ArticleWorld journal of surgical oncology2025
Targeting NETO2 suppresses cell proliferation, invasion, and migration and inactivates the STAT3/C-MYC pathway in hepatocellular carcinoma.
Article in World journal of surgical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- PHLDA1 is a shared diagnostic and key mediator of inflammatory fibrosis in heart and kidney.Frontiers in immunology · 2026Article
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6 authors.
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Abstract
backgroundNeuropilin and tolloid-like 2 (NETO2) facilitates the progression of various cancers, but its role in hepatocellular carcinoma (HCC) is not known. This study aimed to assess the potential of targeting NETO2 in HCC and its relationship with the STAT3/C-MYC pathway.
methodsHCC cells (Huh7 and MHCC-97 H) were cultured and transfected with control siRNA (siCtrl), NETO2 siRNA (siNETO2), control overexpression (oeCtrl), or NETO2 overexpression (oeNETO2), with non-transfected cells used as blank controls.
resultsNETO2 mRNA and protein expressions were reduced in both Huh7 and MHCC-97 H cells. EdU and CCK-8 assays indicated that cell proliferation was decreased after siNETO2 transfection in Huh7 and MHCC-97 H cells. TUNEL assay found revealed that the cell apoptosis rate was greater after siNETO2 transfection in MHCC-97 H cells, and tended to be greater in Huh7 cells (but the difference was not statistically significant). Transwell invasion assay revealed that the number of invasive Huh7 and MHCC-97 H cells decreased after siNETO2 transfection. Cell scratch assay revealed that the cell migration rate was reduced after siNETO2 transfection in Huh7 cells but was not significantly different in MHCC-97 H cells. Western blotting revealed that p-STAT3 and C-MYC expressions were decreased after siNETO2 transfection in Huh7 and MHCC-97 H cells. Overexpression experiments revealed that cell proliferation and invasion were promoted but that the cell apoptosis rate was reduced after oeNETO2 transfection in Huh7 and MHCC-97 H cells.
conclusionNETO2 knockdown suppresses HCC cell proliferation, invasion, and migration and inactivates the STAT3/C-MYC pathway, suggesting that NETO2 is a potential target for HCC treatment.
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