title: INHIBITORY ACTION OF CoCl2-INDUCED MCF-7 CELL HYPOXIA MODEL OF BREAST CANCER AND ITS INFLUENCE ON VASCULAR ENDOTHELIAL GROWTH FACTOR.
abstract: Breast cancer, a malignant tumor frequently occurring in females, is traditionally treated with excision. In the search for a new treatment, we analyzed the influence of CoCl2 on MCF-7 cell proliferation of breast cancer and tumor angiogenesis factor and discussed the results. Having applied CoCl2 as chemical hypoxia-induced agent, in-vitro MCF-7 cell hypoxia model of breast cancer was established, after which methyl thiazolyl tetrazolium (MTT) staining was performed in detecting inhibitory action of CoCl2 to proliferation of MCF-7 cells cultured in-vitro, and inverted phase contrast microscope was adopted to observe morphological changes of MCF-7 cell in hypoxia model. Furthermore, reverse transcription-polymerase chain reaction (RT-PCR) was made to determine how CoCl2 influences mRNA expression changes of hypoxia inducible factor-1α (HIF-1α), chemokine receptor-4 (CXCR4) and vascular endothelial growth factor (VEGF) in MCF-7 cells. Western blot was designed to study and record data on the influence of CoCl2 on protein expression changes of HIF-1α, CXCR4 and VEGF. As a result, CoCl2 was proved to control MCF-7 cell proliferation and increase expression of HIF-1α, CXCR4 and VEGF.
authors.affiliation: Department of Breast and Thyroid Surgery, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
authors.forename: M
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Department of Breast Surgery, Qi Lu Hospital of Shandong University, Jinan, China.
authors.forename: R
authors.initials: R
authors.lastname: Ma
authors.affiliation: Department of Breast and Thyroid Surgery, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
authors.forename: Q
authors.initials: Q
authors.lastname: Li
mesh_terms: D016587:Antimutagenic Agents / Q000494:pharmacology*; D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology; D015687:Cell Hypoxia / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D003035:Cobalt / Q000494:pharmacology*; D005260:Female; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D009363:Neoplasm Proteins / Q000378:metabolism*; D019718:Receptors, CXCR4 / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis*
chemical_list: D016587:Antimutagenic Agents; C527276:CXCR4 protein, human; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D009363:Neoplasm Proteins; D019718:Receptors, CXCR4; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D003035:Cobalt; C018021:cobaltous chloride