ArticleCell death & disease2023
Nuclear complement C3b promotes paclitaxel resistance by assembling the SIN3A/HDAC1/2 complex in non-small cell lung cancer.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- The Complosome: An Emerging Intracellular Complement Network in Cancer Development and Therapy.International journal of molecular sciences · 2026Review
- Tumour cell-intrinsic complement C1r and C1s regulate cancer cell fitness and shape the immune microenvironment in triple-negative breast cancer.Cellular and molecular life sciences : CMLS · 2026Article
- [Potential Mechanisms and Research Advances of HDAC1 in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- VDAC1 protein derived from extracellular vesicles promotes paclitaxel resistance in gastric cancer through autophagy and mitophagy.Cancer biology & medicine · 2026Article
- The insider's perspective: The intracellular complosome and immune cell dynamics in cancer.Clinical and translational medicine · 2026Review
- SIN3A promotes lung adenocarcinoma by repressing MIR22HG/Beclin1 axis-mediated autophagy and ferroptosis.European journal of medical research · 2026Article
- Targeting the C3 signaling axis of the complement system: immune microenvironment regulation and emerging therapeutic strategies for glioblastoma.Frontiers in immunology · 2026Review
- Integrated multi-omics characterization across clinically relevant subgroups of long COVID.National science review · 2025Article
- Marine natural product Methyl mycophenolate inhibits gastric cancer growth through regulating p53 and the downstream pathways.Cancer cell international · 2025Article
- HDAC inhibitors modulate Hippo pathway signaling in hormone positive breast cancer.Clinical epigenetics · 2025Article
- The role of complement in tumor immune tolerance and drug resistance: a double-edged sword.Frontiers in immunology · 2025Review
- Quiescent cancer cells induced by high-density cultivation reveals cholesterol-mediated survival and lung metastatic traits.British journal of cancer · 2024Article
- The complement cascade in lung injury and disease.Respiratory research · 2024Review
- HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to the classical role as a serum effector system of innate immunity, accumulating evidence suggests that intracellular complement components have indispensable functions in immune defense, T cell homeostasis, and tumor cell proliferation and metastasis. Here, we revealed that complement component 3 (C3) is remarkably upregulated in paclitaxel (PTX)-resistant non-small cell lung cancer (NSCLC) cells and that knockdown of C3 promoted PTX-induced cell apoptosis, sensitizing resistant cells to PTX therapy. Ectopic C3 decreased PTX-induced apoptosis and induced resistance to PTX treatment in original NSCLC cells. Interestingly, C3b, the activated fragment of C3, was found to translocate into the nucleus and physically associate with the HDAC1/2-containing SIN3A complex to repress the expression of GADD45A, which plays an important role in cell growth inhibition and apoptosis induction. Importantly, C3 downregulated GADD45A by enhancing the binding of the SIN3A complex with the promoter of GADD45A, thus decreasing the H3Ac level to compress chromatin around the GADD45A locus. Subsequently, ectopic GADD45A promoted PTX-induced cell apoptosis, sensitizing resistant cells to PTX therapy, and insufficiency of GADD45A in original cancer cells induced resistance to PTX treatment. These findings identify a previously unknown nucleus location and oncogenic property for C3 in chemotherapy and provide a potential therapeutic opportunity to overcome PTX resistance.
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