ArticleOncotarget2015
Nutrient/serum starvation derived TRIP-Br3 down-regulation accelerates apoptosis by destabilizing XIAP.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 19 citations in OpenAlex.
- Drosophila Pyruvate Kinase Links Metabolic State with Circadian Output via TARANIS and PDF.Research square · 2025Article
- Drosophila Pyruvate Kinase Links Metabolic State with Circadian Output via TARANIS and PDF.bioRxiv : the preprint server for biology · 2025Article
- TARANIS Interacts with VRILLE and PDP1 to Modulate the Circadian Transcriptional Feedback Mechanism inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Ubiquitin-independent proteasomal degradation driven by C-degron pathways.Molecular cell · 2023Article
- Low-Nutrient Environment-Induced Changes in Inflammation, Cell Proliferation, and PGC-1α Expression in Stromal Cells with Ovarian Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Inhibitory role of TRIP-Br1 oncoprotein in anticancer drug-mediated programmed cell death via mitophagy activation.International journal of biological sciences · 2022Article
- CDCA4 as a novel molecular biomarker of poor prognosis in patients with lung adenocarcinoma.Frontiers in oncology · 2022Article
- CDCA4 suppresses epithelial-mesenchymal transtion (EMT) and metastasis in Non-small cell lung cancer through modulating autophagy.Cancer cell international · 2021Article
- Exploring the Role of TRIP-Brs in Human Breast Cancer: An Investigation of Expression, Clinicopathological Significance, and Prognosis.Molecular therapy oncolytics · 2020Article
- Inhibitory Role of TRIP-Br1/XIAP in Necroptosis under Nutrient/Serum Starvation.Molecules and cells · 2020Article
- CDCA4, a downstream gene of the Nrf2 signaling pathway, regulates cell proliferation and apoptosis in the MCF‑7/ADM human breast cancer cell line.Molecular medicine reports · 2018Article
- Δ2-Troglitazone promotes cytostatic rather than pro-apoptotic effects in breast cancer cells cultured in high serum conditions.Cell cycle (Georgetown, Tex.) · 2016Article
- TRIP-Br1 oncoprotein inhibits autophagy, apoptosis, and necroptosis under nutrient/serum-deprived condition.Oncotarget · 2015Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TRIP-Br3 and TRIP-Br1 have shown to have important biological functions. However, the function of TRIP-Br3 in tumorigenesis is not well characterized compared to oncogenic TRIP-Br1. Here, we investigated the function of TRIP-Br3 in tumorigenesis by comparing with that of TRIP-Br1. Under nutrient/serum starvation, TRIP-Br3 expression was down-regulated slightly in cancer cells and significantly in normal cells. Unexpectedly, TRIP-Br1 expression was greatly up-regulated in cancer cells but not in normal cells. Moreover, TRIP-Br3 activated autophagy while TRIP-Br1 inactivated it under serum starvation. In spite of different expression and roles of TRIP-Br3 and TRIP-Br1, both of them alleviate cell death by directly binding to and stabilizing XIAP, a potent apoptosis inhibitor, through blocking its ubiquitination. Taken together, we propose that TRIP-Br3 primarily activates the autophagy and suppresses apoptosis in nutrient sufficient condition. However, the prolonged extreme stressful condition of nutrient starvation causes a dramatic decrease of TRIP-Br3, which in turn induces apoptosis by destabilizing XIAP. Up-regulated TRIP-Br1 in cancer cells compensates this effect and delays apoptosis. This can be explained by the competitive alternative binding of TRIP-Br3 and TRIP-Br1 to the BIR2 domain of XIAP. In an extended study, our immunohistochemical analysis revealed a markedly lower level of TRIP-Br3 protein in human carcinoma tissues compared to normal epithelial tissues, implying the role of TRIP-Br3 as a tumor suppressor rather than onco-protein.
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