Research Paper|Volume 13, Issue 24|pp 25778—25798

PKMYT1, exacerbating the progression of clear cell renal cell carcinoma, is implied as a biomarker for the diagnosis and prognosis

Juan Chen¹, Xiaoliang Hua^2,^3,⁴, Heying Chen¹, Xiangmin Qiu¹, Haibing Xiao^2,^3,⁴, Shengdong Ge^2,^3,⁴, Chaozhao Liang^2,^3,⁴, Qin Zhou¹

¹The Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, The College of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China
²Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, China
³Anhui Province Key Laboratory of Genitourinary Diseases, Anhui Medical University, Hefei, China
⁴The Institute of Urology, Anhui Medical University, Hefei, China

* Equal contribution

Received: April 14, 2021Accepted: November 22, 2021Published: December 27, 2021

https://doi.org/10.18632/aging.203759

Copyright: © 2021 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Clear cell renal cell carcinoma (ccRCC) is one of the most lethal urological malignancies with high tumor heterogeneity, and reliable biomarkers are still needed for its diagnosis and prognosis. WEE family kinases function as key regulators of the G2/M transition, have essential roles in maintaining cellular genomic stability and have the potential to be promising therapeutic targets in various tumors. However, the roles of WEE family kinases in ccRCC remain undetermined. In the present study, we first explored multiple public datasets and found that PKMYT1 was up-regulated in both RCC tumors and cell lines. Expression levels of PKMYT1 were highly associated with pathological stage and grade. Kaplan-Meier curves showed that high PKMYT1 expression was associated with lower overall survival and disease-free survival. Receiver operating characteristic curves revealed that the expression of PKMYT1 could better distinguish ccRCC from normal samples. Functional enrichment analysis demonstrated that cell cycle- related pathways and epithelial to mesenchymal transition (EMT) might be potential mechanisms of PKMYT1 in ccRCC tumorigenesis. Moreover, knockdown of PKMYT1 in vitro attenuated the proliferation, migration and invasion of RCC cell lines, promoted cell apoptosis and prevented the EMT phenotype in vitro. In conclusion, our study demonstrated that PKMYT1 has the potential to act as a diagnostic and prognostic biomarker for RCC patients. Targeting PKMYT1 may be considered as a new potential therapeutic method and direction in RCCs.