Horm Metab Res 2023; 55(08): 563-572
DOI: 10.1055/a-2084-3112
Original Article: Endocrine Research

Knockdown of CENPN Inhibits Glucose Metabolism and Induces G1 Arrest in Esophageal Cancer Cells by Regulating PI3K/AKT Signaling Pathway

Authors

  • Shasha Xu

    1   Department of Gastroenterology, Hangzhou Ninth People's Hospital, Hangzhou, China
  • Xing Wei

    2   Department of Biochemistry and Cell Biology, Youjiang Medical University for Nationalities, Baise, China

Abstract

Esophageal carcinoma (ESCA) is a deadly malignancy with an increasing incidence year by year. The purpose of this study was to explore the function of CENPN in ESCA. Based on TCGA public data platform, the transcription level of CENPN in ESCA was analyzed. Subsequently, ESCA cells with CENPN overexpression or knockdown were constructed. The proliferation and migration levels of ESCA cells were evaluated by CCK-8, colony formation assay, and transwell analysis. Western blotting was used to detect protein levels associated with CyclinD1, CDK2, GLUT1, and PI3K/AKT signaling pathways. Cell cycle distribution was measured by flow cytometry. Glucose consumption and lactate production in ESCA cells were measured. CENPN was overexpressed in ESCA. In vitro experiments showed that CENPN promoted the proliferation and migration of ESCA cells, and upregulated the levels of CyclinD1, CDK2, and GLUT1, promoting the cell cycle process, increasing glucose consumption and lactic acid production. In addition, CENPN overexpression increased the phosphorylation levels of PI3K and AKT. The results suggest that the abnormal expression of CENPN in ESCA may enhance the malignant phenotype of ESCA cells by activating the PI3K/AKT signaling pathway. CENPN is expected to be a new target for ESCA treatment.



Publication History

Received: 23 December 2022
Received: 01 May 2023

Accepted after revision: 01 May 2023

Accepted Manuscript online:
01 May 2023

Article published online:
13 June 2023

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