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PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways
Renal cell carcinoma (RCC) is the most common type of kidney cancer. By analysing The Cancer Genome Atlas (TCGA) database, 16 genes were identified to be consistently highly expressed in RCC tissues compared with the matched para-tumour tissues. Using a high-throughput cell viability screening metho...
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/PMC6561616/ https://www.ncbi.nlm.nih.gov/pubmed/31180521 http://dx.doi.org/10.3892/ijo.2019.4819 |
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author | Yu, Zi Li, Qiang Zhang, Gejun Lv, Chengcheng Dong, Qingzhuo Fu, Cheng Kong, Chuize Zeng, Yu |
author_facet | Yu, Zi Li, Qiang Zhang, Gejun Lv, Chengcheng Dong, Qingzhuo Fu, Cheng Kong, Chuize Zeng, Yu |
author_sort | Yu, Zi |
collection | PubMed |
description | Renal cell carcinoma (RCC) is the most common type of kidney cancer. By analysing The Cancer Genome Atlas (TCGA) database, 16 genes were identified to be consistently highly expressed in RCC tissues compared with the matched para-tumour tissues. Using a high-throughput cell viability screening method, it was found that downregulation of only two genes significantly inhibited the viability of 786-O cells. Among the two genes, pleckstrin homology domain containing O1 (PLEKHO1) has never been studied in RCC, to the best of our knowledge, and its expression level was shown to be associated with the prognosis of patients with RCC in TCGA dataset. The upregulation of PLEKHO1 in RCC was first confirmed in 30 paired tumour and para-tumour tissues. Then, the effect of PLEKHO1 on cell proliferation and apoptosis was assessed in vitro. Additionally, xenograft tumour models were established to investigate the function of PLEKHO1 in vivo. The results showed that PLEKHO1 knockdown significantly inhibited cell viability and facilitated apoptosis in vitro and impaired tumour formation in vivo. Thus, PLEKHO1 is likely to be associated with the viability of RCC cells in vitro and in vivo. Further gene expression microarray and co-expression analyses showed that PLEKHO1 may be involved in the serine/threonine-protein kinase hippo and JNK signalling pathways. Together, the results of the present study suggest that PLEKHO1 may contribute to the development of RCC, and therefore, further study is needed to explore its potential as a therapeutic target. |
format | Online Article Text |
id | pubmed-6561616 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-65616162019-06-26 PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways Yu, Zi Li, Qiang Zhang, Gejun Lv, Chengcheng Dong, Qingzhuo Fu, Cheng Kong, Chuize Zeng, Yu Int J Oncol Articles Renal cell carcinoma (RCC) is the most common type of kidney cancer. By analysing The Cancer Genome Atlas (TCGA) database, 16 genes were identified to be consistently highly expressed in RCC tissues compared with the matched para-tumour tissues. Using a high-throughput cell viability screening method, it was found that downregulation of only two genes significantly inhibited the viability of 786-O cells. Among the two genes, pleckstrin homology domain containing O1 (PLEKHO1) has never been studied in RCC, to the best of our knowledge, and its expression level was shown to be associated with the prognosis of patients with RCC in TCGA dataset. The upregulation of PLEKHO1 in RCC was first confirmed in 30 paired tumour and para-tumour tissues. Then, the effect of PLEKHO1 on cell proliferation and apoptosis was assessed in vitro. Additionally, xenograft tumour models were established to investigate the function of PLEKHO1 in vivo. The results showed that PLEKHO1 knockdown significantly inhibited cell viability and facilitated apoptosis in vitro and impaired tumour formation in vivo. Thus, PLEKHO1 is likely to be associated with the viability of RCC cells in vitro and in vivo. Further gene expression microarray and co-expression analyses showed that PLEKHO1 may be involved in the serine/threonine-protein kinase hippo and JNK signalling pathways. Together, the results of the present study suggest that PLEKHO1 may contribute to the development of RCC, and therefore, further study is needed to explore its potential as a therapeutic target. D.A. Spandidos 2019-05-30 /pmc/articles/PMC6561616/ /pubmed/31180521 http://dx.doi.org/10.3892/ijo.2019.4819 Text en Copyright: © Yu 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 Yu, Zi Li, Qiang Zhang, Gejun Lv, Chengcheng Dong, Qingzhuo Fu, Cheng Kong, Chuize Zeng, Yu PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways |
title | PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways |
title_full | PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways |
title_fullStr | PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways |
title_full_unstemmed | PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways |
title_short | PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways |
title_sort | plekho1 knockdown inhibits rcc cell viability in vitro and in vivo, potentially by the hippo and mapk/jnk pathways |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6561616/ https://www.ncbi.nlm.nih.gov/pubmed/31180521 http://dx.doi.org/10.3892/ijo.2019.4819 |
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