Journal
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
Volume 86, Issue 3, Pages 340-350Publisher
OXFORD UNIV PRESS
DOI: 10.1093/bbb/zbab217
Keywords
NSCLC; NXPH4; CDKN2A; EZH2; cyclinD
Categories
Funding
- Beijing Municipal Natural Science Foundation [7202042]
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This study discovered the high expression of NXPH4 in non-small cell lung cancer and confirmed that knocking down NXPH4 can inhibit cell proliferation and migration, causing cell cycle arrest in the S1 phase. Moreover, NXPH4 was found to be regulated by the transcriptional activation of EZH2 and interacted with CDKN2A to participate in cell cycle regulation.
NXPH4 is discovered to be a neuropeptide-like glycoprotein, belonging to the Neurexophilins (Nxphs) family. NXPH4 shares a similar domain structure with NXPH1, which, however, is poorly understood in terms of its function. Bioinformatics analysis and experimental verification in this study confirmed the abnormal high expression of NXPH4 in non-small cell lung cancer (NSCLC) tissues and cells. Knockdown of NXPH4 by siRNA can inhibit the proliferation and migration of cells, resulting in significant cell cycle arrest in S1 phase. Furthermore, in NSCLC cells, NXPH4 was regulated by transcriptional activation of enhancer of zeste homolog 2 (EZH2) in its upstream. While downstream, NXPH4 could interact with CDKN2A and downregulate its protein stability, thus participating in the cell cycle regulation through interacting with cyclinD-CDK4/6-pRB-E2F signaling pathway. To sum up, the present study reveals a regulatory pathway of EZH2/NXPH4/CDKN2A in NSCLC, providing possible reference for understanding the function of NXPH4 in tumors.
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