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MicroRNA-16 sensitizes breast cancer cells to paclitaxel through suppression of IKBKB expression

Xueyuan Tang, Long Jin, Peiguo Cao, Ke Cao, Chenghui Huang, Yanwei Luo, Jian Ma, Shourong Shen, Ming Tan, Xiayu Li and Ming Zhou _

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Oncotarget. 2016; 7:23668-23683. https://doi.org/10.18632/oncotarget.8056

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Xueyuan Tang1,4, Long Jin1, Peiguo Cao1, Ke Cao1, Chenghui Huang1, Yanwei Luo3,4, Jian Ma3,4, Shourong Shen2,4, Ming Tan5, Xiayu Li2,4, Ming Zhou3,4

1Department of Oncology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China

2Department of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China

3The Key Laboratory of Carcinogenesis of The Chinese Ministry of Health and The Key Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China

4Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

5Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, USA

Correspondence to:

Ming Zhou, email: zhouming2001@163.com

Xiayu Li, email: lixiayu@163.com

Keywords: miR-16, IKBKB, Taxol, breast cancer, chemosensitivity

Received: October 08, 2015     Accepted: February 29, 2016     Published: March 14, 2016


Paclitaxel (Taxol) is an effective chemotherapeutic agent for treating breast cancer patients. However, chemoresistance is a major obstacle in cancer treatment. Here, we showed that overexpression of miR-16 promoted Taxol-induced cytotoxicity and apoptosis in breast cancer cells. Furthermore, IκB kinase β (IKBKB) was identified as a direct target of miR-16. Up-regulation of IKBKB suppressed Taxol-induced apoptosis and led to an increased resistance to Taxol, and restoring IKBKB expression in miR-16-overexpressing breast cancer cells recovered Taxol resistance. Moreover, miR-16 was highly expressed in Taxol-sensitive breast cancer tissues compared with Taxol-resistant tissues, and there was an inverse correlation between miR-16 expression and IKBKB expression in breast cancer tissues. The expression levels of miR-16 were negatively associated with T stages, whereas the expression of IKBKB was positively correlated with T stages, lymph node metastasis and clinical stages. Taken together, our data demonstrates that miR-16 sensitizes breast cancer cells to Taxol through the suppression of IKBKB expression, and targeting miR-16/IKBKB axis will be a promising strategy for overcoming Taxol resistance in breast cancer.

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