Mechanism of Thymosin Beta 10 Inhibiting the Apoptosis and Prompting Proliferation in A549 Cells
10.3779/j.issn.1009-3419.2014.11.03
- VernacularTitle:胸腺素β10在人肺腺癌细胞株A549中抑制细胞凋亡、促进细胞增殖机制研究
- Author:
LI ZIXUAN
1
,
2
;
QU LIANYUE
;
ZHONG HONGSHAN
;
XU KE
;
QIU XUESHAN
Author Information
1. 110001 沈阳，中国医科大学附属第一医院放射科，辽宁省影像诊断与介入治疗重点实验室
2. 110001 沈阳，中国医科大学附属第一医院病理科，基础医学院病理学教研室
- Keywords:
Lung neoplasms;
hTymosinβ10;
Proliferation;
Apoptosis
- From:
Chinese Journal of Lung Cancer
2014;(11):783-788
- CountryChina
- Language:Chinese
-
Abstract:
Background and objective Thymosin beta 10 (Tβ10) is one ofβ-thymosin family members, has a highly conserved polar 5 kDa peptides. hTis peptide is now regarded to be a small actin-binding protein and thereby induce depolymerization of the intracellular F-actin networks. Alteration of Tβ10 expression may alter the balance of cell growth, cell death, cell attachment and cell migration. Tβ10 also affects cell metastasis as well as proliferation, apoptosis and vasculariza-tion of cancer cells. But function of Tβ10 appear to be rather different between cancer cells, and the molecular mechanisms ofβ-thymosins to regulate cell apoptosis and proliferation in NSCLC (non-small cell lung cancer) cell lines are unclear. In this study, we used lung adenocarcinoma cell line A549, added Tβ10 or down-regulated the expression of Tβ10. We observed the change of apoptosis, proliferation and cell cyclin ability in A549 and the mechanisms underline them were also identiifed. Methods Atfer A549 was treated with 100 ng/mL recombinant human Tβ10 or siTβ10, apoptosis rate of A549 and cell cycle distribution were detected by lfow cytometry (FCM). CCK-8 assay was employed to determine the proliferation of A549. hTe mRNA level of P53, Caspase-3, Cyclin A and Cyclin E were determined by real-time PCR. hTe protein level of P53, Caspase-3, Cyclin A and Cyclin E were detected by Western blot. Results Add Tβ10 can inhibit the apoptosis and prompt the prolifera-tion of A549. It can also increase the cell rates of S-phrase and G2/M-phrase, decrease the expression of P53 and Caspase-3,but increase the expression of Cyclin A and Cyclin E. Interferance of Tβ10 can prompt the apoptosis and inhibit the prolifera-tion of A549. It can also increase the cell rates of G0/G1-phrase, increase the expression of P53 and Caspase-3, but decrease the expression of Cyclin A and Cyclin E. Conclusion In lung cancer cell line, Tβ10 can inhibit the apoptosis by increase P53, drive cells into the S and G2/M-phase, prompt cell proliferation by increase the expression of Cyclin A and Cyclin E. Tβ10 may become a potential biomarker and therapy target for non-small cell lung cancer.
