4.3 Article

miR-1273h-5p suppresses CXCL12 expression and inhibits gastric cancer cell invasion and metastasis

期刊

OPEN MEDICINE
卷 17, 期 1, 页码 930-946

出版社

DE GRUYTER POLAND SP Z O O
DOI: 10.1515/med-2022-0486

关键词

gastric cancer; miR-1273h-5p; proliferation; apoptosis; migration; invasion

资金

  1. National Natural Science Foundation of China [81773778]
  2. China Postdoctoral Science Foundation [2019M650775, 2020T130438]

向作者/读者索取更多资源

This study demonstrates that miR-1273h-5p plays a significant role in gastric cancer by regulating cell proliferation, migration, invasion, and apoptosis. Downregulation of miR-1273h-5p leads to upregulation of CXCL12, which may serve as a novel diagnostic and therapeutic target for gastric cancer.
The aim of this study was to verify the biological function of miR-1273h-5p in gastric cancer (GC) and its underlying mechanisms. The differential expression of microRNAs between GC and tumor-adjacent normal tissues was detected using microarrays, miR-1273h-5p, and chemokine (C-X-C motif) ligand 12 (CXCL12) mRNA, and protein levels were evaluated using polymerase chain reaction and Western blotting methods, cell proliferation, apoptosis, migration, and invasion were determined by CCK-8, flow cytometry, and transwell assay. Compared to tumor-adjacent normal tissue and gastric epithelial mucosa cell line cells, miR-1273h-5p was significantly downregulated in tissues and cells of GC. The overexpression of miR-1273h-5p could inhibit cell proliferation, migration, invasion, and promote cell apoptosis; in contrast, inhibition of miR-1273h-5p expression could reverse this process. Moreover, a significant upregulation of CXCL12 was observed when the miR-1273h-5p was downregulated in GC cells. Additionally, miR-1273h-5p significantly reduces tumor volume and weight. Thus, this study suggests that miR-1273h-5p regulates cell proliferation, migration, invasion, and apoptosis during GC progression by directly binding to CXCL12 mRNA 3 '-untranslational regions, which may be a novel diagnostic and therapeutic target in GC.

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