The molecular mechanisms of chemoresistance in cancers

Hua-Chuan Zheng _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:59950-59964. https://doi.org/10.18632/oncotarget.19048

Metrics: PDF 8088 views  |   HTML 14064 views  |   ?  


Hua-Chuan Zheng1

1Department of Experimental Oncology and Animal Center, Shengjing Hospital of China Medical University, Shenyang 110004, China

Correspondence to:

Hua-Chuan Zheng, email: [email protected]

Keywords: cancer, chemoresistance, molecular mechanisms, chemotherapy

Received: March 31, 2017     Accepted: June 24, 2017     Published: July 06, 2017


Overcoming intrinsic and acquired drug resistance is a major challenge in treating cancer patients because chemoresistance causes recurrence, cancer dissemination and death. This review summarizes numerous molecular aspects of multi-resistance, including transporter pumps, oncogenes (EGFR, PI3K/Akt, Erk and NF-κB), tumor suppressor gene (p53), mitochondrial alteration, DNA repair, autophagy, epithelial-mesenchymal transition (EMT), cancer stemness, and exosome. The chemoresistance-related proteins are localized to extracellular ligand, membrane receptor, cytosolic signal messenger, and nuclear transcription factors for various events, including proliferation, apoptosis, EMT, autophagy and exosome. Their cross-talk frequently appears, such as the regulatory effects of EGFR-Akt-NF-κB signal pathway on the transcription of Bcl-2, Bcl-xL and survivin or EMT-related stemness. It is essential for the realization of the target, individualized and combine therapy to clarify these molecular mechanisms, explore the therapy target, screen chemosensitive population, and determine the efficacy of chemoreagents by cell culture and orthotopic model.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 19048