ArticleThe Journal of biological chemistry2015
Cellular inhibitor of apoptosis protein 1 (cIAP1) stability contributes to YM155 resistance in human gastric cancer cells.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Targeting the inhibitors of apoptosis proteins (IAPs) to combat drug resistance in cancers.Frontiers in pharmacology · 2025Review
- Cancer genes disfavoring T cell immunity identified via integrated systems approach.Cell reports · 2022Article
- Article
- A comprehensive review of the roles of E2F1 in colon cancer.American journal of cancer research · 2020Review
- cIAP1 promotes proliferation and migration and prevents apoptosis in gallbladder cancerBioscience reports · 2019Article
- Potential Involvement ofOxidative medicine and cellular longevity · 2019Article
- Mixed lineage kinase-4 promotes gastric carcinoma tumorigenesis through suppression of the c-Jun N-terminal kinase signaling pathway.Experimental and therapeutic medicine · 2018Article
- Bone morphogenetic protein and activin membrane-bound inhibitor overexpression inhibits gastric tumor cell invasion via the transforming growth factor-β/epithelial-mesenchymal transition signaling pathway.Experimental and therapeutic medicine · 2018Article
- Application of novel targeting nanoparticles contrast agent combined with contrast-enhanced computed tomography during screening for early-phase gastric carcinoma.Experimental and therapeutic medicine · 2018Article
- Article
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
YM155, which blocks the expression of survivin, a member of the inhibitor of apoptosis (IAP) family, induces cell death in a variety of cancer types, including prostate, bladder, breast, leukemia, and non-small lung cancer. However, the mechanism underlying gastric cancer susceptibility and resistance to YM155 is yet to be specified. Here, we demonstrate that cIAP1 stability dictates resistance to YM155 in human gastric cancer cells. Treatment of human gastric cancer cells with YM155 differentially induced cell death dependent on the stability of cIAP1 as well as survivin. Transfection with cIAP1 expression plasmids decreased cell sensitivity to YM155, whereas knockdown of endogenous cIAP1 using RNA interference enhanced sensitivity to YM155. In addition, double knockdown of survivin and cIAP1 significantly induced cell death in the YM155-resistant cell line, MKN45. We also showed that YM155 induced autoubiquitination and proteasome-dependent degradation of cIAP1. Surprisingly, survivin affected the stability of cIAP1 through binding, contributing to cell sensitivity to YM155. Thus, our findings reveal that YM155 sensitizes human gastric cancer cells to apoptotic cell death by degrading cIAP1, and furthermore, cIAP1 in gastric cancer cells may act as a PD marker for YM155 treatment.
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