Abstract
Breast cancer is the most commonly diagnosed cancer in women. Triple-negative (TN) breast cancer lacks expression of estrogen receptor (ER), progesterone receptor (PR) as well as the expression and/or gene amplification of human epidermal growth factor receptor 2 (HER2). TN breast cancer is aggressive and does not respond to hormone therapy, therefore new treatments are urgently needed. Plant-derived chemicals have contributed to the establishment of chemotherapy agents. In previous studies, rosemary extract (RE) has been found to reduce cell proliferation and increase apoptosis in some cancer cell lines. However, there are very few studies examining the effects of RE in TN breast cancer. In the present study, we examined the effects of RE on TN MDA-MB-231 breast cancer cell proliferation, survival/apoptosis, Akt, and mTOR signaling. RE inhibited MDA-MB-231 cell proliferation and survival in a dose-dependent manner. Furthermore, RE inhibited the phosphorylation/activation of Akt and mTOR and enhanced the cleavage of PARP, a marker of apoptosis. Our findings indicate that RE has potent anticancer properties against TN breast cancer and modulates key signaling molecules involved in cell proliferation and survival.
Highlights
Breast cancer is the most frequently diagnosed cancer in women, accounting for over 1.3 million diagnosed cases annually worldwide [1]
We have previously prepared a methanol-based extract of rosemary leaves in our lab and when tested in lung cancer cells, we found a significant inhibition of proliferation and survival as well as an inhibition of Akt, mechanistic target of rapamycin (mTOR), and p70S6K [57]
In the present study we investigated the effects of rosemary extract (RE) on MDA-MB-231 TN breast cancer cell proliferation and survival/apoptosis
Summary
Breast cancer is the most frequently diagnosed cancer in women, accounting for over 1.3 million diagnosed cases annually worldwide [1]. Cancer cells are characterized by their ability to proliferate uncontrollably and evade apoptosis [5,6] These characteristics are often acquired as a result of mutations in key proteins involved in the signaling pathways responsible for regulating cell function and maintaining homeostasis [7,8,9,10]. Molecular signaling pathways of growth factor receptors [9], such as epidermal growth factor receptor (EGFR/HER1) initiate signal transduction pathways [11] including the phosphatidylinositol 3-kinase (PI3K)/Akt [10,12,13,14,15,16] and the Ras/mitogen-activated protein kinase (MAPK) pathways [17,18], which lead to increased cell proliferation and survival. Akt overexpression is associated with increased resistance to chemotherapeutic agents such as cisplatin, methotrexate, or paclitaxel [16,21]
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