ArticleOncology research2026
Plexin A2 Knockdown Enhances Apoptosis in Chemotherapy Treated Melanoma Cells.
Article in Oncology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
9 authors.
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Abstract
Background: Cancer cells are characterized by the ability to exit reversibly from the cell cycle to resist an unfavorable environment. This study elucidates alterations in adhesion molecule expression in melanoma cells acquiring resistance to dacarbazine (DTIC) and entering the G0 state. Plexin A2 (PLXNA2) was identified as a focal adhesion-related molecule implicated in carcinogenesis. Methods: Applying siRNA-mediated knockdown, the effects of altered Results: Our findings indicated that DTIC treatment modulates melanoma cell interactions with the extracellular matrix, facilitating adhesion to collagen IV, fibronectin, and laminin. Concurrently, integrin expression diminishes upon DTIC exposure. Delete Crucially, focal adhesion signaling molecules, including PLXNA2, Phosphoinositide-3-Kinase Regulatory Subunit 1, and Fibroblast Growth Factor Receptor 2, exhibit increased expression. Conclusions: These findings suggest that PLXNA2 down-regulation in DTIC-treated cancer cells promotes their apoptosis. Therefore, targeting focal adhesion molecules during chemotherapy can increase the sensitivity of tumor cells to anticancer treatment.
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