ArticleInternational journal of molecular sciences2021
Loss of FADD and Caspases Affects the Response of T-Cell Leukemia Jurkat Cells to Anti-Cancer Drugs.
Article in International journal of molecular sciences, 2021. 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, 13 citations in OpenAlex.
- FOXO1 Inhibition and FADD Knockdown Have Opposing Effects on Anticancer Drug-Induced Cytotoxicity and p21 Expression in Osteosarcoma Cells.International journal of molecular sciences · 2026Article
- IAPs in cancers: molecular mechanisms, clinical prognostic value, and translational therapeutic potential.Journal of translational medicine · 2026Review
- Evaluation of the Apoptotic, Prooxidative and Therapeutic Effects of Odoroside A on Lung Cancer: An In Vitro Study Extended with In Silico Analyses of Human Lung Cancer Datasets.Life (Basel, Switzerland) · 2025Article
- Research Progress in the Small Molecule Smac Mimetics in Combination Therapy of Cancer.Current medicinal chemistry · 2025Review
- The interaction between RIPK1 and FADD controls perinatal lethality and inflammation.Cell reports · 2024Article
- Quaternary Benzophenanthridine Alkaloids Act as Smac Mimetics and Overcome Resistance to Apoptosis.International journal of molecular sciences · 2023Article
- ZBP1-Mediated Necroptosis: Mechanisms and Therapeutic Implications.Molecules (Basel, Switzerland) · 2022Review
- A Dual Role for FADD in Human Precursor T-Cell Neoplasms.International journal of molecular sciences · 2022Article
- FADD as a key molecular player in cancer progression.Molecular medicine (Cambridge, Mass.) · 2022Review
- Contribution of Cancer-Targeting Drugs toward Faster Clinical Application.International journal of molecular sciences · 2022Article
- Cpd-42 protects against calcium oxalate nephrocalcinosis-induced renal injury and inflammation by targeting RIPK3-mediated necroptosis.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Programmed cell death (PCD) pathways play a crucial role in the response of cancer cells to treatment. Their dysregulation is one of the cancer hallmarks and one of the reasons of drug resistance. Here, we studied the significance of the individual members of PCD signaling pathways in response to treatment with common anti-cancer drugs using the T-cell leukemia Jurkat cells with single or double knockouts of necroptosis and/or apoptosis genes. We identified apoptosis as the primary cell death pathway upon anti-cancer drugs treatment. The cells with knocked out either Fas-associated protein with death domain (FADD) or all executioner caspases were resistant. This resistance could be partially overcome by induction of RIP1-dependent necroptosis through TNFR1 activation using combined treatment with TNF-α and smac mimetic (LCL161). RIP1 was essential for cellular response to TNF-α and smac mimetic, but dispensable for the response to anti-cancer drugs. Here, we demonstrated the significance of FADD and executioner caspases in carrying out programmed cell death upon anti-cancer drug treatments and the ability of combined treatment with TNF-α and smac mimetic to partially overcome drug resistance of FADD and/or CASP3/7/6-deficient cells via RIP1-dependent necroptosis. Thus, a combination of TNF-α and smac mimetic could be a suitable strategy for overcoming resistance to therapy in cells unable to trigger apoptosis.
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