ArticleCell death and differentiation2020
Membrane-bound TNF mediates microtubule-targeting chemotherapeutics-induced cancer cytolysis via juxtacrine inter-cancer-cell death signaling.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- M196R-TNFR2 and membrane TNFα down-regulate soluble TNFα-induced pro-metastatic functions in triple-negative breast cancer cells.Cancer cell international · 2026Article
- Chimeric antigen receptor cells as a tool for localized delivery of TNFα in solid cancer treatment.Human vaccines & immunotherapeutics · 2025Review
- Oral and transdermal administration of lipopolysaccharide safely enhances self-healing ability through the macrophage network.Frontiers in immunology · 2025Review
- HSPA8 inhibitors augment cancer chemotherapeutic effectiveness via potentiating necroptosis.Molecular biology of the cell · 2024Article
- Apoptotic dysregulation mediates stem cell competition and tissue regeneration.Nature communications · 2023Article
- HSPA8 acts as an amyloidase to suppress necroptosis by inhibiting and reversing functional amyloid formation.Cell research · 2023Article
- Unveiling the landscape of cytokine research in glioma immunotherapy: a scientometrics analysis.Frontiers in pharmacology · 2023Review
- Ccl3 enhances docetaxel chemosensitivity in breast cancer by triggering proinflammatory macrophage polarization.Journal for immunotherapy of cancer · 2022Article
- Review
- Platinum drugs and taxanes: can we overcome resistance?Cell death discovery · 2021Review
- miR-4721, Induced by EBV-miR-BART22, TargetsMolecular therapy. Nucleic acids · 2020Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microtubule-targeting agents (MTAs) are a class of most widely used chemotherapeutics and their mechanism of action has long been assumed to be mitotic arrest of rapidly dividing tumor cells. In contrast to such notion, here we show-in many cancer cell types-MTAs function by triggering membrane TNF (memTNF)-mediated cancer-cell-to-cancer-cell killing, which differs greatly from other non-MTA cell-cycle-arresting agents. The killing is through programmed cell death (PCD), either in way of necroptosis when RIP3 kinase is expressed, or of apoptosis in its absence. Mechanistically, MTAs induce memTNF transcription via the JNK-cJun signaling pathway. With respect to chemotherapy regimens, our results establish that memTNF-mediated killing is significantly augmented by IAP antagonists (Smac mimetics) in a broad spectrum of cancer types, and with their effects most prominently manifested in patient-derived xenograft (PDX) models in which cell-cell contacts are highly reminiscent of human tumors. Therefore, our finding indicates that memTNF can serve as a marker for patient responsiveness, and Smac mimetics will be effective adjuvants for MTA chemotherapeutics. The present study reframes our fundamental biochemical understanding of how MTAs take advantage of the natural tight contact of tumor cells and utilize memTNF-mediated death signaling to induce the entire tumor regression.
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