Affiliation:
1. Department of Gastroenterology, Hangzhou Ninth People's
Hospital, Hangzhou, China
2. Department of Biochemistry and Cell Biology, Youjiang Medical
University for Nationalities, Baise, China
Abstract
AbstractEsophageal 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.
Subject
Biochemistry (medical),Clinical Biochemistry,Endocrinology,Biochemistry,General Medicine,Endocrinology, Diabetes and Metabolism
Cited by
1 articles.
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