ArticleClinical and experimental medicine2012
A monoclonal antibody (Mc178-Ab) targeted to the ecto-ATP synthase β-subunit-induced cell apoptosis via a mechanism involving the MAPKase and Akt pathways.
Article in Clinical and experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- The function of Cav-1 in MDA-MB-231 breast cancer cell migration and invasion induced by ectopic ATP5B.Medical oncology (Northwood, London, England) · 2021Article
- Identification of Multi-Target Anti-AD Chemical Constituents From Traditional Chinese Medicine Formulae by Integrating Virtual Screening andFrontiers in pharmacology · 2021Article
- Tanshinone I inhibited growth of human chronic myeloid leukemia cells via JNK/ERK mediated apoptotic pathways.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- Natural products and other inhibitors of FEuropean journal of medicinal chemistry · 2020Review
- Multiomics Reveals Ectopic ATP Synthase Blockade Induces Cancer Cell Death via a lncRNA-mediated Phospho-signaling Network.Molecular & cellular proteomics : MCP · 2020Article
- Cellular Mechanisms of Circulating Tumor Cells During Breast Cancer Metastasis.International journal of molecular sciences · 2020Review
- A novel RNA aptamer identifies plasma membrane ATP synthase beta subunit as an early marker and therapeutic target in aggressive cancer.Breast cancer research and treatment · 2019Article
- BAMLET kills chemotherapy-resistant mesothelioma cells, holding oleic acid in an activated cytotoxic state.PloS one · 2018Article
- A humanized chimeric antibody Hai178 targeted to the β subunit of F1F0 ATP synthase.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- The F0F1 ATP Synthase Complex Localizes to Membrane Rafts in Gonadotrope Cells.Molecular endocrinology (Baltimore, Md.) · 2016Article
- Temporal Phosphoproteome Dynamics Induced by an ATP Synthase Inhibitor Citreoviridin.Molecular & cellular proteomics : MCP · 2015Article
- ATP synthase: the right size base model for nanomotors in nanomedicine.TheScientificWorldJournal · 2014Review
- ATP synthase: a molecular therapeutic drug target for antimicrobial and antitumor peptides.Current medicinal chemistry · 2013Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ecto-ATP synthase has been considered to be an effective target for cancer recently. As inhibitors of ecto-ATP synthase were found to be cytotoxic for tumor cells, a monoclonal antibody (Mc178-Ab) against ecto-ATP synthase was generated in our previous study that exhibited both anti-angiogenic and anti-tumorigenic effects. However, the mechanism of action of Mc178-Ab and its downstream pathways for anti-tumor effects remain unclear. In this research, we intended to investigate the mechanism of the anti-tumor action of Mc178-Ab. The expressions of cell surface ATP synthase on A549 and CHO cells were confirmed by flow cytometry and confocal microscope. Proliferation and apoptosis were examined after the treatment with Mc178-Ab. In order to examine the activity of ecto-ATP synthase changed by Mc178-Ab, extracellular ATP generation and intracellular pH levels were assessed. The phosphorylation of the signaling molecules, MAPKase and Akt, was analyzed by western blot. Cell proliferation was blocked, and apoptosis was induced in A549 cells treated with Mc178-Ab, as determined by MTT assay and flow cytometry analysis of Annexin-V/PI staining separately. The intracellular pH level and extracellular ATP generation were also decreased after Mc178-Ab treatment. Finally, western blot data revealed that the phosphorylation of JNK and p38 was increased, while the phosphorylation of ERK and Akt was decreased in A549 cells treated with Mc178-Ab. Compared with A549 cells, Mc178-Ab had less effect on CHO cells. The decreased intracellular pH levels and the altered concentration of extracellular ATP may contribute to the mechanisms of the effect of Mc178-Ab on A549 and CHO cells. The results also suggested that the anti-tumor effect of Mc178-Ab was associated with MAPKase and Akt pathways.
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