ArticleBritish journal of cancer2016
Mitochondrial dysfunction-mediated apoptosis resistance associates with defective heat shock protein response in African-American men with prostate cancer.
Article in British journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Targeting mitochondria and programmed cell death as potential interventions for metastatic castration-resistant prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Dichloroacetate for Cancer Treatment: Some Facts and Many Doubts.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The association between methylmalonic acid, a biomarker of mitochondrial dysfunction, and risk of prostate cancer.International urology and nephrology · 2024Article
- Genetic and biological drivers of prostate cancer disparities in Black men.Nature reviews. Urology · 2024Review
- Targeting the Metabolic Paradigms in Cancer and Diabetes.Biomedicines · 2024Review
- Mitochondrial Alterations in Prostate Cancer: Roles in Pathobiology and Racial Disparities.International journal of molecular sciences · 2023Review
- Racial disparity in prostate cancer in the African American population with actionable ideas and novel immunotherapies.Cancer reports (Hoboken, N.J.) · 2021Review
- Dichloroacetate and PX-478 exhibit strong synergistic effects in a various number of cancer cell lines.BMC cancer · 2021Article
- Pyruvate dehydrogenase kinase 1 interferes with glucose metabolism reprogramming and mitochondrial quality control to aggravate stress damage in cancer.Journal of Cancer · 2020Article
- Hsp60 and IL-8 axis promotes apoptosis resistance in cancer.British journal of cancer · 2019Article
- CytochromeCancer research · 2019Article
- Dichloroacetic acid upregulates apoptosis of ovarian cancer cells by regulating mitochondrial function.OncoTargets and therapy · 2019Article
- Mitochondrial biology and prostate cancer ethnic disparity.Carcinogenesis · 2018Review
- Mitochondrial determinants of cancer health disparities.Seminars in cancer biology · 2017Review
- Investigation of Mitochondrial Metabolic Response to Doxorubicin in Prostate Cancer Cells: An NADH, FAD and Tryptophan FLIM Assay.Scientific reports · 2017Article
- Inhibition of COX2 enhances the chemosensitivity of dichloroacetate in cervical cancer cells.Oncotarget · 2017Article
- Differential expression of miR-34b and androgen receptor pathway regulate prostate cancer aggressiveness between African-Americans and Caucasians.Oncotarget · 2017Article
- Article
- Endoplasmic reticulum-mediated unfolded protein response and mitochondrial apoptosis in cancer.Biochimica et biophysica acta. Reviews on cancer · 2017Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAfrican-American (AA) patients with prostate cancer (PCa) respond poorly to current therapy compared with Caucasian American (CA) PCa patients. Although underlying mechanisms are not defined, mitochondrial dysfunction is a key reason for this disparity.
methodsCell death, cell cycle, and mitochondrial function/stress were analysed by flow cytometry or by Seahorse XF24 analyzer. Expression of cellular proteins was determined using immunoblotting and real-time PCR analyses. Cell survival/motility was evaluated by clonogenic, cell migration, and gelatin zymography assays.
resultsGlycolytic pathway inhibitor dichloroacetate (DCA) inhibited cell proliferation in both AA PCa cells (AA cells) and CA PCa cells (CA cells). AA cells possess reduced endogenous reactive oxygen species, mitochondrial membrane potential (mtMP), and mitochondrial mass compared with CA cells. DCA upregulated mtMP in both cell types, whereas mitochondrial mass was significantly increased in CA cells. DCA enhanced taxol-induced cell death in CA cells while sensitising AA cells to doxorubicin. Reduced expression of heat shock proteins (HSPs) was observed in AA cells, whereas DCA induced expression of CHOP, C/EBP, HSP60, and HSP90 in CA cells. AA cells are more aggressive and metastatic than CA cells.
conclusionsRestoration of mitochondrial function may provide new option for reducing PCa health disparity among American men.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.