The aim of the present study was to explore the mechanism by which microRNA (miR)-642a-5p regulates the migration and invasion of colon cancer cells via collagen type I α1 (COL1A1). The characteristics of miR-642a-5p and COL1A1 were analysed through bioinformatics. Cancer and normal tissues were collected from patients with colon cancer. miR-642a-5p- and COL1A1-overexpressing cell lines were constructed by transfection. A Dual-luciferase reporter assay was used to verify the targeting of COL1A1 by miR-642a-5p. Cell Counting Kit-8, wound healing and Transwell assays were used to detect cell viability, migration and invasion, respectively. Protein and mRNA expression levels were examined by western blotting and reverse transcription-quantitative PCR, respectively. The results revealed that miR-642a-5p expression was significantly upregulated and COL1A1 expression was downregulated in patients with colon cancer. Low levels of miR-642a-5p and high levels of COL1A1 were associated with a poor prognosis in patients with colon cancer. miR-642a-5p directly targeted the 3′-untranslated region of COL1A1 and inhibited COL1A1 expression. Overexpression of miR-642a-5p inhibited cell viability, migration, invasion and epithelial mesenchymal transition. Overexpression of COL1A1 promoted cell viability, migration, invasion and EMT, and partially reversed the inhibitory effects of miR-642a-5p on colon cancer cells. In conclusion, miR-642a-5p inhibited colon cancer cell migration, invasion and EMT by regulating COL1A1.

Aim This research aimed at clarifying the intracellular effect of SERPINE1 in the progression of colon adenocarcinoma (COAD) and the underlying mechanism. Methods We obtained the expression profile of SERPINE1 in COAD via the Starbase database and verified it on COAD tissue samples through qRT-PCR and immunoblotting, respectively. Also, miRWalk, TargetScan and miRDB databases were adopted to generate the miRNA prediction that might target SERPINE1, and the gene target miR-148a-3p was confirmed using dual-luciferase assays. The effect of SERPINE1 and miR-148a-3p on COAD was further evaluated by cell experiments. MTT assay was used to detect the change of cell proliferation ability. The invasive and migratory capability of COAD cells was examined using transwell and would healing assays. Cell apoptosis was determined through flow cytometry. The expressions of genes and EMT-associated proteins were evaluated by qRT-PCR and immunoblotting. Further lucubration of the biological relevance of SERPINE1 and miR-148a-3p was conducted using rescue experiments. Results We found that the expression quantities of SERPINE1 in COAD tissues and cell lines were higher than those in corresponding non-cancerous tissues and normal cells. When SERPINE1 expression is reduced, EMT process is inhibited, invasion and proliferation ability of COAD cells are obviously reduced, and apoptosis level is increased. Moreover, SERPINE1 was identified as the target gene of miR-148a-3p. When the expression of miR-148a-3p was enhanced, it was found that the expression of SERPINE1 was reduced. miR-148a-3p played the similar effect of si-SERPINE1 that suppressed the COAD progression. Additionally, we found out that SERPINE1 is validated in hindering the tumor healing effect of miR148a-3p in COAD, including cell growth and invasion. Conclusion Our study suggests that SERPINE1/miR-148a-3p axis has potential as prognostic markers of COAD and provides reference for the development of new therapies.

Background：Gastric cancer (GC) is one of the most principle malignant cancers in the digestive system. Moreover, the critical role of circular RNAs (circRNAs) has been identified in GC development. Methods：In this context, the purpose of research was to explore the regulatory mechanism circ_0001013, a novel circRNAs predicted by our research, in GC. The differential circRNAs and related mechanism in GC were predicted by microarray analysis. Circ_0001013, miR-136, and TWSG1 expression in GC clinical samples and cells was detected by RT-qPCR. The relationship among circ_0001013, miR-136, and TWSG was assessed by dual-luciferase reporter assay, biotin coupled probe pull-down assay, and biotin coupled miRNA capture. After gain- and loss-of-function assays in GC cells, cell proliferation, migration, invasion, and cell cycle and apoptosis were measured by EdU assay, scratch test, Transwell assay, and flow cytometry respectively. The effect of circ_0001013 on tumor growth was detected by xenograft tumor in nude mice. Results ：Microarray analysis predicted a novel circRNA, circ_0001013, was upregulated in GC, which was confirmed by RT-qPCR detection in GC tissues and cells. Besides, miR-136 was downregulated but TWSG1 was highly expressed in GC tissues. Mechanically, circ_0001013 could bind to miR-136, and miR-136 negatively targeted TWSG1 in GC cells. Silencing circ_0001013 or TWSG1 or overexpressing miR-136 decreased GC cell proliferation, migration, invasion, and cell cycle arrest and accelerated cell apoptosis. Circ_0001013 silencing decreased TWSG1 expression and inhibited transplanted tumor growth in nude mice. Conclusion：Circ_0001013 elevated TWSG1 expression by binding to miR-136, thereby exerting oncogenic effect in GC.

To investigate the mechanism by which ginsenoside Rg3 regulates oxidative stress (OS) and inflammation through NF/KB pathway to delay mouse liver injury. This work randomized Balbc mice as four groups: Normal, D-gal, Rg3-L, Rg3-H. Paraffin-embedded liver tissue sections were prepared, later, BAX/BCL-2 protein expression was observed by HE, Sirius red, TUNEL and immunofluorescence to detect apoptotic injury and α-SMA/TGF-β protein expression to detect fibrosis, and liver inflammation-related protein NF-KB was detected. HE and TUNEL staining showed that Rg3 reduced necrotic cells and fibrosis in liver-injured mice, Rg3 increased anti-inflammatory cytokine IL-18 and reduced TNF-α, IL-1β and IL-6 expression. Conclusion: Ginsenoside Rg3 can effectively antagonize D-gal's role in mouse liver injury, and its mechanism may be associated with regulating inflammatory pathway by Rg.

Background：Gastric cancer (GC) is one of the most principle malignant cancers in the digestive system. Moreover, the critical role of circular RNAs (circRNAs) has been identified in GC development. Methods：In this context, the purpose of research was to explore the regulatory mechanism circ_0001013, a novel circRNAs predicted by our research, in GC. The differential circRNAs and related mechanism in GC were predicted by microarray analysis. Circ_0001013, miR-136, and TWSG1 expression in GC clinical samples and cells was detected by RT-qPCR. The relationship among circ_0001013, miR-136, and TWSG was assessed by dual-luciferase reporter assay, biotin coupled probe pull-down assay, and biotin coupled miRNA capture. After gain- and loss-of-function assays in GC cells, cell proliferation, migration, invasion, and cell cycle and apoptosis were measured by EdU assay, scratch test, Transwell assay, and flow cytometry respectively. The effect of circ_0001013 on tumor growth was detected by xenograft tumor in nude mice. Results ：Microarray analysis predicted a novel circRNA, circ_0001013, was upregulated in GC, which was confirmed by RT-qPCR detection in GC tissues and cells. Besides, miR-136 was downregulated but TWSG1 was highly expressed in GC tissues. Mechanically, circ_0001013 could bind to miR-136, and miR-136 negatively targeted TWSG1 in GC cells. Silencing circ_0001013 or TWSG1 or overexpressing miR-136 decreased GC cell proliferation, migration, invasion, and cell cycle arrest and accelerated cell apoptosis. Circ_0001013 silencing decreased TWSG1 expression and inhibited transplanted tumor growth in nude mice. Conclusion：Circ_0001013 elevated TWSG1 expression by binding to miR-136, thereby exerting oncogenic effect in GC.