ArticleNeoplasia (New York, N.Y.)2009
Human melanoma cells under endoplasmic reticulum stress acquire resistance to microtubule-targeting drugs through XBP-1-mediated activation of Akt.
Article in Neoplasia (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 60 citations in OpenAlex.
- Vemurafenib potently induces endoplasmic reticulum stress-mediated apoptosis in BRAFV600E melanoma cells.Science signaling · 2013Trial
- Targeting the unfolded protein response for cancer therapy: mitigating tumor adaptation and immune suppression.Biomarker research · 2025Review
- Live and let die: signaling AKTivation and UPRegulation dynamics in SARS-CoVs infection and cancer.Cell death & disease · 2022Review
- Anticancer effect of caudatin in diethylnitrosamine‑induced hepatocarcinogenesis in rats.Molecular medicine reports · 2020Article
- Review
- Novel mTORC1 Mechanism Suggests Therapeutic Targets for COMPopathies.The American journal of pathology · 2019Article
- IRE1α-XBP1 signaling pathway regulates IL-6 expression and promotes progression of hepatocellular carcinoma.Oncology letters · 2018Article
- The unfolded protein response impacts melanoma progression by enhancing FGF expression and can be antagonized by a chemical chaperone.Scientific reports · 2017Article
- IRE1α-XBP1 pathway promotes melanoma progression by regulating IL-6/STAT3 signaling.Journal of translational medicine · 2017Article
- GALNT6 Stabilizes GRP78 Protein by O-glycosylation and Enhances its Activity to Suppress Apoptosis Under Stress Condition.Neoplasia (New York, N.Y.) · 2017Article
- Upregulated ATF6 contributes to chronic intermittent hypoxia-afforded protection against myocardial ischemia/reperfusion injury.International journal of molecular medicine · 2016Article
- Salubrinal-Mediated Upregulation of eIF2α Phosphorylation Increases Doxorubicin Sensitivity in MCF-7/ADR Cells.Molecules and cells · 2016Article
- Article
- RIPK1 regulates survival of human melanoma cells upon endoplasmic reticulum stress through autophagy.Autophagy · 2015Article
- Oncogenic activation of MEK/ERK primes melanoma cells for adaptation to endoplasmic reticulum stress.The Journal of investigative dermatology · 2014Article
- Article
- Suppression of antifolate resistance by targeting the myosin Va trafficking pathway in melanoma.Neoplasia (New York, N.Y.) · 2013Article
- Modulation of the Akt pathway reveals a novel link with PERK/eIF2α, which is relevant during hypoxia.PloS one · 2013Article
- 1,3-Bis(3,5-dichlorophenyl) urea compound 'COH-SR4' inhibits proliferation and activates apoptosis in melanoma.Biochemical pharmacology · 2012Article
- The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Past studies have shown that melanoma cells have largely adapted to endoplasmic reticulum (ER) stress. In this study, we report that melanoma cells under ER stress are more resistant to apoptosis induced by the microtubule-targeting chemotherapeutic drugs, docetaxel and vincristine, and this is, at least in part, due to activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway mediated by the X-box-binding protein 1 (XBP-1) axis of the unfolded protein response. Treatment with the ER stress-inducer tunicamycin (TM) or thapsigargin before the addition of docetaxel or vincristine reduced the levels of apoptosis induced by the drugs. This was associated with inhibition of mitochondrial release of apoptogenic proteins and activation of Bax and Bak. Induction of ER stress resulted in the rapid activation of the PI3K/Akt pathway that seemed to be important in antagonizing docetaxel and vincristine, in that inhibition of Akt blocked the effect of pretreatment with TM on apoptosis induced by the drugs. Neither docetaxel nor vincristine triggered ER stress in melanoma cells, but the basal activity of XBP-1 signaling seemed to play a role in the protection against the drugs because small interfering RNA knockdown of XBP-1 enhanced docetaxel- and vincristine-induced apoptosis. In addition, inhibition of XBP-1 decreased the constitutive levels of activation of Akt and blocked the activation of Akt induced by TM. Taken together, these results identify activation of the PI3K/Akt pathway by XBP-1-mediated signaling of the unfolded protein response as a resistance mechanism against docetaxel and vincristine in melanoma cells under ER stress.
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