The expression of RBM7 and its relationship with P21 in breast cancer cell BT474
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    Abstract:

    Objective:This study aims to investigate the relationship between RNA binding protein 7(RBM7) and P21 via overexpressing and knocking down RBM7 in human breast cancer cell BT474. Methods:BT474 cells were respectively transfected with RBM7 overexpressing,knocking down lentivirus(experimental group)and corresponding control lentivirus(control group). The expression of RBM7 was verified after BT474 stably transfected with RBM7 letivirus by the qRT-PCR and Western blot assays. The effects of RBM7 overexpression or knock down on breast cancer proliferation were evaluated by using CCK-8 assays. At the same time,the flow cytometry assays were used to detect the cell cycle distribution of RBM7 overexpression or knock down. The qRT-PCR and Western blot assays were used to investigate the expression of P21 following the variation of RBM7. Furthermore,the relationship between RBM7 and P21 was studied by RNA binding protein immunoprecipitation(RIP) assays. Results:The green fluorescence was observed by fluorescence microscope when BT474 was transfected with RBM7 overexpression and knock down lentivirus after 48 h. After stably screening,the fluorescence expression of cells was significantly stronger. CCK-8 and the flow cytometry assays showed that overexpressing RBM7 could promote the proliferation of breast cancer cells,while knocking down RBM7 could inhibit the proliferation of breast cancer cells. It was observed that overexpression of RBM7 could downregulate mRNA(P < 0.05)and protein expression of P21,and knockdown of RBM7 upregulated mRNA(P < 0.05)and protein expression of P21 by qRT-PCR and Western blot. It was revealed that RBM7 could directly bind to mRNA of P21 by RNA-binding protein immunoprecipitation(RIP)assays. Conclusion:RBM7 can downregulate the expression of P21 by binding to its transcript in breast cancer cell BT474.

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奚佩雯,胡 玥,张 旭,戴欣媛,石 靓,丁 强. RBM7在乳腺癌细胞BT474中的表达及其与P21的关系[J].南京医科大学学报(自然科学版英文版),2020,(2):160-165.

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  • Received:June 30,2019
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  • Online: March 14,2020
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