogenesis of renal cell carcinoma through the VEGF/VEGFR2 signal transduction pathway and lead to poor prognosis of renal cell carcinoma. These findings suggest a potential target for the development of anticancer strategies for renal cancer.