Research Papers:
TXNIP interaction with the Her-1/2 pathway contributes to overall survival in breast cancer
Metrics: PDF 2919 views | HTML 2695 views | ?
Abstract
Weiwei Nie1,*, Weisun Huang1,*, Wenwen Zhang2, Jing Xu2, Wei Song1, Yanru Wang1, Aiyu Zhu1, Jiayan Luo2, Guichun Huang2, Yucai Wang3 and Xiaoxiang Guan1,2
1 Department of Medical Oncology, Jinling Hospital, School of Medicine, Southern Medical University, Guangzhou, P.R. China
2 Department of Medical Oncology, Jinling Hospital, Medical School of Nanjing University, Nanjing, P.R. China
3 Department of Medicine, Rutgers New Jersey Medical School, Newark, NJ, USA
* These authors contributed equally to this work
Correspondence:
Xiaoxiang Guan, email:
Keywords: TXNIP, p27, Her-1/2 inhibitor, breast cancer
Received: November 07, 2014 Accepted: December 24, 2014 Published: December 30, 2014
Abstract
Previous studies have indicated that Her-2 induction causes a strong decrease in thioredoxin interaction protein (TXNIP) in breast cancer cells. However, little is known regarding the prognostic value of TXNIP in clinical breast cancer patients with anti-Her-2 treatment. Using a tissue microarray, we detected TXNIP and p27 expression in breast cancer tissue, as well as corresponding noncancerous tissues. We found that TXNIP expression was associated with better overall survival (OS) in these 150 breast cancer patients and that TXNIP and Her-2 expression status were significantly inversely correlated (r=-0.334, P<0.001). These results were validated in another 101 breast cancer tissue samples (r=-0.422, P<0.001). Moreover, TXNIP expression increased significantly following treatment of the human breast cancer cell lines BT474 and SK-BR-3 with a Her-1/2 inhibitor. Furthermore, TXNIP transfection induced p27 expression and G1 cell cycle arrest and apoptosis. Taken together, our findings suggest that TXNIP plays a critical role in anti-Her-1/Her-2 treatment and may be a potential prognostic marker in breast cancer.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 3096