miR-708–3p promotes gastric cancer progression through downregulating ETNK1

MicroRNAs (miRNAs) are small, evolutionarily conserved, non-coding RNAs playing a role in the proliferation, metastasis, apoptosis, chemo-sensitivity, and chemo-resistance of gastric cancer, as well as the stemness of gastric cancer stem cells. miR-708–3p induces gastric cancer cell chemo-resistance...

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Veröffentlicht in:Heliyon 2023-09, Vol.9 (9), p.e19544-e19544, Article e19544
Hauptverfasser: Shang, Jincai, Wang, Qingdong, Wang, Jingren, Xu, Bo, Liu, Shuang
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Sprache:eng
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Zusammenfassung:MicroRNAs (miRNAs) are small, evolutionarily conserved, non-coding RNAs playing a role in the proliferation, metastasis, apoptosis, chemo-sensitivity, and chemo-resistance of gastric cancer, as well as the stemness of gastric cancer stem cells. miR-708–3p induces gastric cancer cell chemo-resistance, but its actual role in gastric cancer progression remains unclear. This paper shows that miR-708–3p is upregulated in gastric cancer samples and that a high miR-708–3p expression in gastric cancer patients is associated with poor overall survival. Our functional study results indicate that miR-708–3p overexpression promotes gastric cancer cell proliferation and migration, inhibits cell apoptosis, and facilitates the transition from the G0/G1 to the G2/M phase. Furthermore, reducing miR-708–3p levels yielded opposite effects. Next, our in vivo experiments revealed that miR-708–3p advanced gastric cancer cell growth in nude mice. The underlying mechanism was the regulation of ethanolamine kinase 1 (ETNK1) expression by miR-708–3p, which bound to the 3′UTR of the ETNK1 gene in gastric cancer cells. Finally, the recovery assay results showed that ETNK1 overexpression could slow miR-708-3p-induced gastric cancer progression. In conclusion, we identified a new miR-708–3p/ETNK1 pathway involved in gastric cancer progression. These results may offer new targets for gastric cancer therapy and markers for gastric cancer prognosis.
ISSN:2405-8440
2405-8440
DOI:10.1016/j.heliyon.2023.e19544