LncRNA IGFL2-AS1 Promotes the Proliferation, Migration, and Invasion of Colon Cancer Cells and is Associated with Patient Prognosis.

BACKGROUND: LncRNAs play an important role in tumor initiation and development. However, the underlying involvement of lncRNA expression in colorectal carcinoma remains to be clarified. METHODS: All analyses were performed in R software v4.0, SPSS v13.0, and GraphPad Prism 8. The "limma" package was used to identify differentially expressed lncRNAs between two groups with the threshold of |logFC| >1 and P <0.05. The "Survival" package was used to conduct survival analysis. HCT8 and SE480 cell lines were used to conduct further phenotype experiments, including transwell, wound-healing, CCK8 and colony formation assay. Gene set enrichment analysis was used to explore the biological pathway difference in high and low IGFL2-AS1 patients. RESULTS: The lncRNA IGFL2-AS1 was highly expressed in colon adenocarcinoma (COAD) tissue and cell lines (HCT116, HCT8, HCT129, and SW480). The COAD patients with high IGFL2-AS1 were associated with a worse prognosis. Meanwhile, the knockdown of IGFL2-AS1 could significantly suppress the proliferation and invasion of COAD cells. Gene set enrichment analysis showed that the top five biological pathways involving IGFL2-AS1 were angiogenesis, epithelial-mesenchymal transition, KRAS signaling, myogenesis, and coagulation. Western blot results showed that the inhibition of IGFL2-AS1 could significantly reduce the N-cadherin, HIF1A and KRAS protein expression, yet increase the E-cadherin protein level. IGFL2-AS1 was also positively correlated with M0 macrophages, M2 macrophages, and neutrophils but negatively correlated with CD4+ memory T cells and CD8+ T cells. CONCLUSION: IGFL1-AS1 could seriously worsen patient outcomes and facilitate COAD progression, thus serving as an independent tumor marker.

Association of cytotoxic T lymphocyte-associated protein 4 gene -1772T/C polymorphism with gastric cancer risk: A prisma-compliant meta-analysis.

BACKGROUND: We performed a meta-analysis to more precisely evaluate the association between the cytotoxic T lymphocyte-associated protein 4 (CTLA-4) -1772T/C polymorphism and overall gastric cancer (GC) risk and the influence of ethnicity and the source of controls on that association. METHODS: A systematic literature search was performed in PubMed, EMBASE, the Cochrane Library, Web of Science (WOS) Database, Chinese National Knowledge Infrastructure (CNKI), China biomedical literature database (CBM), Wanfang database, and VIP. Two investigators independently reviewed the articles, and disagreements were resolved by discussion and consensus. The odds ratio (OR) with 95% confidence intervals (CIs) was used to assess the strength of the association between the CTLA-4 -1722T/C polymorphism and GC risk, based on the genotype frequencies in cases and controls. The meta-analyses were performed with Stata 12.0, using two-sided P values. Trial sequential analysis (TSA) was calculated by TSA Software. RESULTS: Overall, we identified 5 studies including 1039 GC cases and 2136 controls that evaluated the association of the CTLA-4 -1722T/C polymorphism and GC risk. Overall, there was no significant association between the CTLA-4-1722T/C polymorphism and the risk of GC. In the subgroup analysis based on ethnicity, the results showed that the relationship between the CTLA-4 -1722T/C polymorphism and GC susceptibility was strongest in the Chinese population rather than in the Iranian population (TC vs CC: OR = 1.405, 95% CI: 1.100-1.796, P = .007; TC+TT vs CC: OR = 1.329, 95% CI: 1.052-1.680, P = .017). Then, there was a significant association between the CTLA-4 -1722T/C polymorphism and the risk of GC in studies with HB controls. However, the above correlation can only be reflected in specific populations and gene models. Therefore, we believe that the evidence of this correlation is insufficient. CONCLUSION: Our meta-analysis showed that the CTLA-4 -1722T/C polymorphism may be associated with the susceptibility to GC. However, the slight correlation can only be reflected in specific populations and gene models. Therefore, we believe that this association is negligible. The large and well-designed case-control studies are needed to validate our findings.

Exosomal linc-FAM138B from cancer cells alleviates hepatocellular carcinoma progression via regulating miR-765.

Exosomes are small vesicles with a diameter of 30-150 nm secreted by cells, which can be used as signal carriers to transfer nucleic acids, proteins, lipids and other functional substances to the recipient cells and play a role in cell communication. Hepatocellular carcinoma is the fourth most common cause of cancer-related death worldwide. Studies have shown that long non-coding RNAs (lncRNAs) are involved in the development and progression of many types of tumors. Our present study found that linc-FAM138B was reduced in HCC tissues and cell lines, low expression of linc-FAM138B indicated a poor prognosis in HCC patients. Interestingly, linc-FAM138B could be packaged into cancer cells. And exo-FAM138B inhibited the proliferation, migration and invasion of HCC cells. Furthermore, linc-FAM138B sponged miR-765 levels. And exo-si-FAM138B promoted HCC progression, while deletion of miR-765 reversed the role of exo-si-FAM138B. In vivo tumorigenesis experiments showed that exo-FAM138B suppressed HCC growth via modulating miR-765. In conclusion, exo-linc-FAM138B secreted by cancer cells inhibited HCC development via targeting miR-765, which provided a new idea and perspective for in-depth understanding of the complex signal regulation in HCC process.