MicroRNAs are involved in the development and progression of gastric cancer

Abstract

MicroRNAs (miRNAs) are recognized as an essential component of the RNA family, exerting multiple and intricate biological functions, particularly in the process of tumorigenesis, proliferation, and metastatic progression. MiRNAs are altered in gastric cancer (GC), showing activity as both tumor suppressors and oncogenes, although their true roles have not been fully understood. This review will focus upon the recent advances of miRNA studies related to the regulatory mechanisms of gastric tumor cell proliferation, apoptosis, and cell cycle. We hope to provide an in-depth insight into the mechanistic role of miRNAs in GC development and progression. In particular, we summarize the latest studies relevant to miRNAs' impact upon the epithelial-mesenchymal transition, tumor microenvironment, and chemoresistance in GC cells. We expect to elucidate the molecular mechanisms involving miRNAs for better understanding the etiology of GC, and facilitating the development of new treatment regimens for the treatment of GC.

Keywords: angiogenesis; chemoresistance; epithelial-mesenchymal transition (EMT); gastric cancer; microRNA; signaling pathway; tumor microenvironment.

Fig. 1. MiRNAs are involved in the regulation of gastric cancer cell proliferation by targeting PI3K/Akt/mTOR and Wnt/β-catenin signaling pathways.

15-PGDH 15-hydroxyprostaglandin dehydrogenase, β-cat β-catenin, Akt protein kinase B, APC adenomatous polyposis coli, DIXDC1 disheveled–axin domain containing 1, GFs growth factors, GSK-3 glycogen synthase kinase-3, mTOR mammalian target of rapamycin, PI3K phosphoinositide 3-kinases, PGE2 prostaglandin E2, PTEN phosphatase and tensin homolog, SFRP1 secreted frizzled-related protein 1, SOX5 SRY-box transcription factor 5, SOX9 SRY-box transcription factor 9, STRA6 stimulated by retinoic acid 6, SUFU suppressor of fused homolog, TRIM24 tripartite motif-containing 24.

Fig. 2. MiRNAs modulate the chemoresistance in gastric cancer cells.

5-FU 5-fluorouracil, DTX docetaxel, DDP/CDDP cisplatin, PTX paclitaxel, VCR vincristine, ABCG2 ATP binding cassette subfamily G member 2, Akt protein kinase B, ANK2 ankyrin 2, ANXA2 annexin A2, ARHGAP10 rho GTPase activating protein 10, ATG12 autophagy-related 12, CAPNS1 calpain small subunit 1, E2F5 E2F transcription factor 5, ERBB2 erb-b2 receptor tyrosine kinase 2, HMGA2 high mobility group AT-Hook 2, MALAT1 metastasis-associated lung adenocarcinoma transcript 1, MDR1 multidrug resistance mutation 1, mTOR mammalian target of rapamycin, PI3K phosphoinositide 3-kinases, PTEN phosphatase and tensin homolog, RECK reversion-inducing cysteine-rich protein with Kazal motifs, SIRT1 sirtuin 1, SLC34A2 solute carrier family 34 member 2, TGFBR2 transforming growth factor beta receptor 2.