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Long intergenic noncoding RNA00265 promotes proliferation of gastric cancer via the microRNA-144-3p/Chromobox 4 axis.

ABSTRACT: The expression and biological function of long intergenic noncoding RNA00265 (LINC00265) in gastric cancer (GC) have not yet been explored. This study aimed to detect LINC00265 expression in GC tissues and cell lines, investigate its roles in the proliferation of GC cells in vitro, and elucidate the regulatory mechanisms of LINC00265 action. It was found that LINC00265 expression was significantly upregulated in GC tissue samples and cell lines compared with their normal counterparts. Additionally, LINC00265 knockdown could inhibit GC cell proliferation in vitro. Further investigation revealed that LINC00265 acted as a competing endogenous RNA for microRNA-144-3p (miR-144-3p) and inhibition of miR-144-3p markedly counteracted LINC00265 knockdown-meditated suppression on GC cell proliferation. Additionally, Chromobox 4 (CBX4) was upregulated in GC and silencing CBX4 could reduce GC cell proliferation. Then, CBX4 mRNA was demonstrated to be a direct target of miR-144-3p in GC cells and LINC00265/miR-144-3p axis could regulate CBX4 expression. Taken together, LINC00265 may promote GC cell proliferation via the miR-144-3p/CBX4 axis.

SUBMITTER: Yang Z

PROVIDER: S-EPMC8291797 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background Therapy for patients with liver cancer in the advanced stage remains a great challenge, and there are very few approved treatments. Although accumulated evidence demonstrates the importance of lncRNAs in liver cancer, data on the functional roles and molecular mechanisms of endogenous bornavirus-like nucleoprotein (EBLN3P) have been rarely reported. Materials and Methods The bioinformatics prediction software ENCORI was used to predict the putative binding sites of EBLN3P. The regulatory roles of EBLN3P and miR-144-3p in cell proliferation, migration and invasion ability were verified by the Cell Counting Kit-8, wound healing and Transwell assays, respectively. The interactions among EBLN3P, miR-144-3p and DOCK4 were explored by a luciferase assay and Western blotting. The expression of EBLN3P and microRNA (miR)-144-3p in liver cancer tissues was quantified by reverse transcription-quantitative PCR, and the expression of dedicator of cytokinesis 4 (DOCK4) was quantified by immunohistochemical analysis. Results The present results revealed that overexpression of EBLN3P or knockdown of miR-144-3p promoted liver cancer cell proliferation, migration and invasion. Bioinformatics analysis and a luciferase assay demonstrated that EBLN3P directly interacts with miR-144-3p to attenuate miR-144-3p binding to the 3?-untranslated region of DOCK4. Furthermore, the mechanistic investigations showing that the miR-144-3p/DOCK4 regulatory loop was activated by knockdown of miR?144-3p or overexpression of DOCK4 validate the roles of EBLN3P in promoting liver cancer cell proliferation, migration and invasion in vitro. Elevated levels of EBLN3P and DOCK4 and decreased miR-144-3p expression were observed in both liver cancer tissues and cell lines. Conclusion The present study is the first to demonstrate that EBLN3P may act as a ceRNA to modulate DOCK4 expression by competitively sponging miR-144-3p, leading to the regulation of liver cancer progression, which provides new insights for liver cancer diagnosis and treatment.

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Long intergenic noncoding RNA00265 promotes proliferation of gastric cancer via the microRNA-144-3p/Chromobox 4 axis.

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