ArticleCancer science2021
The survival and proliferation of osteosarcoma cells are dependent on the mitochondrial BIG3-PHB2 complex formation.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- The investigational anti-B7-H3 antibody-drug conjugate vobramitamab duocarmazine exerts anti-tumor activity in vitro and in vivo in pediatric sarcoma preclinical models.Cell death & disease · 2026Article
- Arfgef3 knockout ameliorates ischemia reperfusion-induced acute kidney injury via mitochondrial dysfunction alleviation in mice.Renal failure · 2025Article
- The role of mitochondria-related lncRNAs in characterizing the immune landscape and supervising the prognosis of osteosarcoma.Journal of bone oncology · 2023Article
- Article
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- Development of artesunate intelligent prodrug liposomes based on mitochondrial targeting strategy.Journal of nanobiotechnology · 2022Article
- miR-30 inhibits the progression of osteosarcoma by targeting MTA1.Journal of musculoskeletal & neuronal interactions · 2022Article
- A mitochondria-related signature for predicting immune microenvironment and therapeutic response in osteosarcoma.Frontiers in oncology · 2022Article
- Prohibitins: A Key Link between Mitochondria and Nervous System Diseases.Oxidative medicine and cellular longevity · 2022Review
- The survival and proliferation of osteosarcoma cells are dependent on the mitochondrial BIG3-PHB2 complex formation.Cancer science · 2021Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
Previous studies reported the critical role of the brefeldin A-inhibited guanine nucleotide exchange protein 3-prohibitin 2 (BIG3-PHB2) complex in modulating estrogen signaling activation in breast cancer cells, yet its pathophysiological roles in osteosarcoma (OS) cells remain elusive. Here, we report a novel function of BIG3-PHB2 in OS malignancy. BIG3-PHB2 complexes were localized mainly in mitochondria in OS cells, unlike in estrogen-dependent breast cancer cells. Depletion of endogenous BIG3 expression by small interfering RNA (siRNA) treatment led to significant inhibition of OS cell growth. Disruption of BIG3-PHB2 complex formation by treatment with specific peptide inhibitor also resulted in significant dose-dependent suppression of OS cell growth, migration, and invasion resulting from G2/M-phase arrest and in PARP cleavage, ultimately leading to PARP-1/apoptosis-inducing factor (AIF) pathway activation-dependent apoptosis in OS cells. Subsequent proteomic and bioinformatic pathway analyses revealed that disruption of the BIG3-PHB2 complex might lead to downregulation of inner mitochondrial membrane protein complex activity. Our findings indicate that the mitochondrial BIG3-PHB2 complex might regulate PARP-1/AIF pathway-dependent apoptosis during OS cell proliferation and progression and that disruption of this complex may be a promising therapeutic strategy for OS.
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