ArticleCell death & disease2015
Akt phosphorylates Prohibitin 1 to mediate its mitochondrial localization and promote proliferation of bladder cancer cells.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- MDK Activates the PI3K/AKT Axis to Induce AP2A1 Expression and Epithelial-Mesenchymal Transition in Colorectal Cancer.Cancers · 2026Article
- ZNF468/AURKA/PI3K/AKT Positive Feedback Loop Promotes Proliferation and Metastasis of Oesophageal Squamous Cell Carcinoma.Journal of cellular and molecular medicine · 2025Article
- The E3 Ubiquitin Ligase ARIH1 Facilitates Colorectal Cancer Progression by Promoting Oxidative Phosphorylation via the Mitochondrial Translocation of K63-Linked Ubiquitinated PHB1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Emerging roles of prohibitins in cancer: an update.Cancer gene therapy · 2025Review
- Investigation of new autoantibodies in urothelial bladder cancer for biomarker discovery using immunoproteomics.Discover oncology · 2025Article
- Insights into the Mode of Action of Novel Morpholinated Curcumin Derivatives Exhibiting Potent Antitumor Activity in Bladder Cancer Cells In Vitro.Molecules (Basel, Switzerland) · 2025Article
- Phosphoglycerate mutase 5 exacerbates alcoholic cardiomyopathy in male mice by inducing prohibitin-2 dephosphorylation and impairing mitochondrial quality control.Clinical and translational medicine · 2024Article
- UBXN1 promotes liver tumorigenesis by regulating mitochondrial homeostasis.Journal of translational medicine · 2024Article
- Prohibitions in the meta-inflammatory response: a review.Frontiers in molecular biosciences · 2024Review
- Targeting PHB1 to inhibit castration-resistant prostate cancer progression in vitro and in vivo.Journal of experimental & clinical cancer research : CR · 2023Article
- Pgam5-mediated PHB2 dephosphorylation contributes to endotoxemia-induced myocardial dysfunction by inhibiting mitophagy and the mitochondrial unfolded protein response.International journal of biological sciences · 2023Article
- Fatty acid translocase: a culprit of lipid metabolism dysfunction in disease.Immunometabolism (Cobham, Surrey) · 2022Review
- Combinatorial Delivery of Gallium (III) Nitrate and Curcumin Complex-Loaded Hollow Mesoporous Silica Nanoparticles for Breast Cancer Treatment.Nanomaterials (Basel, Switzerland) · 2022Article
- PGAM5-Mediated PHB2 Dephosphorylation Contributes to Diabetic Cardiomyopathy by Disrupting Mitochondrial Quality Surveillance.Research (Washington, D.C.) · 2022Article
- Prohibitin regulates mTOR pathway via interaction with FKBP8.Frontiers of medicine · 2021Article
- Resveratrol Ameliorates Intestinal Damage Challenged With Deoxynivalenol Through MitophagyFrontiers in veterinary science · 2021Article
- The Synthetic Small Molecule FL3 Combats Intestinal Tumorigenesis via Axin1-Mediated Inhibition of Wnt/β-Catenin Signaling.Cancer research · 2020Article
- Prohibitin ligands: a growing armamentarium to tackle cancers, osteoporosis, inflammatory, cardiac and neurological diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Flavagline synthetic derivative induces senescence in glioblastoma cancer cells without being toxic to healthy astrocytes.Scientific reports · 2020Article
- Prohibitin 1 in liver injury and cancer.Experimental biology and medicine (Maywood, N.J.) · 2020Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer (BC) is very common and associated with significant morbidity and mortality, though the molecular underpinnings of its origination and progression remain poorly understood. In this study, we demonstrate that Prohibitin 1 (PHB) was overexpressed in human BC tissues and that PHB upregulation was associated with poor prognosis. We also found that PHB was necessary and sufficient for BC cell proliferation. Interestingly, the overexpressed PHB was primarily found within mitochondria, and we provide the first direct evidence that phosphorylation by Akt at Thr258 of PHB induces this mitochondrial localization. Inhibiton of Akt reverses these effects and inhibited the proliferation of BC cells. Finally, the phosphorylation of PHB was required for BC cell proliferation, further implicating the importance of the Akt in BC. Taken together, these findings identify the Akt/PHB signaling cascade as a novel mechanism of cancer cell proliferation and provide the scientific basis for the establishment of PHB as a new prognostic marker and treatment target for BC.
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