PMID- 35226830 OWN - NLM STAT- MEDLINE DCOM- 20220405 LR - 20220405 IS - 2165-5987 (Electronic) IS - 2165-5979 (Print) IS - 2165-5979 (Linking) VI - 13 IP - 3 DP - 2022 Mar TI - MicroRNA-200b-3p restrains gastric cancer cell proliferation, migration, and invasion via C-X-C motif chemokine ligand 12/CXC chemokine receptor 7 axis. PG - 6509-6520 LID - 10.1080/21655979.2022.2034585 [doi] AB - This study was conducted to investigate the impact of microRNA (miR)-200b-3p on viability, migration, and invasion of gastric cancer (GC) cells and its mechanism. Quantitative real-time PCR (qRT-PCR) was conducted to measure miR-200b-3p expression in GC tissues and cells; besides, the relationship between miR-200b-3p expression and overall survival time (OS) was analyzed with OncomiR database; cell counting kit-8 (CCK-8), colony formation assay, flow cytometry, scratch healing assay, and Transwell assay were performed to detect the proliferation, cell cycle progression, migration, and invasion of GC cells; a lung metastasis model in nude mice was used to examine the effect of miR-200b-3p on the metastasis of GC cells in vivo; the interplay between miR-200b-3p and C-X-C motif chemokine ligand 12 (CXCL12) mRNA 3' UTR was predicted by bioinformatics and verified with a dual-luciferase reporter gene assay; besides, the expression of CXCL12 and CXC chemokine receptor 7 (CXCR7) was probed by Western blot. It was found that miR-200b-3p expression was down-regulated in GC tissues, which was remarkably associated with the lymph node metastasis and decrease of differentiation of GC; transfection with miR-200b-3p mimics restrained the growth, migration, and invasion of GC cells in vitro, induced cell cycle arrest, and inhibited CXCL12 and CXCR7 expression levels; transfection of miR-200b-3p inhibitors worked oppositely in vitro and promoted lung metastasis in vivo. CXCL12 was confirmed as the downstream target of miR-200b-3p and was negatively modulated by miR-200b-3p. In conclusion, miR-200b-3p inhibited GC progression via regulating CXCL12/CXCR7 axis. FAU - Li, Dinuo AU - Li D AUID- ORCID: 0000-0001-7317-5045 AD - Department of General Gastropathy, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China. FAU - Li, Qiang AU - Li Q AD - Department of Gastrosurgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Bioengineered JT - Bioengineered JID - 101581063 RN - 0 (ACKR3 protein, human) RN - 0 (CXCL12 protein, human) RN - 0 (Chemokine CXCL12) RN - 0 (MIRN200 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (Receptors, CXCR) SB - IM MH - Animals MH - Cell Line, Tumor MH - Cell Movement/genetics MH - Cell Proliferation/genetics MH - Chemokine CXCL12/*genetics MH - Humans MH - Male MH - Mice MH - Mice, Inbred BALB C MH - MicroRNAs/*genetics MH - Middle Aged MH - Receptors, CXCR/*genetics MH - Signal Transduction/genetics MH - *Stomach Neoplasms/genetics/metabolism/pathology PMC - PMC8974025 OTO - NOTNLM OT - CXCL12/CXCR7 OT - GC OT - miR-200b-3p OT - migration and invasion OT - proliferation COIS- No potential conflict of interest was reported by the author(s). EDAT- 2022/03/01 06:00 MHDA- 2022/04/06 06:00 PMCR- 2022/02/28 CRDT- 2022/02/28 20:03 PHST- 2022/02/28 20:03 [entrez] PHST- 2022/03/01 06:00 [pubmed] PHST- 2022/04/06 06:00 [medline] PHST- 2022/02/28 00:00 [pmc-release] AID - 2034585 [pii] AID - 10.1080/21655979.2022.2034585 [doi] PST - ppublish SO - Bioengineered. 2022 Mar;13(3):6509-6520. doi: 10.1080/21655979.2022.2034585.