ArticleTranslational lung cancer research2026
CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer.
Article in Translational lung cancer 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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Abstract
Background: Chemotherapy resistance caused by paclitaxel (PTX) is a thorny issue in the treatment of non-small cell lung cancer (NSCLC). In recent years, it has been reported that PTX can induce the formation of polyploid giant cancer cells (PGCCs). Most PTX induced PGCCs would die, but there are still a few PGCCs that can generate daughter cells via neosis, which have stronger proliferative capability, further causing tumor repopulation. The transition from primitive tumor cells to the generation of daughter cells after induction with PTX is a complex biological process involving multiple mechanisms. Therefore, to further investigate this transformation process and explore the underlying mechanisms would help to overcome PTX resistance in clinic. Methods: Flow cytometry assays were used to detect the changes in PGCCs content. Immunofluorescence was used to observe the process of PTX inducing PGCCs and the production of daughter cells. Differentially expressed genes (DEGs) were identified through RNA sequencing (RNA-seq) analysis of primitive cancer cells of A549, as well as descendant PGCCs and daughter cells. Western blot, senescence-associated beta-galactosidase (SA-β-gal) staining, and xenograft models elucidated CDKN1A's role in complex biological process. Results: CDKN1A was highly expressed in descendant PGCCs and lowly expressed in primitive A549 and its daughter cells. We found that when CDKN1A was interfered with short hairpin RNAs (shRNAs) or inhibited with inhibitors, it could significantly reduce the generation of PGCCs and decrease the number of daughter cells. Our research found that CDKN1A knockdown was associated with dysregulation of AKT, ERK, autophagy markers and stemness/EMT-related proteins in this process, phosphorylated protein kinase B (p-AKT) and phosphorylated extracellular signal-regulated kinase (p-ERK) were found to be lowly expressed in PGCCs and daughter cells after CDKN1A was interfered. Low expression of CDKN1A could reduce the senescence of PGCCs too. Conclusions: A critical role for CDKN1A in PTX-induced PGCCs formation and subsequent neosis in NSCLC was identified. CDKN1A inhibition reduces PGCCs formation, suppresses neosis and enhances tumor sensitivity
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