ArticleCell death & disease2014
A novel antagonist to the inhibitors of apoptosis (IAPs) potentiates cell death in EGFR-overexpressing non-small-cell lung cancer cells.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Dioscin inhibits non-small cell lung cancer cells and activates apoptosis by downregulation of Survivin.Journal of Cancer · 2024Article
- Multi-kinase compensation rescues EGFR knockout in a cell line model of head and neck squamous cell carcinoma.Archives of oral biology · 2023Article
- Small molecule profiling to define synergistic EGFR inhibitor combinations in head and neck squamous cell carcinoma.Head & neck · 2022Article
- Claudin1 decrease induced by 1,25-dihydroxy-vitamin D3 potentiates gefitinib resistance therapy through inhibiting AKT activation-mediated cancer stem-like properties in NSCLC cells.Cell death discovery · 2022Article
- The Ubiquitin System: An Emerging Therapeutic Target for Lung Cancer.International journal of molecular sciences · 2021Review
- CHMP4C regulates lung squamous carcinogenesis and progression through cell cycle pathway.Journal of thoracic disease · 2021Article
- Dual targeting of survivin and X-linked inhibitor of apoptosis protein suppresses the growth and promotes the apoptosis of gastric cancer HGC-27 cells.Oncology letters · 2018Article
- XIAP BIR domain suppresses miR-200a expression and subsequently promotes EGFR protein translation and anchorage-independent growth of bladder cancer cell.Journal of hematology & oncology · 2017Article
- Inducing death in tumor cells: roles of the inhibitor of apoptosis proteins.F1000Research · 2017Review
- Differential Impacts of Alternative Splicing Networks on Apoptosis.International journal of molecular sciences · 2016Review
- Cytotoxic effects of SMAC-mimetic compound LCL161 in head and neck cancer cell lines.Clinical oral investigations · 2016Article
- Suppression of gain-of-function mutant p53 with metabolic inhibitors reduces tumor growth in vivo.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the effort to develop an efficient chemotherapy drug for the treatment of non-small-cell lung cancer (NSCLC), we analyzed the anti-tumorigenic effects of a novel small molecule targeting the inhibitor of apoptosis (IAPs), HM90822B, on NSCLC cells. HM90822B efficiently decreased IAP expression, especially that of XIAP and survivin, in several NSCLC cells. Interestingly, cells overexpressing epidermal growth factor receptor (EGFR) due to the mutations were more sensitive to HM90822B, undergoing cell cycle arrest and apoptosis when treated. In xenograft experiments, inoculated EGFR-overexpressing NSCLC cells showed tumor regression when treated with the inhibitor, demonstrating the chemotherapeutic potential of this agent. Mechanistically, decreased levels of EGFR, Akt and phospho-MAPKs were observed in inhibitor-treated PC-9 cells on phosphorylation array and western blotting analysis, indicating that the reagent inhibited cell growth by preventing critical cell survival signaling pathways. In addition, gene-specific knockdown studies against XIAP and/or EGFR further uncovered the involvement of Akt and MAPK pathways in HM90822B-mediated downregulation of NSCLC cell growth. Together, these results support that HM90822B is a promising candidate to be developed as lung tumor chemotherapeutics by targeting oncogenic activities of IAP together with inhibiting cell survival signaling pathways.
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