|Table of Contents|

NCAPD3 Inhibits Apoptosis of Prostate Cancer Cellsby Activating AKT-FOXO Signaling Pathway(PDF)

《南京师大学报(自然科学版)》[ISSN:1001-4616/CN:32-1239/N]

Issue:
2021年03期
Page:
90-95
Research Field:
·生物学·
Publishing date:

Info

Title:
NCAPD3 Inhibits Apoptosis of Prostate Cancer Cellsby Activating AKT-FOXO Signaling Pathway
Author(s):
He WenzhengWu QingxinLiu Ping
School of Life Sciences,Nanjing Normal University,Institute of Biochemistry and Biological Products,Nanjing 210023,China
Keywords:
prostate cancerapoptosisNCAPD3AKTFOXO1/3A
PACS:
R36
DOI:
10.3969/j.issn.1001-4616.2021.03.014
Abstract:
NCAPD3(non SMC condensin II complex subunit D3)is a subunit of condensin II complex. Its main function in cells is to regulate the condensation and stabilization of chromatin during mitosis. NCAPD3 also plays a role in promoting cancer in prostate cancer. This study was to explore the molecular mechanism of NCAPD3 in promoting the development of prostate cancer. Firstly,the expression of NCAPD3 in different cancers was analyzed by using the database,and then the expression of p-AKT and NCAPD3 in normal prostate cells and various prostate cancer cells were detected. Secondly,siRNA was used to knock down NCAPD3 in LNCaP and overexpression of NCAPD3 in DU145. Western blot was used to detect the phosphorylation level of AKT(Thr308 and Ser473),the expression level of FOXO1/3A and downstream apoptosis related factors,and flow cytometry was used to detect the apoptosis of prostate cancer cells. The results showed that NCAPD3 was highly expressed in prostate cancer. NCAPD3 activated AKT through phosphorylation,and then regulated the transcriptional activities of FOXO1 and FOXO3A,inhibited the apoptosis of prostate cancer cells,and was beneficial to the growth of prostate cancer cells,eventually lead to the malignant progression of prostate cancer. This study found that NCAPD3,as a tumor promoting gene in prostate cancer,may become a new target gene for clinical diagnosis and treatment of prostate cancer.

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Last Update: 2021-09-15