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- 저자 : Ping Hongyan (검색결과 4 건)
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Ping Hongyan,Wang Degang,Fu Maxian,Chen Kaihong,Zhang Jiuhong,Li Ke,Jiang Xuewu,Duan Shouxing,Zhang Xuan 대한독성 유전단백체 학회 2022 Molecular & cellular toxicology Vol.18 No.4
Background Diethylstilbestrol (DES) has been shown to disrupt the morphology and proliferation of gubernaculum testis cells. Objective This study aimed to elucidate the mechanism underlying DES induced damage to gubernaculum testis based on proteome analysis. Results Neonatal mice were exposed to DES or control vehicle and the gonads were collected for isobaric tags for relative and absolute quantitation based proteomics analysis. We found that at the early and late stages of gubernaculum development, treatment with different concentrations of DES upregulated the expression of proteins which were generally involved in several function categories including single-organism process, cellular process, binding, catalytic activity, cell part and organelle. KEGG pathway analysis showed that cardiac muscle contraction, oxidative phosphorylation, calcium signaling and cGMP-PKG signaling pathway were the most dysregulated pathways associated with DES in the late stage of gubernaculum development, while steroid biosynthesis was the only enriched pathway in the early stage of gubernaculum development. Conclusion Proteomics profi ling and functional analysis reveal new clues on how DES interferes with cellular processes and disrupts the development of gubernaculum. These findings have potential applications in the treatment of genitourinary diseases such as cryptorchidism.
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Degradation Characteristics and Metabolic Pathway of 17β-estradiol (E2) by Rhodococcus sp. DS201
Qingmiao Yu,Ping Wang,Dongbo Liu,Ruixia Gao,Huanhuan Shao,Hongyan Zhao,Zhe Ma,Dan Wang,Hongliang Huo 한국생물공학회 2016 Biotechnology and Bioprocess Engineering Vol.21 No.6
In this study an E2-degrading bacterium was isolated from the activated sludge of a municipal treatment plant that treats the waste from a contraceptive medicineprocessing factory in Beijing, China. Using the observed morphological and physiological features of the bacterium and 16S rRNA sequence analysis, this bacterial strain was identified as Rhodococcus sp. DS201. Using single-factor experiments and orthogonal tests, it was demonstrated that, when strain DS210 bacteria were inoculated into MM medium at an initial concentration of 1 mg/L with an initial pH of 7 and an inoculum amount of 1%, complete degradation of E2 by this strain was achieved within 3 days at 30oC. After strain DS201 had degraded the E2, several E2 metabolites were detected in the culture extracts using high-performance liquid chromatography (HPLC); they were then further identified using HPLC with tandem mass spectrometry (LC-MS/MS). Mass spectrum analysis of the E2 degradation identified the following products: pent- 4-enoic acid; 2-ethyl-3-hydroxy-6-methylcyclohexane-1- carboxylic acid; 3-(7a-methyl-1,5-dioxooctahydro-1H-inden- 4-yl) propanoic acid; and 5-hydroxy-4-(3-hydroxypropyl)- 7a-methyloctahydro-1H-inden-1-one. These products have not previously been reported as parts of a mechanism for microbial E2 degradation and were suspected to be new metabolite products. Therefore, the E2 degradation pathway by strain DS201 is proposed herein.
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Liu Xiaoyi,Wei Qinglv,Yang Chenyue,Zhao Hongyan,Xu Jie,Mobet Youchaou,Luo Qingya,Yang Dan,Zuo Xinzhao,Chen Ningxuan,Yang Yu,Li Li,Wang Wei,Yu Jianhua,Xu Jing,Liu Tao,Yi Ping 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-
5-Methylcytosine (m5C) is a common RNA modification that modulates gene expression at the posttranscriptional level, but the crosstalk between m5C RNA modification and biomolecule condensation, as well as transcription factor-mediated transcriptional regulation, in ovarian cancer, is poorly understood. In this study, we revealed that the RNA methyltransferase NSUN2 facilitates mRNA m5C modification and forms a positive feedback regulatory loop with the transcription factor E2F1 in ovarian cancer. Specifically, NSUN2 promotes m5C modification of E2F1 mRNA and increases its stability, and E2F1 binds to the NSUN2 promoter, subsequently reciprocally activating NSUN2 transcription. The RNA binding protein YBX1 functions as the m5C reader and is involved in NSUN2-mediated E2F1 regulation. m5C modification promotes YBX1 phase separation, which upregulates E2F1 expression. In ovarian cancer, NSUN2 and YBX1 are amplified and upregulated, and higher expression of NSUN2 and YBX1 predicts a worse prognosis for ovarian cancer patients. Moreover, E2F1 transcriptionally regulates the expression of the oncogenes MYBL2 and RAD54L, driving ovarian cancer progression. Thus, our study delineates a NSUN2-E2F1-NSUN2 loop regulated by m5C modification in a manner dependent on YBX1 phase separation, and this previously unidentified pathway could be a promising target for ovarian cancer treatment.
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Hong Yan,Min Zhao,Shan Huang,Ping Chen,Wen-yong Wu,Jin Huang,Zheng-sheng Wu,Qiang Wu 한국유방암학회 2016 Journal of breast cancer Vol.19 No.1
Purpose: Prolactin (PRL) plays a critical role in breast cancer progression by activating its cognate receptor and promotes the growth and differentiation of breast cancer cells. Studies have shown that B-cell lymphoma 6 (BCL6) is the target gene of microRNA- 339-5p (miR-339-5p) and that BCL6 expression contributes to breast cancer progression. Herein, we identified PRL as a potent suppressor of BCL6 expression in human breast cancer cells. Methods: Western blotting and quantitative reverse transcription-polymerase chain reaction were used to investigate molecular mechanisms underlying miR-339-5p expression and BCL6 manipulation in MCF-7, T47D, and SKBR3 breast cancer cells. Phenotypic changes in these breast cancer cell lines were assessed by performing cell viability (MTT), colony formation, migration, and invasion assays. Results: PRL suppressed BCL6 protein and mRNA expression and upregulated miR-339-5p expression in MCF-7 and T47D breast cancer cells. Selective downregulation of miR-339-5p expression significantly reversed PRL-induced suppression of BCL6 mRNA and protein expression. Exogenous PRL stimulation significantly decreased the proliferation, colony formation, migration, and invasion of breast cancer cells, and suppression of miR-339-5p expression reversed these processes in vitro. Conclusion: These results indicated that PRL inhibited BCL6 expression and regulated breast cancer progression through a miR-339-5p-dependent pathway.
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