In:
Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics, Computers, Materials and Continua (Tech Science Press), Vol. 23, No. 1 ( 2016-01-21), p. 61-68
Abstract:
It is largely recognized that PDCD4 is frequently lost in tumors of various origins, including lung cancer, and its loss contributes to tumor progression. However, its role and molecular mechanism remain largely unexplored in non-small cell lung cancer (NSCLC). In this study, downregulated
PDCD4 mRNA expression was found in NSCLC tissues compared to their corresponding paracarcinoma tissues and distal paracarcinoma tissues. Induced expression of PDC D4 inhibited cell growth and proliferation and cell cycle transition in vitro. Conversely, knocking down PDCD4 expression promoted
cell growth and proliferation. Mechanistically, PDCD4 inactivated PI3K/Akt signaling and its downstream cell cycle factors CCND1 and CDK4 to regulate cell growth in NSCLC. Additionally, PI3K-specific inhibitor Ly294002 suppressed the expression of pPI3K (Tyr458), pAkt (Ser473), CCND1, and CDK4 in PC9-shPDCD4 and A549-shPDCD4 cells. Furthermore, Akt-specific inhibitor MK2206 inhibited the expression of pAkt (Ser473), CCND1, and CDK4 in PC9-shPDCD4 and A549-shPDCD4 cells. Taken together, our study provides evidence that PDCD4 inhibits cell growth through PI3K/Akt signaling in
NSCLC and may be a potential therapeutic target for NSCLC.
Type of Medium:
Online Resource
ISSN:
0965-0407
DOI:
10.3727/096504015X14478843952861
Language:
English
Publisher:
Computers, Materials and Continua (Tech Science Press)
Publication Date:
2016
detail.hit.zdb_id:
1114699-0
detail.hit.zdb_id:
2044620-2
