ArticleOncotarget2015
The Vacuolar ATPase a2-subunit regulates Notch signaling in triple-negative breast cancer cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- The V-ATPases in cancer and cell death.Cancer gene therapy · 2022Review
- Inhibition of autophagy by chloroquine prevents resistance to PI3K/AKT inhibitors and potentiates their antitumor effect in combination with paclitaxel in triple negative breast cancer models.Journal of translational medicine · 2022Article
- Disruption of pH Dynamics Suppresses Proliferation and Potentiates Doxorubicin Cytotoxicity in Breast Cancer Cells.Pharmaceutics · 2021Article
- Inhibiting ATP6V0D2 Aggravates Liver Ischemia-Reperfusion Injury by Promoting NLRP3 Activation via Impairing Autophagic Flux Independent of Notch1/Hes1.Journal of immunology research · 2021Article
- In vivo anti-V-ATPase antibody treatment delays ovarian tumor growth by increasing antitumor immune responses.Molecular oncology · 2020Article
- Quantitative label-free imaging of iron-bound transferrin in breast cancer cells and tumors.Redox biology · 2020Article
- RHOQ is induced by DLL4 and regulates angiogenesis by determining the intracellular route of the Notch intracellular domain.Angiogenesis · 2020Article
- Cancer-associated V-ATPase induces delayed apoptosis of protumorigenic neutrophils.Molecular oncology · 2020Article
- Targeting V-ATPase Isoform Restores Cisplatin Activity in Resistant Ovarian Cancer: Inhibition of Autophagy, Endosome Function, and ERK/MEK Pathway.Journal of oncology · 2019Article
- Rhamnetin induces apoptosis in human breast cancer cells via the miR-34a/Notch-1 signaling pathway.Oncology letters · 2019Article
- The "Yin and Yang" of Natural Compounds in Anticancer Therapy of Triple-Negative Breast Cancers.Cancers · 2018Review
- Hematopoietic stem cell specific V-ATPase controls breast cancer progression and metastasis via cytotoxic T cells.Oncotarget · 2018Article
- Vacuolar ATPase as a potential therapeutic target and mediator of treatment resistance in cancer.Cancer medicine · 2018Review
- Autophagy flux inhibition augments gastric cancer resistance to the anti-human epidermal growth factor receptor 2 antibody trastuzumab.Oncology letters · 2018Article
- The curious case of vacuolar ATPase: regulation of signaling pathways.Molecular cancer · 2018Review
- Identification of Novel Bisbenzimidazole Derivatives as Anticancer Vacuolar (H⁺)-ATPase Inhibitors.Molecules (Basel, Switzerland) · 2017Article
- The V-ATPase a2 isoform controls mammary gland development through Notch and TGF-β signaling.Cell death & disease · 2016Article
- The Function of V-ATPases in Cancer.Physiological reviews · 2016Review
- Selective inhibition of tumor cell associated Vacuolar-ATPase 'a2' isoform overcomes cisplatin resistance in ovarian cancer cells.Molecular oncology · 2016Article
- Cancer: fundamentals behind pH targeting and the double-edged approach.OncoTargets and therapy · 2016Article
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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
Triple Negative Breast Cancer (TNBC) is a subtype of breast cancer with poor prognosis for which no targeted therapies are currently available. Notch signaling has been implicated in breast cancer but the factors that control Notch in TNBC are unknown. Because the Vacuolar ATPase has been shown to be important in breast cancer invasiveness, we investigated the role of a2-subunit isoform of Vacuolar ATPase (a2V) in regulating Notch signaling in TNBC. Confocal microscopy revealed that among all the 'a' subunit isoforms, a2V was uniquely expressed on the plasma membrane of breast cancer cells. Both a2V and NOTCH1 were elevated in TNBC tumors tissues and cell lines. a2V knockdown by siRNA as well as V-ATPase inhibition by Bafilomycin A1 (Baf A1) in TNBC cell lines enhanced Notch signaling by increasing the expression of Notch1 intracellular Domain (N1ICD). V-ATPase inhibition blocked NICD degradation by disrupting autophagy and lysosomal acidification as demonstrated by accumulation of LC3B and diminished expression of LAMP1 respectively. Importantly, treatment with Baf A1 or anti-a2V, a novel-neutralizing antibody against a2V hindered cell migration of TNBC cells. Our findings indicate that a2V regulates Notch signaling through its role in endolysosomal acidification and emerges as a potential target for TNBC.
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