Abstract
Triple-negative breast cancer is a high-risk breast cancer with poor survival rate. To date, there is a lack of targeted therapy for this type of cancer. One unique phenomenon is that inflammatory breast cancer is frequently triple negative. However, it is still ambiguous how inflammation influences triple-negative breast cancer growth and responding to chemotherapy. Herein, we investigated the levels of inflammation-associated enzyme, iNOS, in 20 triple-negative breast cancer patients’ tumors, and examined its correlation with patients’ responses to platinum-based neoadjuvant chemotherapy. Our studies showed that triple-negative breast cancer patients with attenuated iNOS levels in tumor cells after treatment showed better responses to platinum-based neoadjuvant chemotherapy than other triple-negative breast cancer patients. Our further in vitro studies confirmed that induction of proper levels of NO increased the resistance to cisplatin in triple-negative MDA-MB-231 cells. Our data suggest that aberrant high level of iNOS/NO are associated with less effectiveness of platinum-based neoadjuvant chemotherapy in triple-negative breast cancer. Therefore, we propose to monitor iNOS levels as a new predictor for triple-negative breast cancer patient’s response to platinum-based neoadjuvant chemotherapy. Moreover, iNOS/NO is considered as a potential target for combination therapy with platinum drugs for triple-negative breast cancer.
Highlights
Triple-negative breast cancers (TNBCs) refer to describe those cancers which do not express oestrogen receptor (ER), progesterone receptor (PR) or overexpress human epidermal growth factor receptor 2 (Her2/neu) [1]
By employing IHC, we examined the expression of inducible nitric oxide synthase (iNOS) protein in human tumor tissues from 20 TNBC patients before and after platinum-based drugs neoadjuvant chemotherapy
We observed that positive expression of iNOS protein was 18/20
Summary
Triple-negative breast cancers (TNBCs) refer to describe those cancers which do not express oestrogen receptor (ER), progesterone receptor (PR) or overexpress human epidermal growth factor receptor 2 (Her2/neu) [1]. TNBCs account for approximately 15%-25% of all breast cancer cases [2]. Because of lack of targeted receptors, treatment options for TNBCs are restrictive. It has been reported that their phenotypic and molecular similarity to BRCA1-related breast cancers might provide implications in terms of treatment [3]. PLOS ONE | DOI:10.1371/journal.pone.0130286 July 21, 2015
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