ArticleClinical and experimental medicine2013
Recombinant human leptin induces growth inhibition and apoptosis in human gastric cancer MGC-803 cells.
Article in Clinical and experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- A Variant ofPharmacogenomics and personalized medicine · 2020Article
- Anti-neuropilin-1 monoclonal antibody suppresses the migration and invasion of human gastric cancer cells via Akt dephosphorylation.Experimental and therapeutic medicine · 2018Article
- Effects of UCP4 on the Proliferation and Apoptosis of Chondrocytes: Its Possible Involvement and Regulation in Osteoarthritis.PloS one · 2016Article
- A suppressor of cytokine signaling 1 antagonist enhances antigen-presenting capacity and tumor cell antigen-specific cytotoxic T lymphocyte responses by human monocyte-derived dendritic cells.Clinical and vaccine immunology : CVI · 2013Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
The aim of this study is to investigate the effect of recombinant human leptin (rhLep) on the proliferation of human gastric cancer MGC-803 cells and its underlying mechanisms. RT-PCR was performed to identify the expression of leptin receptor (Ob-R). Cell proliferation was measured with MTT assay. DNA content and cell cycle were analyzed by flow cytometry. Apoptosis was assessed by DNA ladder assay and flow cytometry analysis using Annexin V-FITC/PI double staining. Underlying mechanisms of rhLep-induced apoptosis were evaluated by the activities of caspase-3, -8, -9, and cytochrome c release from mitochondria. Moreover, the phosphorylation of STAT3 in MGC-803 cells upon rhLep administration was detected by Western blot analysis. Our results demonstrated that two leptin receptors (Ob-Ra and Ob-Rb) were expressed in MGC-803 cells. rhLep diminished the proliferation rate of MGC-803 cells in a time- and concentration-dependent manner and induced MGC-803 cell apoptosis involving in the activation of caspase-8 and caspase-3 but not caspase-9. In addition, rhLep failed to induce cytochrome c release from mitochondria and had no effect on the activation of STAT3 in MGC-803 cells. Therefore, from these results, we concluded that rhLep significantly inhibited cell proliferation via G0/G1 phase cell cycle arrest and induced apoptosis through the extrinsic apoptotic pathway in human gastric cancer MGC-803 cells.
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