Objective: LncRNAs are non-coding RNAs exerting vital roles in the occurrence and development of various cancer types. This study tended to describe the expression pattern of FENDRR in colorectal cancer (CRC), and further investigate the role of FENDRR in CRC cell biological behaviors. Methods: Gene expression profile of colon cancer was accessed from the TCGA database, and then processed for differential analysis for identification of differentially expressed lncRNAs and miRNAs. Some in vitro experiments like qRT-PCR, MTT, colony formation assay, wound healing assay and Transwell assay were performed to assess the effect of FENDRR on cell biological behaviors. Dual-luciferase reporter assay was conducted to further validate the targeting relationship between FENDRR and miR-424-5p, and rescue experiments were carried out for determining the mechanism of FENDRR/miR-424-5p underlying the proliferation, migration and invasion of CRC cells. Results: Bioinformatics analysis suggested that FENDRR was significantly down-regulated in CRC tissue, and low FENDRR was intimately correlated to poor prognosis. FENDRR overexpression could greatly inhibit cell proliferation, migration and invasion. Besides, there was a negative correlation between FENDRR and miR-424-5p. Dual-luciferase reporter assay indicated that miR-424-5p was a direct target of FENDRR. Rescue experiments discovered that FENDRR exerted its role in cell proliferation, migration and invasion in CRC via targeting miR-424-5p. Conclusion: FENDRR is poorly expressed in CRC tissue and cells, and low FENDRR is responsible for the inhibition of cell proliferation, migration and invasion of CRC by means of targeting miR-424-5p.

Objectives. This study investigated the functional mechanism of transmembrane protein 100 (TMEM100) as a tumor inhibitor gene in CRC cells and offered a reference for the treatment of CRC. Methods. The mRNA expression data of CRC were acquired from the TCGA database to mine differentially expressed mRNAs. The role of TMEM100 in the progression of CRC cells was evaluated by MTT, colony formation, scratch healing, and Transwell assays. The influence of TMEM100 on the TGF-β signaling pathway was detected by western blot. Results. TMEM100 was markedly lowly expressed in CRC. CRC cell growth was significantly suppressed by overexpressing TMEM100 but noticeably facilitated by silencing TMEM100. Overexpression of TMEM100 inhibited the activation of the TGF-β signaling pathway, thus inhibiting malignant progression of CRC. Conclusion. TMEM100 is lowly expressed in CRC, which can suppress CRC cell growth by regulating the TGF-β signaling pathway.

Objectives: Colon cancer (CC) is the third largest cancer worldwide. Investigation of the molecular mechanism of CC progression helps to explore novel therapeutic targets. We attempted to understand the modulatory mechanism of miR-142-3p in CC cell autophagy and CC progression, which will lay a theoretical groundwork for seeking potential diagnostic and therapeutic targets for CC. Methods: Through bioinformatics methods, miRNA expression data were subjected to differential analysis for identification of target miRNA. Downstream target mRNAs were predicted and gene set enrichment analysis (GSEA) was completed. qRT-PCR assessed gene expression in cells. Cell Counting Kit-8, cell doubling time calculation, colony formation, and flow cytometry were used to assess cellular biological functions. Dual-luciferase assay was used for targeting relationship validation of the target miRNA and mRNA. Western blot was performed to evaluate expression of proteins related to HEDGEHOG signaling pathway and autophagy. Results: miR-142-3p was markedly highly expressed in CC, and high miR-142-3p expression in CC patients was implicated with relatively poor prognosis. Over-expressing miR-142-3p facilitated proliferation and inhibited apoptosis of CC cells, whereas silencing it produced an opposite result. miR-142-3p targeted and decreased TP53INP2 level. TP53INP2 over-expression suppressed the HEDGEHOG signaling pathway and induced the activation of CC cell autophagy. Rescue experiments revealed that influence of miR-142-3p inhibitor on CC cell proliferation and apoptosis could be reversed by silencing TP53INP2. Conclusion: miR-142-3p hampered tumor cell autophagy and promoted CC progression via targeting TP53INP2, which will offer a fresh research orientation for the diagnosis of CC.

Colon cancer is a kind of common intestinal disease, and early diagnosis of colon cancer is crucial for patient’s prognosis. RNA alternative splicing (AS) is an RNA modification that affects cancer occurrence. RNA AS detection is promising to improve the in-depth understanding of the pathological mechanisms in colon cancer. In this study, differential analysis was performed to determine colon cancer-related AS events and the corresponding parental genes. Subsequently, GO functional annotation analysis was carried out on the parental genes, which revealed that these AS events might affect cell adhesion and cell growth. Besides, protein-protein interaction (PPI) network was established with the parental genes, in which MCODE was utilized to identify major functional modules. Enrichment analysis for the major functional module was implemented again, which demonstrated that these genes were mainly concentrated in the ribosome, protein ubiquitination, cell adhesion molecule binding, and other relevant biological functions. Next, differentially expressed genes (DEGs) were screened from colon cancer and normal tissues and overlapped with the parental genes, by which 55 gene expression-associated AS and the corresponding 45 genes were obtained. Moreover, a correlation analysis between splicing factors (SFs) and AS was done to identify interactions. On this basis, an SF-AS network was constructed. The univariate Cox regression analysis was employed to screen prognostic AS signature and establish a risk model. To assess the model, K-M and ROC analyses were done for model assessment, indicating the effective prediction performance. Combined with common clinicopathological features, the multivariate Cox regression analysis was conducted to confirm whether the risk model could be considered as an independent prognostic indicator. Finally, the expression status of the parental genes for the prognostic AS was evaluated between normal and colon cancer cells using qRT-PCR. In summary, TCGA SpliceSeq data were comprehensively analyzed, and a 5-AS prognostic model was constructed for colon cancer.