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Effect of CTP-mediated PTEN on 5637 bladder cancer cells and the underlying molecular mechanism

OBJECTIVE: The aim of the present study was to explore the effect of cytoplasmic transduction peptide (CTP)-phosphatase and tensin homolog (PTEN) on the proliferation, cell cycle, apoptosis, migration and invasion of bladder cancer cells and the underlying molecular mechanism. METHODS: A eukaryotic...

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Autores principales: Yu, Bei, Huang, Yuan, Yang, Yue, Hu, Haifeng, Yang, Jin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9741776/
https://www.ncbi.nlm.nih.gov/pubmed/36496361
http://dx.doi.org/10.1186/s12894-022-01152-y
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author Yu, Bei
Huang, Yuan
Yang, Yue
Hu, Haifeng
Yang, Jin
author_facet Yu, Bei
Huang, Yuan
Yang, Yue
Hu, Haifeng
Yang, Jin
author_sort Yu, Bei
collection PubMed
description OBJECTIVE: The aim of the present study was to explore the effect of cytoplasmic transduction peptide (CTP)-phosphatase and tensin homolog (PTEN) on the proliferation, cell cycle, apoptosis, migration and invasion of bladder cancer cells and the underlying molecular mechanism. METHODS: A eukaryotic expression vector, pTT5-CTP-PTEN, was constructed. The constructed vector was transfected into HEK 293-6E cells to express a fusion protein, CTP-PTEN. The fusion protein was purified. 5637 bladder cancer cells were cocultured with purified CTP-PTEN fusion protein. Target gene expression, protein expression, cell proliferation, cell cycle, apoptosis, cell invasion and cell migration were examined by reverse transcription polymerase chain reaction (RT-PCR), western blot, MTT assay, flow cytometry, Transwell assay, and cell scratch assay, respectively. RESULTS: Both PTEN and CTP-PTEN fusion protein inhibited the proliferation, cell cycle, invasion and migration of bladder cancer cells and promoted the apoptosis of bladder cancer cells. The effect of CTP-PTEN was more significant. CONCLUSIONS: The fused expression of CTP and PTEN significantly increased the penetrability of the tumor suppressor gene PTEN into cancer cells. The CTP-PTEN fusion protein exhibited a significant carcinostatic effect on 5637 bladder cancer cells. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12894-022-01152-y.
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spelling pubmed-97417762022-12-12 Effect of CTP-mediated PTEN on 5637 bladder cancer cells and the underlying molecular mechanism Yu, Bei Huang, Yuan Yang, Yue Hu, Haifeng Yang, Jin BMC Urol Research OBJECTIVE: The aim of the present study was to explore the effect of cytoplasmic transduction peptide (CTP)-phosphatase and tensin homolog (PTEN) on the proliferation, cell cycle, apoptosis, migration and invasion of bladder cancer cells and the underlying molecular mechanism. METHODS: A eukaryotic expression vector, pTT5-CTP-PTEN, was constructed. The constructed vector was transfected into HEK 293-6E cells to express a fusion protein, CTP-PTEN. The fusion protein was purified. 5637 bladder cancer cells were cocultured with purified CTP-PTEN fusion protein. Target gene expression, protein expression, cell proliferation, cell cycle, apoptosis, cell invasion and cell migration were examined by reverse transcription polymerase chain reaction (RT-PCR), western blot, MTT assay, flow cytometry, Transwell assay, and cell scratch assay, respectively. RESULTS: Both PTEN and CTP-PTEN fusion protein inhibited the proliferation, cell cycle, invasion and migration of bladder cancer cells and promoted the apoptosis of bladder cancer cells. The effect of CTP-PTEN was more significant. CONCLUSIONS: The fused expression of CTP and PTEN significantly increased the penetrability of the tumor suppressor gene PTEN into cancer cells. The CTP-PTEN fusion protein exhibited a significant carcinostatic effect on 5637 bladder cancer cells. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12894-022-01152-y. BioMed Central 2022-12-10 /pmc/articles/PMC9741776/ /pubmed/36496361 http://dx.doi.org/10.1186/s12894-022-01152-y Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Yu, Bei
Huang, Yuan
Yang, Yue
Hu, Haifeng
Yang, Jin
Effect of CTP-mediated PTEN on 5637 bladder cancer cells and the underlying molecular mechanism
title Effect of CTP-mediated PTEN on 5637 bladder cancer cells and the underlying molecular mechanism
title_full Effect of CTP-mediated PTEN on 5637 bladder cancer cells and the underlying molecular mechanism
title_fullStr Effect of CTP-mediated PTEN on 5637 bladder cancer cells and the underlying molecular mechanism
title_full_unstemmed Effect of CTP-mediated PTEN on 5637 bladder cancer cells and the underlying molecular mechanism
title_short Effect of CTP-mediated PTEN on 5637 bladder cancer cells and the underlying molecular mechanism
title_sort effect of ctp-mediated pten on 5637 bladder cancer cells and the underlying molecular mechanism
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9741776/
https://www.ncbi.nlm.nih.gov/pubmed/36496361
http://dx.doi.org/10.1186/s12894-022-01152-y
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