Cancer management and research · 2026
LONP2 Enhances Cervical Cancer Growth and Metastatic Potential by Upregulating PLS3 and Activating PI3K/AKT Signaling.
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Yang Ying, Sun Jing, Tian Liu, Liao Jing
Аннотация
PURPOSE: This study aimed to investigate the role of LONP2 in cervical cancer progression and elucidate the underlying signaling mechanisms.
METHODS: HeLa cervical cancer cells were transduced with lentiviral vectors to overexpress LONP2 or simultaneously overexpress LONP2 and knock down plastin 3 (PLS3). Protein expression was assessed by Western blotting. Cell viability, apoptosis, migration, and invasion were evaluated using CCK-8 assays, flow cytometry, and Transwell assays, respectively. The involvement of the PI3K/AKT signaling pathway was examined by detecting the phosphorylation levels of PI3K and AKT. A nude mouse xenograft model was established to validate the in vitro findings.
RESULTS: LONP2 overexpression significantly increased PLS3 protein expression in cervical cancer cells. Functionally, LONP2 promoted cell proliferation, migration, invasion, and tumor growth while suppressing apoptosis. Knockdown of PLS3 markedly attenuated these tumor-promoting effects both in vitro and in vivo. Mechanistically, LONP2 overexpression enhanced the phosphorylation of PI3K and AKT without significantly affecting total PI3K or AKT expression, indicating activation of the PI3K/AKT signaling pathway. Importantly, silencing PLS3 effectively reversed LONP2-induced PI3K/AKT pathway activation. Consistent findings were observed in xenograft tumors, where PLS3 knockdown suppressed tumor growth and reduced p-PI3K and p-AKT expression.
CONCLUSION: LONP2 promotes cervical cancer progression by upregulating PLS3 expression and activating the PI3K/AKT signaling pathway. The LONP2/PLS3/PI3K-AKT signaling axis represents a novel mechanism driving cervical cancer progression and may serve as a potential therapeutic target for cervical cancer treatment.
METHODS: HeLa cervical cancer cells were transduced with lentiviral vectors to overexpress LONP2 or simultaneously overexpress LONP2 and knock down plastin 3 (PLS3). Protein expression was assessed by Western blotting. Cell viability, apoptosis, migration, and invasion were evaluated using CCK-8 assays, flow cytometry, and Transwell assays, respectively. The involvement of the PI3K/AKT signaling pathway was examined by detecting the phosphorylation levels of PI3K and AKT. A nude mouse xenograft model was established to validate the in vitro findings.
RESULTS: LONP2 overexpression significantly increased PLS3 protein expression in cervical cancer cells. Functionally, LONP2 promoted cell proliferation, migration, invasion, and tumor growth while suppressing apoptosis. Knockdown of PLS3 markedly attenuated these tumor-promoting effects both in vitro and in vivo. Mechanistically, LONP2 overexpression enhanced the phosphorylation of PI3K and AKT without significantly affecting total PI3K or AKT expression, indicating activation of the PI3K/AKT signaling pathway. Importantly, silencing PLS3 effectively reversed LONP2-induced PI3K/AKT pathway activation. Consistent findings were observed in xenograft tumors, where PLS3 knockdown suppressed tumor growth and reduced p-PI3K and p-AKT expression.
CONCLUSION: LONP2 promotes cervical cancer progression by upregulating PLS3 expression and activating the PI3K/AKT signaling pathway. The LONP2/PLS3/PI3K-AKT signaling axis represents a novel mechanism driving cervical cancer progression and may serve as a potential therapeutic target for cervical cancer treatment.