Affiliations: [a] Department of Breast Surgery, Sichuan Academy of Medical Sciences and Sichuan Provincial People’s Hospital, Chengdu 610072, China | [b] Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu 610072, China | [c] Department of Oncology, The General Hospital of Western Theater Command, Chengdu 610072, China | [d] Department of Oncology, Sichuan Academy of Medical Sciences and Sichuan Provincial People’s Hospital, Chengdu 610072, China
Correspondence:
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Corresponding author: Haixia Pan, Department of Oncology, Sichuan Academy of Medical Sciences and Sichuan Provincial People’s Hospital, 32 West Section 2, Yihuan Road, Chengdu 610072, China. Tel./Fax: +86 28 87394133; E-mail: [email protected].
Note: [1] These authors contributed equally to this work.
Abstract: BACKGROUND: The PANDAR, a novel identified long non-coding RNA, is previously reported to function as oncogene in various cancers including breast cancer. the study aims to explore the role of lncRNA PANDAR for cell proliferation and invasion of breast cancer, and its underlying mechanism. METHODS: The expression of lncRNA PANDAR in 65 pairs of breast cancer tissues and adjacent normal tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR) assay. The association between lncRNA PANDAR expression and clinical factors of breast cancer was analyzed. Cell proliferation, cell colony formation and cell invasion assays were performed to detect the effects of lncRNA PANDAR expression tumor proliferation and invasion abilities. The western blot analysis was also performed to detected the EMT related makers expression of E-cadherin, Vimentin, MMP2 and MMP9. RESULTS: We demonstrated that lncRNA PANDAR expression was higher in breast cancer tissues and cells compared with adjacent normal tissues and the normal mammary epithelial cell line, respectively. Higher lncRNA PANDAR expression positively associated with lymph node metastasis and advanced clinical stage in patients. In vitro, we demonstrated that knockdown of lncRNA PANDAR significantly suppressed cell proliferation, cell colony formation and cell invasion ability in breast cells. Furthermore, we verified that knockdown of lncRNA PANDAR dramatically inhibited cell epithelial-mesenchymal transition (EMT) pathway by downregulating Vimentin, MMP2 and MMP9 expression, but upregulating E-cadherin expression in breast cancer. CONCLUSIONS: Our results proved that PANDAR may serve as potential target of breast cancer treatment.
