1. Academic Validation
  2. PP4C facilitates lung cancer proliferation and inhibits apoptosis via activating MAPK/ERK pathway

PP4C facilitates lung cancer proliferation and inhibits apoptosis via activating MAPK/ERK pathway

  • Pathol Res Pract. 2020 May;216(5):152910. doi: 10.1016/j.prp.2020.152910.
Bin Wang 1 Xun-Xia Zhu 1 Lin-Yue Pan 2 He-Feng Chen 3 Xiao-Yong Shen 4
Affiliations

Affiliations

  • 1 Department of Thoracic Surgery, The Affiliated Huadong Hospital of Fudan University, No. 221 West Yan-an Road, Shanghai 200040, China.
  • 2 Department of Respiration, The Affiliated Huadong Hospital of Fudan University, No. 221 West Yan-an Road, Shanghai 200040, China.
  • 3 Department of Respiration, The Affiliated Huadong Hospital of Fudan University, No. 221 West Yan-an Road, Shanghai 200040, China. Electronic address: 13917472201@163.com.
  • 4 Department of Thoracic Surgery, The Affiliated Huadong Hospital of Fudan University, No. 221 West Yan-an Road, Shanghai 200040, China. Electronic address: shenxiaoyong2014@163.com.
Abstract

Purpose: Protein Phosphatase 4 catalytic subunit (PP4C) has been shown to play crucial regulatory roles in biological process and is frequently upregulated in Cancer such as breast and colorectal carcinoma. However, the function and potential molecular mechanism of PP4C in lung Cancer remains unclear.

Methods: Bioinformatic analysis was used to detect the expression level and prognosis of patients. Western blot, quantitative Real-Time PCR (qRT-PCR), CCK8, 5-Ethynyl-2'-deoxyuridine (Edu) proliferation assay and flow cytometric were used to explore the function in lung Cancer cells.

Results: In this study, we found that PP4C was upregulated in lung Cancer tissues as compared with that in normal lung tissues. Furthermore, patients with high expression level of PP4C were correlated with a poor prognosis in lung Cancer patients. In vitro, CCK8, Edu proliferation assays and flow cytometry analysis showed that PP4C could promote lung Cancer cell growth and inhibit Apoptosis. Mechanistic investigations revealed that PP4C may interact with PP4R1 and promote ERK activation. Additionally, PP4C depletion resulted in lower tumor growth in vivo.

Conclusions: Taken together, these data showed the oncogenic of PP4C in NSCLC tumorigenesis and provide a new insight of PP4C in the progression of NSCLC.

Keywords

Apoptosis; ERK; Non-small-cell lung cancer; PP4C; Proliferation.

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