连接蛋白
缝隙连接
癌症研究
生物
乳腺癌
癌症
癌细胞
内科学
下调和上调
细胞培养
细胞生物学
转移
作者
Jennifer Jones,Amanda M. Miceli,Mary M. Chaudhry,Mallika A. Jai,Romel N. Pancho,Alan Lazzar,Bradley S. Taylor,Vishnupriya Bodempudi,Prarthana P. Jain,Sheeri Hanjra,Alexander E. Urban,Brian Zanotti,Ellen K Kohlmeir,Thomas M. Bodenstine
出处
期刊:Cancer Research
[American Association for Cancer Research]
日期:2020-08-15
卷期号:80: 5997-5997
标识
DOI:10.1158/1538-7445.am2020-5997
摘要
Dysregulation of gap junction intercellular communication (GJIC) is a common feature during cancer progression. GJIC is a means of direct cell-cell communication mediated by regulated membrane channels composed of connexin proteins. This communication is frequently lost between primary tumor cells but may be upregulated at secondary metastatic sites with stromal cells. Control of this process by cancer cells has been shown to facilitate aggressive qualities both in vitro and in vivo. During the process of metastasis, cells encounter numerous metabolic challenges that must be overcome, particularly during growth of primary tumors. In this study, we set out to evaluate if changes to cancer cell metabolism affect GJIC in breast cancer cells. To address this question, we generated a metabolic variant of the MDA-MB-231 cell line conditioned to grow in glucose-limiting conditions. These cells were grown in FBS supplemented RPMI with Citation Format: Jennifer C. Jones, Amanda M. Miceli, Mary M. Chaudhry, Mallika A. Jai, Romel N. Pancho, Alan Lazzar, Bradley S. Taylor, Vishnupriya Bodempudi, Prarthana P. Jain, Sheeri Hanjra, Alexander E. Urban, Brian Zanotti, Ellen K. Kohlmeir, Thomas M. Bodenstine. Increased connexin 43 expression and gap junction communication correlates with invasion following reduced glucose metabolism in breast cancer cells [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 5997.
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