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Effect of RRS1 gene knockdown on BT549 cell line proliferation and apoptosis in breast cancer
Author(s) -
Yanan Hua,
Junying Song,
Zeng Z.-L.,
Liqun Wu,
Z. Zhang,
L. Zhang,
N. Li,
Shaobo Cong,
Lin Hou
Publication year - 2019
Publication title -
neoplasma
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.628
H-Index - 50
eISSN - 1338-4317
pISSN - 0028-2685
DOI - 10.4149/neo_2018_171229n853
Subject(s) - gene knockdown , apoptosis , cell growth , cancer research , mtt assay , flow cytometry , microbiology and biotechnology , biology , viability assay , genetics
The RRS1 regulator of ribosome synthesis has recently been reported a new target gene linked to cancer development. This study therefore investigates RRS1effectsb on BT549 cell proliferation and apoptosis in breast cancer. Western blot (WB) and real - time quantitative PCR (qPCR) were used to detect the relative expression of RRS1 in breast cancer cells BT-549 and the normal HMEC mammary gland epithelial cells. BT-549 cells were cultured and infected with retroviruses and RRS1 expression was detected by qPCR and WB. The MTT assay, Caspase-3/7 and flow cytometry (FCM) then detected growth and apoptosis in the BT549 breast cancer BT cell. WB detected the expression of Bcl-2 and Bax genes related to apoptosis at the protein level, and MTT assay confirmed that RRS1 knockdown significantly decreased cell viability (p<0.05) and induced apoptosis which was rescued by shRNA-RRS1 expression. The amount of caspase-3 increased significantly and apoptosis was obvious. The apoptotic cells amount analyzed by FCM was significantly increased and RRS1 knockdown also decreased the expression of apoptosis related protein bcl-2 and simultaneously increased the expression of Bax (p<0.05). Finally, the RRS1 gene was highly expressed in breast cancer cell line BT549 and its knockdown significantly reduced proliferation and apoptosis in BT549 cell. These results suggest that RRS1 is a novel gene related to breast cancer and has an important role in breast cancer proliferation and apoptosis.

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