Regulatory effect and mechanism of RNA binding motif protein 38 on the expression of progesterone receptor in human breast cancer ZR-75-1 cell
10.3760/cma.j.issn.0253-3766.2016.06.005
- VernacularTitle:人乳腺癌ZR-75-1细胞中RNA结合蛋白38对孕激素受体表达的调节作用及其机制
- Author:
Peipei Lou S
1
;
Chunlian LI
;
Tiansong XIA
;
Liang SHI
;
Jing WU
;
Xujie ZHOU
;
Ying WANG
;
Qiang DING
Author Information
1. 210029,南京医科大学第一附属医院乳腺外科
- Keywords:
Breast neoplasms;
RNA binding motif protein 38;
RNPC1;
Progesterone
- From:
Chinese Journal of Oncology
2016;38(6):425-429
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the regulatory mechanism of RNA binding motif protein 38 (RNPC1) on the expression of progesterone receptor (PR) in breast cancer cell line ZR?75?1. Methods Lentiviral vector was used to induce overexpression of RNPC1 in ZR?75?1 cells. qRT?PCR and Western blot were used to assess the regulatory effect of RNPC1 on PR expression. Actinomycin was used to detect the regulatory mechanism involved. Immunohistochemical ( IHC) staining was used to determine the protein expression of RNPC1 and PR in 80 breast cancer tissues. Results IHC staining showed that the expression of RNPC1 was significantly higher in the PR positive breast cancer tissues than that in the PR negative breast cancer tissues ( P<0.05) . The qRT?PCR results showed that overexpression of RNPC1 in ZR?75?1 cells significantly upregulated the mRNA level of PR (1.764±0.028 vs. 1.001±0.037, P<0.01), whereas knockdown of RNPC1 did the opposite (0.579± 0.007 vs. 1.000±0.002, P<0.01).The Western blot results also showed that overexpression of RNPC1 up?regulated PR levels, while knockdown of RNPC1 resulted in down?regulation of PR levels in the ZR?75?1 cells. The actinomycin assay showed that overexpression of RNPC1 increased the mRNA stability of PR. The half?life of PR mRNA was increased from 4. 0 h to 6. 5 h. Knockdown of RNPC1 decreased the mRNA stability of PR and the half?life of PR transcript was decreased from 4.1 h to 3.0 h. Conclusion RNPC1 plays a crucial role in regulating the expression of PR in breast cancer ZR?75?1 cells.
