الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Breast Cancer is a global disease and considered as the most common cancer between women over the world. The triple-negative breast cancer (TNBC) is considered as a subtype of breast cancer representing about 15% of breast cancer. These malignant diseases present a serious public health and their treatment with traditional chemotherapy cannot considered an all-round solution due to toxic side effects. Search for new anticancer compounds still feverish to avoid the undesirable harmful effects of chemicals on the host. Previous studies revealed that the organoselenium compounds can affect cell division and act as antitumor agents. Therefore, the present work aimed at surveying the antitumor activity of selenourea compound (4C) against triple negative breast cancer cell line and investigating their mechanism of towards the TNBC cell lines (MDA-MB-231-human source) and (4T1-murine source). The evaluation of 4C efficacy was shown through demonstration of proliferation; formation of colonies; wound healing; cell cycle analysis; estimation of ROS and the anticancer activity of compound 4C was in part via the down regulation of PI3K/AKT/mTOR/FASN pathway. The results showed that, Selenourea compound 4C exhibited antiproliferation and proapoptotic activity through the elevations in the cell populations at annexin V apoptotic phases. The ability of the two types of TNBC cells for healing the wound and formation of the colony were decreased after treating them with 4C. Cell cycle analysis revealed treated cells were arrested at G1 phase. Treatment of TNBC cells with IC50 showed more DNA damage via comet assay. The cytotoxic effect of 4C on the TNBC cells is increased by induction of free radicals that cause cell death compared to untreated cells. Our results showed that the mechanism of 4C compound was in part via modulation of the PI3K/AKT/mTOR signaling pathway which regulates the proliferation, metabolism, survival, and metastasis. from the present study, it may be concluded that: The antitumor activity of selenocompound (4C) on human (MDA- MB-231) or murine (4T1) TNBC cell lines may be attributed to the induction of ROS and apoptotic signaling pathway proteins leading to DNA fragmentation of TNBC cells.