ArticleOncogene2010
BAX inhibitor-1 enhances cancer metastasis by altering glucose metabolism and activating the sodium-hydrogen exchanger: the alteration of mitochondrial function.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- Article
- Targeting metabolic reprogramming promotes the efficacy of transarterial chemoembolization in the rabbit VX2 liver tumor model.Oncology letters · 2024Article
- Transmembrane BAX inhibitor motif containing 6 suppresses presenilin-2 to preserve mitochondrial integrity after myocardial ischemia-reperfusion injury.International journal of biological sciences · 2023Article
- TMBIM6 (transmembrane BAX inhibitor motif containing 6) enhances autophagy through regulation of lysosomal calcium.Autophagy · 2021Article
- TMBIM6/BI-1 contributes to cancer progression through assembly with mTORC2 and AKT activation.Nature communications · 2020Article
- BAX inhibitor-1: between stress and survival.The FEBS journal · 2020Review
- Stimulation of cell invasion by the Golgi Ion Channel GAAP/TMBIM4 via an HRedox biology · 2020Article
- Article
- Mitochondrial Involvement in Migration, Invasion and Metastasis.Frontiers in cell and developmental biology · 2019Review
- Microenvironment dependent gene expression signatures in reprogrammed human colon normal and cancer cell lines.BMC cancer · 2018Article
- Review
- Targeting Metabolic Remodeling in Triple Negative Breast Cancer in a Murine Model.Journal of Cancer · 2017Article
- Histone deacetylase inhibitor induces cell apoptosis and cycle arrest in lung cancer cells via mitochondrial injury and p53 up-acetylation.Cell biology and toxicology · 2016Article
- Metabolic changes associated with tumor metastasis, part 2: Mitochondria, lipid and amino acid metabolism.Cellular and molecular life sciences : CMLS · 2016Review
- Golgi anti-apoptotic proteins are highly conserved ion channels that affect apoptosis and cell migration.The Journal of biological chemistry · 2015Article
- Apoptosis, autophagy, necroptosis, and cancer metastasis.Molecular cancer · 2015Review
- TMBIM protein family: ancestral regulators of cell death.Oncogene · 2015Review
- Berberine Regulated Lipid Metabolism in the Presence of C75, Compound C, and TOFA in Breast Cancer Cell Line MCF-7.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anti-apoptotic protein, BAX inhibitor-1 (BI-1), has a role in cancer/tumor progression. BI-1-overexpressing HT1080 and B16F10 cells produced higher lung weights and tumor volumes after injection into the tail veins of mice. Transfection of BI-1 siRNA into cells before injection blocked lung metastasis. in vitro, the overexpression of BI-1 increased cell mobility and invasiveness, with highly increased glucose consumption and cytosolic accumulation of lactate and pyruvate, but decreased mitochondrial O(2) consumption and ATP production. Glucose metabolism-associated extracellular pH also decreased as cells excreted more H(+), and sodium hydrogen exchanger (NHE) activity increased, probably as a homeostatic mechanism for intracellular pH. These alterations activated MMP 2/9 and cell mobility and invasiveness, which were reversed by the NHE inhibitor, 5-(N-ethyl-N-isopropyl) amiloride (EIPA), suggesting a role for NHE in cancer metastasis. In both in vitro and in vivo experiments, C-terminal deleted (CDeltaBI-1) cells showed similar results to control cells, suggesting that the C-terminal motif is required for BI-1-associated alterations of glucose metabolism, NHE activation and cancer metastasis. These findings strongly suggest that BI-1 reduces extracellular pH and regulates metastasis by altering glucose metabolism and activating NHE, with the C-terminal tail having a pivotal role in these processes.
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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.