Yonggang Zuo1, Yue Li2, Zhenyu Zhou2, Mingde Ma2, Kanda Fu2. 1. Department of Breast and Thyroid Surgery, Huaihe Hospital of Henan University, Kaifeng, 475000, China. Electronic address: yonggangzou0071@163.com. 2. Department of Breast and Thyroid Surgery, Huaihe Hospital of Henan University, Kaifeng, 475000, China.
Abstract
BACKGROUND: Long non-coding RNA Metastasis associated lung adenocarcinoma transcript 1(lncRNA MALAT1) play important roles in tumor progression. In the present study, we determined the regulatory function of MALAT1 in triple-negative breast cancer (TNBC). METHODS: A total of 43 cases of TNBC tissues and paired adjacent non-tumor tissues were collected for the research. MALAT1 expression was explored by qRT-PCR. In vitro functional validation experiments were used to determine the effect of MALAT1 on TNBC progression. We further identified the downstream target miRNAs for MALAT1. RESULTS: Relative expression of MALAT1 was increased in TNBC tissues and cell lines. High MALAT1 expression was closely correlated to advance clinical features and poor overall survival in TNBC patients. Function assay showed that MALAT1 silencing significantly decreased cell proliferation, migration, and invasion. Flow cytometry assay revealed that MALAT1 inhibition significantly induced cell cycle arrest in the G0/G1 phase. In addition, we showed that the roles of MALAT1 on TNBC cells progression was mediated by miR-129-5p. CONCLUSION: Our results demonstrated that the "MALAT1-miR-129-5p" axis might play an important role in the progression of TNBC, thereby might provide a potential therapeutic strategy for the treatment of TNBC.
BACKGROUND: Long non-coding RNA Metastasis associated lung adenocarcinoma transcript 1(lncRNA MALAT1) play important roles in tumor progression. In the present study, we determined the regulatory function of MALAT1 in triple-negative breast cancer (TNBC). METHODS: A total of 43 cases of TNBC tissues and paired adjacent non-tumor tissues were collected for the research. MALAT1 expression was explored by qRT-PCR. In vitro functional validation experiments were used to determine the effect of MALAT1 on TNBC progression. We further identified the downstream target miRNAs for MALAT1. RESULTS: Relative expression of MALAT1 was increased in TNBC tissues and cell lines. High MALAT1 expression was closely correlated to advance clinical features and poor overall survival in TNBC patients. Function assay showed that MALAT1 silencing significantly decreased cell proliferation, migration, and invasion. Flow cytometry assay revealed that MALAT1 inhibition significantly induced cell cycle arrest in the G0/G1 phase. In addition, we showed that the roles of MALAT1 on TNBC cells progression was mediated by miR-129-5p. CONCLUSION: Our results demonstrated that the "MALAT1-miR-129-5p" axis might play an important role in the progression of TNBC, thereby might provide a potential therapeutic strategy for the treatment of TNBC.
Authors: Javier Martinez-Useros; Mario Martin-Galan; Maria Florez-Cespedes; Jesus Garcia-Foncillas Journal: Cancers (Basel) Date: 2021-06-27 Impact factor: 6.639