Aspirin Suppresses the Growth and Metastasis of Osteosarcoma through the NF-κB Pathway
PUBLISHED: 2015-12-29  841 total views, 1 today

Dan LiaoLi ZhongTingmei DuanRu-Hua ZhangXin WangGang Wang,Kaishun HuXiaobin Lv, and Tiebang Kang*

Author Affiliations

State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China.

*Corresponding Author:
Tiebang Kang, State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, 651 Dongfeng East Road, Guangzhou 510060, China. Phone: 86-20-8734-3183; Fax: 86-20-8734-3170; E-mail: kangtb@sysucc.org.cn


Abstract

Purpose: Aspirin has recently been reported to reduce both the incidence and the risk of metastasis in colon cancer. However, there is no evidence at the cellular levels or in the animal models for such an effect of aspirin on cancer metastasis.

Experimental Design: MTT assay, colony formation assay, and apoptosis assay were employed to analyze the effects of aspirin on the osteosarcoma cell viability in vitro. The NF-κB activity was measured by the NF-κB p65 luciferase reporter. Western blotting was used to analyze the proteins in cells. The migration and invasion abilities of osteosarcoma cells in vitro were measured by the Transwell assay. Xenograft-bearing mice were used to assess the roles of aspirin in both tumor growth and metastasis of osteosarcoma in vivo(n = 5–8 mice/group). An unpaired Student t test or ANOVA with the Bonferroni post hoctest were used for the statistical comparisons.

Results: Aspirin reduced cell viability in a dose- and time-dependent manner in osteosarcoma cell lines, and aspirin synergistically sensitized osteosarcoma cells to cisplatin (DDP) in vitro and in vivo (P < 0.001). Moreover, aspirin markedly repressed the migration and invasion of osteosarcoma cells in vitro (P < 0.001), and dramatically diminished the occurrence of osteosarcoma xenograft metastases to the lungs in vivo (P< 0.001). Mechanistically, aspirin diminishes osteosarcoma migration, invasion, and metastasis through the NF-κB pathway.

Conclusion: Aspirin suppresses both the growth and metastasis of osteosarcoma through the NF-κB pathway at the cellular level and in the animal models. Clin Cancer Res; 1–11. ©2015 AACR.

Disclaimer: Only abstract of articles from non-members were published. This page aims to promote Chinese scientific research. There is no conflicts of interest with any journals reserved the copyright. For more please contact the author.


Author
Dr. Kang Tiebang
+ Author Profile

Dr.Kang Tiebang

Principal Investigatorof State Key Laboratory of Oncology in South China     

Email: kangtb@mail.sysu.edu.cn,kangtb@sysucc.org.cn

 

Research area

  • Regulationof Cell Cycle

  • Basicresearch of tumor-targeted therapy

  • Regulationof tumor metastasis.

 

Research Results

  • GSK-3 gene was found to play a role of oncogenein osteosarcoma cancer occurrence and development through NFkB pathways.GSK-3/NF-kB pathway can be used as therapeutic targets and prognosticindicators in patients with osteosarcoma. This study provided new thoughts andtargets for the integrated treatment of osteosarcoma (J. Natl Cancer Inst, 2012)

  • Chk1 was found to work as oncogene in livercancer, and its important substrate is SYK (L) that is a tumor suppressor gene.SYK (L) is degraded through its phosphorylation by Chk1. It showed that SYK (L)and Chk1 protein levels were correlated negatively. Chk1 can be used asprognostic indicators of liver cancer patients and therapeutic targets, and Chk1suppressor may enhance the sensitivity of liver cancer cells to chemotherapy. (J.Clin. Invest., 2012)

  • It was the first study to ever report hSSB1 wasa chaperone that can regulate stability of p53 protein and adjust p300-mediatedacetylation of p53 in order to control transcriptional activity of p53. (CellRes., 2012). Meanwhile, as a chaperone, hSSB1 also can directly regulatestability of p21 protein (Oncogene, 2011). 


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