Jianxin Lv1, Ziyi Fu2, Min Shi1, Kai Xia3, Chenbo Ji2, Pengfei Xu2, Mingming Lv2, Bo Pan1, Luxian Dai1, Hui Xie4. 1. Yangzhou Maternal and Child Health Hospital, Affiliated with Yangzhou Medical University, Yangzhou 225002, China. 2. Nanjing Maternal and Child Health Medical Institute, Affiliated Nanjing Maternal and Child Health Hospital, Nanjing Medical University, Nanjing 210004, China. 3. The Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin 214400, China. 4. Nanjing Maternal and Child Health Medical Institute, Affiliated Nanjing Maternal and Child Health Hospital, Nanjing Medical University, Nanjing 210004, China; The People's Hospital of Jiangsu Province/The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China. Electronic address: xhfybj@163.com.
Abstract
BACKGROUND/AIMS: Chemoresistance of breast cancer is a growing problem and still a major clinical obstacle to successful treatment in clinical patients. miR-760 was significantly downregulated in chemoresistance breast cancer tissues compared to chemo-sensitive tissues in our previous study. However, the role of miR-760 in modulating drug resistance remains largely unexplored. In this study, we sought to determine the expression pattern of miR-760 targeted mRNAs, and explore their potential functions and participated-pathways in breast cancer drug resistance cells. RESULTS: Compared to parental cell line MCF-7, miR-760 was downregulated by 6.15 folds in MCF-7/Adr cells. The qRT-PCR result showed that compared to miR-760 negative control cells group, miR-760 was up-regulated 15.817 folds after miR-760 lentiviral transfection in miR-760 mimics group. The microarray data showed that 270 genes were dysregulated over 2-fold change in MCF-7/Adr cells after miR-760 overexpressed, including 241 up-regulated and 29 downregulated genes. GO analysis result appeared that the predicted target genes of miR-760 mainly regulated DNA binding, protein binding, molecular function, nucleic acid binding, and so on; the pathway analysis data demonstrated that these target genes mainly involved in cell cycle, TGF-beta signaling pathway, mRNA processing reactome, G protein signaling, apoptosis, Wnt signaling pathway, and other signaling pathways. There were 3 predicted target genes (RHOB, ANGOTL4, ABCA1) of miR-760 were selected at a P value<0.05 and the fold enrichment was>40. CONCLUSION: Our study explored the genes expression pattern after miR-760 overexpresssed, and confirmed 3 dominantly dysregulated genes, which could expand the insights into the miR-760 function and molecular mechanisms in drug resistance of breast cancer. This study might afford a comprehensive understanding of miR-760 as prognostic biomarkers during clinical treatment, and we supposed that the miR-760 expression levels in drug resistance carcinoma tissues could be pursued to develop new strategies for targeted therapies in chemoresistant breast cancer patients.
BACKGROUND/AIMS: Chemoresistance of breast cancer is a growing problem and still a major clinical obstacle to successful treatment in clinical patients. miR-760 was significantly downregulated in chemoresistance breast cancer tissues compared to chemo-sensitive tissues in our previous study. However, the role of miR-760 in modulating drug resistance remains largely unexplored. In this study, we sought to determine the expression pattern of miR-760 targeted mRNAs, and explore their potential functions and participated-pathways in breast cancer drug resistance cells. RESULTS: Compared to parental cell line MCF-7, miR-760 was downregulated by 6.15 folds in MCF-7/Adr cells. The qRT-PCR result showed that compared to miR-760 negative control cells group, miR-760 was up-regulated 15.817 folds after miR-760 lentiviral transfection in miR-760 mimics group. The microarray data showed that 270 genes were dysregulated over 2-fold change in MCF-7/Adr cells after miR-760 overexpressed, including 241 up-regulated and 29 downregulated genes. GO analysis result appeared that the predicted target genes of miR-760 mainly regulated DNA binding, protein binding, molecular function, nucleic acid binding, and so on; the pathway analysis data demonstrated that these target genes mainly involved in cell cycle, TGF-beta signaling pathway, mRNA processing reactome, G protein signaling, apoptosis, Wnt signaling pathway, and other signaling pathways. There were 3 predicted target genes (RHOB, ANGOTL4, ABCA1) of miR-760 were selected at a P value<0.05 and the fold enrichment was>40. CONCLUSION: Our study explored the genes expression pattern after miR-760 overexpresssed, and confirmed 3 dominantly dysregulated genes, which could expand the insights into the miR-760 function and molecular mechanisms in drug resistance of breast cancer. This study might afford a comprehensive understanding of miR-760 as prognostic biomarkers during clinical treatment, and we supposed that the miR-760 expression levels in drug resistance carcinoma tissues could be pursued to develop new strategies for targeted therapies in chemoresistant breast cancerpatients.
Authors: Alma D Campos-Parra; Gerardo Cuamani Mitznahuatl; Abraham Pedroza-Torres; Rafael Vázquez Romo; Fany Iris Porras Reyes; Eduardo López-Urrutia; Carlos Pérez-Plasencia Journal: Int J Mol Sci Date: 2017-06-02 Impact factor: 5.923
Authors: Naira V Margaryan; Hannah Hazard-Jenkins; Mohamad A Salkeni; Matthew B Smolkin; James A Coad; Sijin Wen; Elisabeth A Seftor; Richard E B Seftor; Mary J C Hendrix Journal: Cancers (Basel) Date: 2019-03-08 Impact factor: 6.639