Pakistan journal of pharmaceutical sciences · 2026
MiR-326 targets ETS1 to activate PI3K/Akt signaling and promote malignant phenotypes in gastric cancer cells.
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Liang Kai, Zhang Xiangyu, Yang Yin
Аннотация
BACKGROUND: Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide and effective therapeutic targets remain limited.
OBJECTIVES: This study aimed to investigate the expression and functional role of miR-326 in gastric cancer, identify its direct target gene and elucidate the underlying molecular mechanisms involving the PI3K/Akt signaling pathway and the regulation of inflammatory cytokines.
METHODS: miR-326 expression was detected by qRT-PCR in 56 paired GC tissues and adjacent normal tissues, as well as in GC cell lines (SGC-7901, MKN-45, AGS) and normal GES-1 cells. CCK-8 assays, flow cytometry, Transwell migration/invasion assays and ELISA were performed to assess cell proliferation, apoptosis, migration/invasion and cytokine secretion. Dual-luciferase reporter assay and Western blotting were used to validate the target gene and pathway activation.
RESULTS: miR-326 was significantly upregulated in GC tissues and cell lines. ETS1 was identified as a direct target of miR-326. Overexpression of miR-326 reduced ETS1 expression, activated the PI3K/Akt pathway (increased p-PI3K and p-AKT), promoted cell proliferation, migration and invasion, inhibited apoptosis and induced an imbalance of inflammatory cytokines (increased IL-6 and TNF-α; decreased IL-10 and IL-17). Co-overexpression of ETS1 or treatment with the PI3K inhibitor LY294002 reversed these effects.
CONCLUSIONS: miR-326 promotes malignant phenotypes in gastric cancer cells by targeting ETS1, activating the PI3K/Akt signaling pathway, and inducing dysregulation of inflammatory cytokines. The miR-326/ETS1/PI3K/Akt axis may serve as a potential diagnostic biomarker and therapeutic target for gastric cancer.
OBJECTIVES: This study aimed to investigate the expression and functional role of miR-326 in gastric cancer, identify its direct target gene and elucidate the underlying molecular mechanisms involving the PI3K/Akt signaling pathway and the regulation of inflammatory cytokines.
METHODS: miR-326 expression was detected by qRT-PCR in 56 paired GC tissues and adjacent normal tissues, as well as in GC cell lines (SGC-7901, MKN-45, AGS) and normal GES-1 cells. CCK-8 assays, flow cytometry, Transwell migration/invasion assays and ELISA were performed to assess cell proliferation, apoptosis, migration/invasion and cytokine secretion. Dual-luciferase reporter assay and Western blotting were used to validate the target gene and pathway activation.
RESULTS: miR-326 was significantly upregulated in GC tissues and cell lines. ETS1 was identified as a direct target of miR-326. Overexpression of miR-326 reduced ETS1 expression, activated the PI3K/Akt pathway (increased p-PI3K and p-AKT), promoted cell proliferation, migration and invasion, inhibited apoptosis and induced an imbalance of inflammatory cytokines (increased IL-6 and TNF-α; decreased IL-10 and IL-17). Co-overexpression of ETS1 or treatment with the PI3K inhibitor LY294002 reversed these effects.
CONCLUSIONS: miR-326 promotes malignant phenotypes in gastric cancer cells by targeting ETS1, activating the PI3K/Akt signaling pathway, and inducing dysregulation of inflammatory cytokines. The miR-326/ETS1/PI3K/Akt axis may serve as a potential diagnostic biomarker and therapeutic target for gastric cancer.