Search

Your search keyword '"ZI-JIE MEI"' showing total 2 results
Start Over Author "ZI-JIE MEI" Search Limiters Academic (Peer-Reviewed) Journals
2 results on '"ZI-JIE MEI"'

1. Altered DNA Methylation and Gene Expression Profiles in Radiation-Induced Heart Fibrosis of Sprague-Dawley Rats

Author

Ye, Yao, Li-Feng, Chen, Jin, Li, Jing, Chen, Xiao-Li, Tian, Hui, Wang, Zi-Jie, Mei, Cong-Hua, Xie, and Ya-Hua, Zhong

Subjects
Rats, Sprague-Dawley, Radiation, Myocardium, Biophysics, Animals, Humans, CpG Islands, Radiology, Nuclear Medicine and imaging, DNA Methylation, Transcriptome, Fibrosis, Epigenesis, Genetic, Rats
Abstract

Radiation-induced heart disease (RIHD) is a serious side effect of radiotherapy for thoracic tumors. Advanced myocardial fibrosis in the late phase of RIHD can lead to myocardial remodeling, heart function impairing and heart failure, resulting in serious clinical consequences, and its pathogenesis remains vague. DNA methylation is one of the important epigenetic mechanisms which often occurs in response to environmental stimuli and is crucial in regulating gene expression. We hypothesized DNA methylation may contribute to pathogenesis in radiation-induced heart fibrosis (RIHF) and altered DNA methylation patterns probably influenced the genes expression in RIHF. In present study, we found genome-wide differences in DNA methylation status and RNA expression were demonstrated and we screened out 44 genes whose altered expression maybe were regulated by CpG island methylation within the gene promoter in RIHF of Sprague-Dawley rat by employing gene expression arrays and human CpG island microarrays. Gene expression and CpG island methylation levels of several candidate genes were further validated. Our investigation provided a new dimension to reveal the specific mechanisms of RIHF and explore the potential therapeutic targets for it.

Published
2022

2. MicroRNA-320 regulates the radiosensitivity of cervical cancer cells C33AR by targeting β-catenin.

Author

CHUN-XU YANG, SHI-MIN ZHANG, JIE LI, BO YANG, WEN OUYANG, ZI-JIE MEI, JING CHEN, JING DAI, SU KE, FU-XIANG ZHOU, YUN-FENG ZHOU, and CONG-HUA XIE

Subjects
CERVICAL cancer diagnosis, CERVICAL cancer, MICRORNA, CATENINS, GENE targeting, POLYMERASE chain reaction, BIOMARKERS, RADIATION-sensitizing agents, GENETICS
Abstract

Cervical cancer is the second most common malignancy in women worldwide and always has recurrence owing to radioresistance. MicroRNA (miRNA or miR) has been identified to relate to the sensitivity of cancer radiotherapy. Here, we investigated the potential of miRNA-320 as a biomarker for radiosensitivity by targeting β-catenin in cervical cancer. A radioresistant cervical cancer cell line, C33AR, was established, and the radioresistance of C33AR cells was confirmed by a colony-formation assay. The expression of miRNA-320 was detected by reverse transcription-quantitative polymerase chain reaction, and compared between C33A and C33AR. β-catenin, the target of miRNA-320, was determined at the protein level by western blotting after transfecting the inhibitor of miRNA-320. The expression of miRNA-320 was markedly decreased in C33AR cells, which appeared to be more radioresistant, compared with its parental cell line C33A. Target prediction suggested that miRNA-320 negatively regulated the expression of β-catenin. Knockdown of β-catenin increased C33AR radiosensitivity, which revealed that the inhibition of β-catenin could rescue the miRNA-320-mediated cell radioresistance. On the other hand, overexpressing miRNA-320 increased C33AR radiosensitivity. In conclusion, miRNA-320 regulated the radiosensitivity of C33AR cells by targeting β-catenin. This finding provides evidence that miRNA-320 may be a potential biomarker of radiosensitivity in cervical cancer. [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results