Abstract
Advanced breast cancer holds a poor prognosis for chemotherapy and endocrine therapy resistance. Autophagy is one of the main causes of tumor drug-therapy failure, and increasing evidence shows that EMT also is responsible for that. Metastasis-associated protein1 (MTA1) is up regulated in lots of tumors, which leads to tumor progression and drug resistance. However, the role of MTA1 in chemotherapeutic resistance in luminal-b breast cancer is still unclear. In this paper, our research shows that higher expression of MTA1 accompanies with worse prognosis in luminal-b breast cancer. Knockdown of MTA1 enhances the sensitivity of MCF-7 to gemcitabine and weakens the metastasis ability of MCF-7 in vitro and in vivo. Further, we find that knockdown of MTA1 strengthens the gemcitabine-mediated tumor growth inhibition effect in vivo, through reversion of the EMT process and inhibition of the autophagy process. Furthermore, our research builds the siMTA1-loaded exosomes, which increases the gemcitabine-mediated tumor growth inhibition effect in vivo.
Highlights
Breast cancer is the most common cancer in women, which causes the second most common tumor-related death events in females [1]
We explore the role of Metastasis-associated protein1 (MTA1) in the gem-induced tumor toxicity effect in vitro and in vivo using small interfere RNA and the adenovirus stable knockdown system
The aim of this study is to explore the tumor growth inhibition effect of down regulation of MTA1 expression when it combines with gemcitabine in luminal-b type breast cancer and triple negative breast cancer (TNBC)
Summary
Breast cancer is the most common cancer in women, which causes the second most common tumor-related death events in females [1]. Recurrence and metastasis are the key issues which lead to a 27% death rate in regression breast cancer [2]. Chemotherapy is well-known as the main strategy to prolong the overall survival for advanced breast cancer, in which gemcitabine (GEM) and capecitabine are the alternative treatments for anthracycline and taxane chemotherapy failure. The clinical outcome of those with advanced breast cancer is still unsatisfactory due to drug resistance induced by unclear factors, especially for the luminal-b type breast cancer and triple negative breast cancer (TNBC) which rely siMTA-Loaded Exosomes in Cancer Therapy more on chemotherapy in the early stage of disease. A strategy to revert the chemotherapy resistance is pivotal in clinical treatment
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