Open Access

PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways

  • Authors:
    • Zi Yu
    • Qiang Li
    • Gejun Zhang
    • Chengcheng Lv
    • Qingzhuo Dong
    • Cheng Fu
    • Chuize Kong
    • Yu Zeng
  • View Affiliations

  • Published online on: May 30, 2019     https://doi.org/10.3892/ijo.2019.4819
  • Pages: 81-92
  • Copyright: © Yu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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.
View Figures
View References

Related Articles

Journal Cover

July-2019
Volume 55 Issue 1

Print ISSN: 1019-6439
Online ISSN:1791-2423

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Yu Z, Li Q, Zhang G, Lv C, Dong Q, Fu C, Kong C and Zeng Y: PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways. Int J Oncol 55: 81-92, 2019
APA
Yu, Z., Li, Q., Zhang, G., Lv, C., Dong, Q., Fu, C. ... Zeng, Y. (2019). PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways. International Journal of Oncology, 55, 81-92. https://doi.org/10.3892/ijo.2019.4819
MLA
Yu, Z., Li, Q., Zhang, G., Lv, C., Dong, Q., Fu, C., Kong, C., Zeng, Y."PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways". International Journal of Oncology 55.1 (2019): 81-92.
Chicago
Yu, Z., Li, Q., Zhang, G., Lv, C., Dong, Q., Fu, C., Kong, C., Zeng, Y."PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways". International Journal of Oncology 55, no. 1 (2019): 81-92. https://doi.org/10.3892/ijo.2019.4819