ArticleCancer science2025
TGF-β Enhances Doxorubicin Resistance and Anchorage-Independent Growth in Cancer Cells by Inducing ALDH1A1 Expression.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- circTGFBR2(3-6) acts as an assembly platform for RNA-binding protein IGF2BP3 and TGFBR1 mRNA to enhance breast cancer cell plasticity.Cell death and differentiation · 2026Article
- TGFβ signaling promotes cell cycle progression and resistance to the CDK4/6 inhibitor palbociclib through SOX4 transcriptional modulation in breast cancer cells.Cell death & disease · 2026Article
- Deciphering the Role of ADAMTS6 in the Epithelial-Mesenchymal Transition of Lung Adenocarcinoma Cells.International journal of molecular sciences · 2025Article
- TGF-β Enhances Doxorubicin Resistance and Anchorage-Independent Growth in Cancer Cells by Inducing ALDH1A1 Expression.Cancer science · 2025Article
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Authors and funding
3 authors.
Funding
Abstract
The transforming growth factor-β (TGF-β)/Smad signaling pathway promotes malignant transformation through various mechanisms, and its effect on enhancing drug resistance can limit the efficacy of treatment. Here, we showed that pre-stimulation of human lung cancer A549 cells with TGF-β increases resistance to doxorubicin-induced growth inhibition in a Smad3- and Smad4-dependent manner. This effect was suppressed by the aldehyde dehydrogenase (ALDH) inhibitor oxyfedrine, suggesting that ALDH family members are involved in drug resistance. TGF-β upregulated the mRNA and protein expression of ALDH1A1. The TGF-β/Smad3 transcriptional enhancer region on ALDH1A1 was identified by Smad3 ChIP-seq analysis using an open database and by reporter assays. Knockdown of ALDH1A1 in A549 cells suppressed TGF-β-induced doxorubicin resistance, and lentivirus-mediated introduction of ALDH1A1 into A549 SMAD3-KO cells restored drug resistance. We also demonstrated that ALDH1A1 is required and sufficient for TGF-β/Smad3 signaling-induced anchorage-independent growth. The results suggest that the TGF-β/Smad3/4 axis promotes resistance to doxorubicin and anchorage-independent growth by inducing the transcription of ALDH1A1.
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