ArticleJournal of cancer research and clinical oncology2013
Perturbation of proteasome function by bortezomib leading to ER stress-induced apoptotic cell death in cholangiocarcinoma.
Article in Journal of cancer research and clinical oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- A phase II trial of the proteasome inhibitor bortezomib in patients with advanced biliary tract cancers.Clinical colorectal cancer · 2014Trial
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- MLN2238 exerts its anti-tumor effectsFrontiers in pharmacology · 2022Article
- Gambogic Acid Inhibits Wnt/β-catenin Signaling and Induces ER Stress-Mediated Apoptosis in Human Cholangiocarcinoma.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Notch3 contributes to T-cell leukemia growth via regulation of the unfolded protein response.Oncogenesis · 2020Article
- Therapeutic Targeting of Signaling Pathways Related to Cancer Stemness.Frontiers in oncology · 2020Review
- ATF6 regulates the development of chronic pancreatitis by inducing p53-mediated apoptosis.Cell death & disease · 2019Article
- A Systematic Investigation of the Malignant Functions and Diagnostic Potential of the Cancer Secretome.Cell reports · 2019Article
- Rapid induction of p62 and GABARAPL1 upon proteasome inhibition promotes survival before autophagy activation.The Journal of cell biology · 2018Article
- Bortezomib promotes KHSV and EBV lytic cycle by activating JNK and autophagy.Scientific reports · 2017Article
- Upregulation of CD147 Promotes Metastasis of Cholangiocarcinoma by Modulating the Epithelial-to-Mesenchymal Transitional Process.Oncology research · 2017Article
- Deregulation of KSHV latency conformation by ER-stress and caspase-dependent RAD21-cleavage.PLoS pathogens · 2017Article
- Curcumin derivative WZ35 efficiently suppresses colon cancer progression through inducing ROS production and ER stress-dependent apoptosis.American journal of cancer research · 2017Article
- Endoplasmic reticulum-mediated unfolded protein response and mitochondrial apoptosis in cancer.Biochimica et biophysica acta. Reviews on cancer · 2017Review
- Inhibition of carbonic anhydrase potentiates bevacizumab treatment in cholangiocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Amblyomin-X induces ER stress, mitochondrial dysfunction, and caspase activation in human melanoma and pancreatic tumor cell.Molecular and cellular biochemistry · 2016Article
- Article
- Endoplasmic reticulum stress-mediated pathways to both apoptosis and autophagy: Significance for melanoma treatment.World journal of experimental medicine · 2015Review
- Phosphatidic Acid Increases Epidermal Growth Factor Receptor Expression by Stabilizing mRNA Decay and by Inhibiting Lysosomal and Proteasomal Degradation of the Internalized Receptor.Molecular and cellular biology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeCholangiocarcinoma (CCA) or cancer of the biliary tract is heterogeneous; however, chronic inflammatory-related features are unique in CCA. Moreover, the genes involved in proteasome functions are evidently increased in CCA. Hence, CCA might be vulnerable to endoplasmic reticulum (ER) stressors, particularly a proteasome inhibitor. Therefore, bortezomib (BTZ), a specific 26S proteasome inhibitor, was selected, and its antitumor effects against CCA were investigated.
methodsLiver fluke-associated CCA cell lines were used. Cell proliferation and apoptosis detection were determined by a tetrazolium-based assay, caspase detection and annexin V binding assay. The accumulations of proteasome substrates, the inductions of ER stress and unfolded protein response (UPR) proteins were demonstrated by western blot and reporter systems. The in vivo anti-proliferative effect was accessed in a subcutaneous transplantation mouse model.
resultsBTZ inhibited CCA proliferation and induced caspase-dependent apoptosis, independently of the NF-κB pathway. Inhibition of protein degradation by BTZ led to the induction of UPR; induction of XBP1 splicing, ATF6 proteolysis and nuclear ATF4 as well as BiP and CHOP expressions were evident. Nevertheless, ER stress-induced UPR was overwhelming, leading to the activation of apoptosis demonstrated by proteolytic cleavages of ER-related caspase 4 and 12 as well as classical caspase 8, 9 and 3. The growth inhibitory effect of BTZ was supported by an in vivo model.
conclusionBTZ treatment could be a promising therapeutic approach for CCA treatment.
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