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PLCε promotes urinary bladder cancer cells proliferation through STAT3/LDHA pathway-mediated glycolysis
Phospholipase Cε (PLCε) and anaerobic glycolysis were determined to be involved in the development of human urinary bladder cancer (UBC), but the mechanisms remain unclear. In the present study, 64 bladder cancer specimens and 42 adjacent tissue specimens were obtained from 64 patients, and immunoch...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448096/ https://www.ncbi.nlm.nih.gov/pubmed/30864733 http://dx.doi.org/10.3892/or.2019.7056 |
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author | Cheng, Honglin Hao, Yanni Gao, Yingying He, Yunfeng Luo, Chunli Sun, Wei Yuan, Mengjuan Wu, Xiaohou |
author_facet | Cheng, Honglin Hao, Yanni Gao, Yingying He, Yunfeng Luo, Chunli Sun, Wei Yuan, Mengjuan Wu, Xiaohou |
author_sort | Cheng, Honglin |
collection | PubMed |
description | Phospholipase Cε (PLCε) and anaerobic glycolysis were determined to be involved in the development of human urinary bladder cancer (UBC), but the mechanisms remain unclear. In the present study, 64 bladder cancer specimens and 42 adjacent tissue specimens were obtained from 64 patients, and immunochemistry indicated that PLCε and lactate dehydrogenase (LDHA) are overexpressed in UBC. PLCε and LDHA were demonstrated to be positively correlated at transcription levels, indicating that one of these two genes may be regulated by another. To elucidate the mechanisms, PLCε was knocked down in T24 cells by short hairpin RNA, and then signal transducer and activator of transcription 3 (STAT3) phosphorylation and LDHA were determined to be downregulated, which indicated that PLCε may serve roles upstream of LDHA through STAT3 to regulate glycolysis in UBC. Furthermore, chromatin immunoprecipitation and luciferase reporter assays were performed to confirm that STAT3 could bind to the promoter of the LDHA gene to enhance its expression. A xenograft tumor mouse model also demonstrated similar results as the in vitro experiments, further confirming the role of PLCε in regulating bladder cell growth in vivo. Collectively, the present study demonstrated that PLCε may regulate glycolysis through the STAT3/LDHA pathway to take part in the development of human UBC. |
format | Online Article Text |
id | pubmed-6448096 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-64480962019-04-05 PLCε promotes urinary bladder cancer cells proliferation through STAT3/LDHA pathway-mediated glycolysis Cheng, Honglin Hao, Yanni Gao, Yingying He, Yunfeng Luo, Chunli Sun, Wei Yuan, Mengjuan Wu, Xiaohou Oncol Rep Articles Phospholipase Cε (PLCε) and anaerobic glycolysis were determined to be involved in the development of human urinary bladder cancer (UBC), but the mechanisms remain unclear. In the present study, 64 bladder cancer specimens and 42 adjacent tissue specimens were obtained from 64 patients, and immunochemistry indicated that PLCε and lactate dehydrogenase (LDHA) are overexpressed in UBC. PLCε and LDHA were demonstrated to be positively correlated at transcription levels, indicating that one of these two genes may be regulated by another. To elucidate the mechanisms, PLCε was knocked down in T24 cells by short hairpin RNA, and then signal transducer and activator of transcription 3 (STAT3) phosphorylation and LDHA were determined to be downregulated, which indicated that PLCε may serve roles upstream of LDHA through STAT3 to regulate glycolysis in UBC. Furthermore, chromatin immunoprecipitation and luciferase reporter assays were performed to confirm that STAT3 could bind to the promoter of the LDHA gene to enhance its expression. A xenograft tumor mouse model also demonstrated similar results as the in vitro experiments, further confirming the role of PLCε in regulating bladder cell growth in vivo. Collectively, the present study demonstrated that PLCε may regulate glycolysis through the STAT3/LDHA pathway to take part in the development of human UBC. D.A. Spandidos 2019-05 2019-03-13 /pmc/articles/PMC6448096/ /pubmed/30864733 http://dx.doi.org/10.3892/or.2019.7056 Text en Copyright: © Cheng et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Cheng, Honglin Hao, Yanni Gao, Yingying He, Yunfeng Luo, Chunli Sun, Wei Yuan, Mengjuan Wu, Xiaohou PLCε promotes urinary bladder cancer cells proliferation through STAT3/LDHA pathway-mediated glycolysis |
title | PLCε promotes urinary bladder cancer cells proliferation through STAT3/LDHA pathway-mediated glycolysis |
title_full | PLCε promotes urinary bladder cancer cells proliferation through STAT3/LDHA pathway-mediated glycolysis |
title_fullStr | PLCε promotes urinary bladder cancer cells proliferation through STAT3/LDHA pathway-mediated glycolysis |
title_full_unstemmed | PLCε promotes urinary bladder cancer cells proliferation through STAT3/LDHA pathway-mediated glycolysis |
title_short | PLCε promotes urinary bladder cancer cells proliferation through STAT3/LDHA pathway-mediated glycolysis |
title_sort | plcε promotes urinary bladder cancer cells proliferation through stat3/ldha pathway-mediated glycolysis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448096/ https://www.ncbi.nlm.nih.gov/pubmed/30864733 http://dx.doi.org/10.3892/or.2019.7056 |
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