Linc00467 promotion of gastric cancer development by directly regulating miR-7-5p expression and downstream epidermal growth factor receptor.

Abstract

Linc00467 is a vital regulator in tumor progression. This study explores the molecular mechanisms of linc00467 in gastric cancer (GC). Linc00467 expression was obtained and analyzed in GC tissue through exploration in the cancer genome atlas database. Then, real-time quantitative polymerase chain reaction was used to detect linc000467 expression in GC cells. Cell functions were observed using cell counting Kit-8, Transwell assay, Western blotting to testify the proliferation, migration, invasion, and the relative expression of epidermal growth factor receptor (EGFR) in GC cells. Moreover, a dual-luciferase reporter gene assay was used to verify the relationship between linc00467 and miR-7-5p. Results showed that the expression of linc00467 was overexpressed in GC. Linc00467 silencing decreased the GC cell proliferation, migration, and invasion. With mRNA verification and combined previous research, linc00467 directly regulated the miR-7-5p expression and downstream EGFR expression. Inhibited miR-7-5p could restore cell function, EGFR expression of GC cells when linc00467 knockdown occurs. Altogether, linc00467 directly regulates the miR-7-5p and EGFR signaling pathway to promote GC proliferation, migration, and invasion.

• Authors: Li-Hao Deng, Hui Zhao, Li-Ping Bai, Jun Xie, Kai Liu, Feng Yan
• Journal: Bioengineered (Bioengineered) Vol. 12 Issue 2 Pg. 9484-9495 (12 2021) ISSN: 2165-5987 [Electronic] United States
• PMID: 34713767 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Video-Audio Media)

Chemical References

• MIRN7 microRNA, human
• MicroRNAs
• Neoplasm Proteins
• RNA, Long Noncoding
• RNA, Neoplasm
• EGFR protein, human
• ErbB Receptors

Topics

• Cell Line, Tumor
• ErbB Receptors (genetics, metabolism)
• Gene Expression Regulation, Neoplastic
• Humans
• MicroRNAs (biosynthesis, genetics)
• Neoplasm Proteins (genetics, metabolism)
• RNA, Long Noncoding (genetics, metabolism)
• RNA, Neoplasm (genetics, metabolism)
• Stomach Neoplasms (genetics, metabolism)