Abstract
Abstract Breast cancer is the most common cancer in women and distant site metastasis is the main cause of death in breast cancer patients. EMT is a natural phenomenon in development and wound healing. EMT is also one of the “Hallmarks of cancer”. EMT is involved in tumor cell progression, invasion, and metastasis. During the process of EMT, epithelial cancer cells acquire molecular alternations that facilitate the loss of epithelial features and gain of mesenchymal phenotype. Such transformation promotes cancer cell migration and invasion. Decrease in E-cadherin expression and gain of N-cadherin and vimentin expression is indicative of EMT phenotype. Working with our recently characterized C4 zinc finger containing RNA binding protein ZAR2 we observed that levels of ZAR2 are significantly lower in the invasive breast cancer cells compared to non-invasive cells. Knockdown of ZAR2 in the non-invasive breast cancer cells increased the in-vitro invasiveness of these cells whereas forced expression of ZAR2 in the invasive breast cancer cells reduced their invasiveness. To understand the possible mechanism of ZAR2-mediated regulation of invasiveness of the breast cancer cells we studied differential gene expression in the ZAR2 knocked down non-invasive breast cancer cells by RNA-seq analysis. One of the genes that are significantly elevated in the ZAR2 knocked down cells is the invasion determining enzyme ATP6V0A4 along with ERBIN and ABCA12. Here we present our observation regarding ZAR2 regulation of ATP6V0A4 and its effect on metastasis and invasion potential of the breast cancer cells. Supported in part by NIH grant 1U54RR026140, Meharry Bridge and 2U54MD007586-32Revised from Meharry RCMI Program in Women’s Health funds to SM and DOD grants BC990678 and BC050641 to GC. Citation Format: Smita Misra, Tanushree Singha, Gautam Chaudhuri. Zygote arrest 1 like (ZAR2): An EMT (epithelial-mesenchymal transition) modulator in breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1886.
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