While, in normal breasts, the histochemical assays show presence of integrins in myoepithelial layer of basement membrane, their concentration and expression pattern are different in breast cancer [12; 20; 21; 22]. Abnormal integrin expression contributes to the migratory properties of tumor cells. This permits them to pass through blood vessels and collagen matrix, invade surrounding cells and tissues, and eventually colonize tumor cells at secondary tissues [20; 21]. Various in vitro and in vivo studies show compromised expression of integrin receptors and their associated signaling pathways. Integrins such as \(\alpha\)v\(\beta\)5, \(\alpha\)v\(\beta\)6, \(\alpha\)2\(\beta\)1, \(\alpha\)6\(\beta\)1, and \(\alpha\)6\(\beta\)4 play critical roles in breast cancer growth, invasion, and metastasis [22]. Integrin \(\alpha\)v (ITG\(\alpha\)v) which forms heterodimer with six \(\beta\) integrin sub is a receptor for various proteins [23]. Each heterodimer of \(\alpha\)v-\(\beta\) plays an important part in the regulation of breast cancer and metastasis. For example, integrin \(\alpha\)v\(\beta\)3 causes bone metastasis in breast cancer through enhanced tumor adhesion. While the expression of this integrin is found in both primary tumors and metastatic cells, it is more active in metastatic cells [24; 25]. Apart from ITG\(\alpha\)v, integrin \(\alpha\)6 (ITG\(\alpha\)6) also has an important role in invasion, adhesion, migration, and progression of breast cancer cells. Overexpression in breast cancer cells and tissues, it is associated with poor prognosis and reduced survival rates. Furthermore, studies show that in various breast cancer cells its overexpression alters the processes such as apoptosis, cell cycle arrest, and DNA damage and double-strand break repair mechanism [26]. This integrin subunit can form heterodimers with \(\beta\)1 or \(\beta\)4 subunits, forming \(\alpha\)6\(\beta\)1 and \(\alpha\)6\(\beta\)4 integrins, with each integrin unit forming receptor for laminins. By participating via different mechanisms, both \(\alpha\)6\(\beta\)1 and \(\alpha\)6\(\beta\)4 contribute to the progression and survival of breast cancer [27]. While there are 8 subunits of \(\beta\) integrin which play important roles in cellular processes, integrins such as \(\beta\)1, \(\beta\)3, \(\beta\)4, \(\beta\)5, \(\beta\)6, and \(\beta\)8 have vital role in breast cancer. Each type of \(\beta\) subunits plays a distinct role in breast cancer where they are essentially involved in pro-tumorigenic processes such as epithelial mesenchymal transition (EMT), tumor development, progression, survival, angiogenesis, neo-angiogenesis, inflammation, and metastasis [16; 28; 29; 30; 31; 32]. For example, the role of \(\beta\)1 integrin based on the type of breast cancer varies, whereby its decreased and increased expression plays essential roles in tumorigenesis. Regular expression of this integrin helps in development of epithelial tissues via cellular proliferation and differentiation, but when overexpressed it can participate in angiogenesis, progression, and metastasis of breast cancer in invasive ductal carcinoma (IDC) [33]. Like \(\alpha\) subunit, \(\beta\) subunit also associates with various receptor molecules, modulating different signaling pathways in breast cancer. For example, ITG\(\beta\)5, which is present in primary and metastatic breast cancer cells, activates TGF-\(\beta\) and ERK signaling pathways via focal adhesion molecules such as focal adhesion kinase (FAK) and paxilin, and epidermal growth factor receptor (EGFR) signaling via proto-oncogene tyrosine-protein kinase (Src), causing tumor cell migration, invasion proliferation, and metastasis [28]. The overexpression of these integrins provides resistance to chemotherapy and radiations, resulting in a decrease in the survival rate of breast cancer patients. Hence, modulating their expressions can help in limiting the growth and invasion of tumor cells, thereby increasing the survival rates.