Breast cancer is the most common type of cancer and the second leading cause of cancer-related deaths in women worldwide [1]. Breast cancer is considered heterogeneous disease characterized by changes in the mammary epithelial cells leading to aggressive cell proliferation [2]. The three main biomarkers of interest in breast cancer include estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). Currently, four molecular subtypes with different levels of expression of these receptors are luminal A, luminal B, HER2-enriched, and basal-like have been identified. Triple-negative breast cancer (TNBC), which is a part of the basal-like subgroup, it is characterized by the lack of PR, ER, and HER2 expression [3]. Different breast cancer subtypes displayed heterogeneity and extremely high mortality due to poor metastatic prognosis, drugs resistance and recurrent diseases [4]. At the most advanced stage of breast cancer, in particular the hormone-independent cancers develop resistance to therapy, thus causing increased mortality. The control and cure of breast cancer includes surgery, radiation therapy and chemotherapy as well as hormone therapy [5]. Several hormones are expressed in tumor tissues that lead to therapy resistance due to the biological actions of peptide hormones in regulating cellular process and proliferation [6]. Somatostatin (SST) is a widely expressed endogenous peptide known to inhibit the cellular processes such as neurotransmission, hormonal secretion and cell proliferation and differentiation as well as promoting apoptosis via five subtypes SSTRs (1-5) encoded by five distinct SSTR genes segregated on chromosomes 14, 16, 17, 20 and 22, respectively [7]. Somatostatin receptors (SSTRs) are G-protein-coupled plasma membrane receptors, initially secreted as a long precursor molecule; it undergoes specific enzymatic degradation generation with two forms of SST peptides, SS-14 and SS-28, as their natural ligands [8]. SSTRs1-5 expression is widely distributed in normal and tumor tissues depending on cell type. In normal tissues, SSTRs are found mainly in brain, pancreas, stomach and kidney, and their expression varies in cancer cells depending on the tumor type and biological characteristics [9]. SSTRs have direct and indirect effects on tumor biology. The direct effect includes the inhibition of tumor proliferation and induction of pro-apoptotic pathways including intrinsic and extrinsic apoptosis pathway [10, 11]. Meanwhile, the indirect effects include the inhibition of hormones and growth factors that promote tumor growth [12, 13] . SSTRs mediate of signal transduction pathways through inhibition of adenylyl cyclase (AC) and guanylyl cyclase (GC), protein phosphorylation and activation of mitogen-activated protein kinase (MAPK)[14,15]. Furthermore, the activation of signaling pathways leads to the induction of cell cycle arrest via activation of cyclin dependent kinase inhibitor (p27Kip1) and apoptosis. Cancer cells with positive SSTRs are less malignant with higher survival rate whereas the lack of SSTRs expression has also been associated with poorly differentiated and invasive tumor. However, a number of effects demonstrated subtype selectivity, and subtype specific signaling has been reported [16]. SSTR1, 2, 4 and 5 frequently interfere with the mitogen-activate protein kinase pathway to modulate cell proliferation, whereas SSTR3 was indicated to have an increased potential to induce apoptosis [2]. In fact, SSTR2 is considered a good prognosis factor because it has association with low proliferative and invasive breast cancer. In addition, SSTRs being frequently expressed in the same cell, and the existence of ligand induced dimerization proposed for G protein coupled receptors, it is hypothesized that SSTRs are functionally excessive and act in concert [10]. Therefore, somatostatain analogues (SSAs) have been used in the treatment of SSTR-positive tumors [12]. However, the therapeutic results of SSAs treatment varied markedly due to the expression of SSTRs, different SSTR expression patterns and reasons that are not fully understood [17]. Expression levels of SSTRs have been determined in multiple human tumour tissues including neuroendocrine and non-endocrine tumor types like hepatocellular carcinoma, pancreatic cancer and breast cancer [18]. SSTRs are highly expressed in neuroendocrine tumors but their level of expression in breast cancer is not well documented [19]. In breast cancer, SSTRs are expressed in different levels and are correlated with various histological markers in a receptor-specific manner [20]. Previous studies have demonstrated the presence of SSTRs in a large variety of tumors and cancer cell lines [21]. In the present study, MCF-7 (estrogen-receptor positive breast cancer cell line) and MDA-MB-231 (estrogen-receptor negative breast cancer cell line) have been used in vitro as a breast cancer models to study the expression of these receptors. The MCF7 line retains several characteristics of differentiated mammary epithelium including ability to process estradiol via cytoplasmic estrogen receptors. MDA-MB-231 is a highly aggressive, invasive but poorly differentiated triple-negative breast cancer (TNBC) cell line that lacks receptors for estrogen (ER) and progesterone (PR) expression, as well as HER2 (human epidermal growth factor receptor 2) amplification [22], and is known to be resistant to several anti-cancer agents [23]. The aim of this study was therefore to evaluate the mRNA expression for SSTRs (1-5) in human breast cancer cell lines MCF7 and MDA-MB231 using quantitative real-time polymerase chain reaction (qRT- PCR).