Xiao-Heng Xu1, Da-Wei Li2, Hui Feng1, Hong-Mei Chen1, Yan-Qiu Song1. 1. Cancer Center, The First Hospital of Jilin University, Changchun Jilin P. R. China. 2. Department of Neurology, Affiliated Hospital of Beihua University Jilin, P. R. China.
Abstract
OBJECTIVE: In this study, we investigated the role of miR-300 in regulating cell proliferation and invasion of breast cancer (BC) cells. METHODS: MicroRNA and protein expression patterns were compared between breast cancer tissue and normal tissue and between two different prognostic groups. The up-regulation of miR-300 was confirmed by real-time reverse transcription polymerase chain reaction and its expression was analyzed in MCF-7 breast cancer cells. RESULTS: We observed that miR-300 expression was frequently and dramatically up-regulated in human breast cancer tissues and cell lines compared with the matched adjacent normal tissues and cells. We further showed that transient and stable over-expression of miR-300 could promote cell proliferation and cell cycle progression. Moreover, p53, a key inhibitor of cell cycle, was verified as a direct target of miR-300, suggesting that miR-300 might promote breast cancer cell proliferation and invasion by regulating p53 expression. CONCLUSION: Our findings indicated that miR-300 up-regulation might exert some sort of antagonistic function by targeting p53 in breast cancer cell proliferation during breast tumorigenesis.
OBJECTIVE: In this study, we investigated the role of miR-300 in regulating cell proliferation and invasion of breast cancer (BC) cells. METHODS: MicroRNA and protein expression patterns were compared between breast cancer tissue and normal tissue and between two different prognostic groups. The up-regulation of miR-300 was confirmed by real-time reverse transcription polymerase chain reaction and its expression was analyzed in MCF-7 breast cancer cells. RESULTS: We observed that miR-300 expression was frequently and dramatically up-regulated in humanbreast cancer tissues and cell lines compared with the matched adjacent normal tissues and cells. We further showed that transient and stable over-expression of miR-300 could promote cell proliferation and cell cycle progression. Moreover, p53, a key inhibitor of cell cycle, was verified as a direct target of miR-300, suggesting that miR-300 might promote breast cancer cell proliferation and invasion by regulating p53 expression. CONCLUSION: Our findings indicated that miR-300 up-regulation might exert some sort of antagonistic function by targeting p53 in breast cancer cell proliferation during breast tumorigenesis.
Entities:
Keywords:
MCF-7; MiR-300; breast cancer; p53; target therapy
Authors: Xiaohui Tan; Jin Peng; Yebo Fu; Shejuan An; Katayoon Rezaei; Sana Tabbara; Christine B Teal; Yan-gao Man; Rachel F Brem; Sidney W Fu Journal: Breast Cancer Res Date: 2014-09-17 Impact factor: 6.466
Authors: J Finlay-Schultz; D M Cittelly; P Hendricks; P Patel; P Kabos; B M Jacobsen; J K Richer; C A Sartorius Journal: Oncogene Date: 2014-09-22 Impact factor: 9.867