ArticleOncology letters2026
Breaking senescence restriction: MAFK-AREG axis promotes NSCLC cells to resist doxorubicin.
Article in Oncology letters, 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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5 authors.
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Abstract
Musculoaponeurotic fibrosarcoma oncogene homolog K (MAFK) and amphiregulin (AREG) promote non-small cell lung cancer (NSCLC) progression. However, whether MAFK regulates AREG to mediate the escape of NSCLC cells from doxorubicin (DOX)-induced senescence remains unclear. In the present study, chemotherapy-modulated senescence-related genes were identified through bioinformatics analysis. Human non-small cell lung adenocarcinoma cell lines (A549 and PC-9 cells) were treated with DOX to generate persistent A549 cells (PACs) and persistent PC-9 cells (PPCs). The expression levels of MAFK, AREG and the senescence-associated protein p21 wild-type p53-activated fragment 1 (p21waf1) were evaluated using western blotting and reverse transcription-quantitative PCR. Senescence-associated β-galactosidase staining and colony formation assays were performed to assess cellular senescence and proliferation. The proportions of senescent and proliferating PACs and PPCs were quantified using flow cytometry. A chromatin-immunoprecipitation assay was performed to examine the regulatory association between MAFK and AREG. AREG was associated with cellular senescence, as demonstrated by changes in senescence markers. In A549 and PC-9 cells, DOX treatment upregulated p21waf1 expression, induced senescence, inhibited proliferation and downregulated both MAFK and AREG expression. By contrast, PACs/PPCs exhibited enhanced proliferation alongside elevated MAFK and AREG levels. PACs and PPCs comprised 60-70% senescent cells and 30-40% proliferating cells. MAFK bound directly to the AREG promoter region. In addition, MAFK overexpression reversed the suppressive effect of AREG knockdown on the proliferation of A549 and PC-9 cells. Collectively, MAFK enabled NSCLC cells to escape DOX-induced senescence by upregulating AREG and facilitated cell proliferation upon DOX treatment.
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