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Your search keyword '"Yan, Jun"' showing total 2 results
2 results on '"Yan, Jun"'

1. PCAF-mediated acetylation of Lin28B increases let-7 biogenesis in lung adenocarcinoma H1299 cells.

Author

Qu TT, Chen F, Wang J, Zhang YJ, Cheng MB, Sun WZ, Shen YF, and Zhang Y

Subjects
Acetylation, Adenocarcinoma pathology, Adenocarcinoma of Lung, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Humans, Lung Neoplasms pathology, Protein Binding, Adenocarcinoma genetics, Lung Neoplasms genetics, MicroRNAs genetics, RNA-Binding Proteins genetics, p300-CBP Transcription Factors genetics
Abstract

Background: Lin28B and its paralog Lin28A are small RNA binding proteins that have similar inhibitory effects, although they target separate steps in the maturation of let-7 miRNAs in mammalian cells. Because Lin28B participates in the promotion and development of tumors mostly by blocking the let-7 tumor suppressor family members, we sought to explore the associated mechanisms to gain insights into how Lin28B might be decreased in human cancer cells to increase let-7 levels and reverse malignancy., Results: We demonstrated that the histone acetyltransferase PCAF, via its cold shock domain, directly interacts with and subsequently acetylates Lin28B in lung adenocarcinoma-derived H1299 cells. RT-qPCR assays showed that both let-7a-1 and let-7g were increased in PCAF-transfected H1299 cells. Lin28B is acetylated by ectopic PCAF and translocates from the nucleus to the cytoplasm in H1299 cells., Conclusions: The effects of acetylated Lin28B on let-7a-1 and let-7g are similar to that of stable knockdown of Lin28B in H1299 cells. The new role of PCAF in mediating Lin28B acetylation and the specific release of its target microRNAs in H1299 cells may shed light on the potential application of let-7 in the clinical treatment of lung cancer patients.

Published
2018
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2. PCAF-mediated acetylation of Lin28B increases let-7 biogenesis in lung adenocarcinoma H1299 cells

Author

Jing Wang, Ting-ting Qu, Mo-bin Cheng, Fei Chen, Wen-zheng Sun, Ye Zhang, Yan-jun Zhang, and Yu-fei Shen

Subjects
0301 basic medicine, Cancer Research, Lung Neoplasms, Adenocarcinoma of Lung, Adenocarcinoma, DNA-binding protein, lcsh:RC254-282, 03 medical and health sciences, let-7, Cell Line, Tumor, microRNA, PCAF, Genetics, Humans, p300-CBP Transcription Factors, Gene knockdown, Chemistry, RNA-Binding Proteins, Acetylation, Cold-shock domain, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Cell biology, Gene Expression Regulation, Neoplastic, MicroRNAs, 030104 developmental biology, Oncology, Cytoplasm, Lin28B, Biogenesis, Research Article, Protein Binding
Abstract

Background Lin28B and its paralog Lin28A are small RNA binding proteins that have similar inhibitory effects, although they target separate steps in the maturation of let-7 miRNAs in mammalian cells. Because Lin28B participates in the promotion and development of tumors mostly by blocking the let-7 tumor suppressor family members, we sought to explore the associated mechanisms to gain insights into how Lin28B might be decreased in human cancer cells to increase let-7 levels and reverse malignancy. Results We demonstrated that the histone acetyltransferase PCAF, via its cold shock domain, directly interacts with and subsequently acetylates Lin28B in lung adenocarcinoma-derived H1299 cells. RT-qPCR assays showed that both let-7a-1 and let-7g were increased in PCAF-transfected H1299 cells. Lin28B is acetylated by ectopic PCAF and translocates from the nucleus to the cytoplasm in H1299 cells. Conclusions The effects of acetylated Lin28B on let-7a-1 and let-7g are similar to that of stable knockdown of Lin28B in H1299 cells. The new role of PCAF in mediating Lin28B acetylation and the specific release of its target microRNAs in H1299 cells may shed light on the potential application of let-7 in the clinical treatment of lung cancer patients.

Published
2018

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