Caspase-3 is the most

important executor of apoptosis in the caspase family. Cell apoptosis can be inhibited by inhibiting the viability and functioning of caspase-3. Activated caspase-3 has a strong capacity to induce apoptosis of tumor cells; Selleckchem Erismodegib the increasing expression level suggests the cell apoptosis [11]. In this experiment, the decrease in ki-67 expression and increase in caspase-3 expression in xenografted tumor is further proof of the ability of these proteins to inhibit proliferation and increase apoptosis of tumor cells. JNk is a member of the mitogen-activated protein kinase (MAPK) family. JNK2 gene is located on 5q35 and mainly mediates in vitro stimulation signals, such as virus, toxin, cytokine, and environmental stimulation signals [12]. IGF-1R is highly expressed in many kinds of tumors and closely related to tumor occurrence, development, and apoptosis. Overexpression of IGF-1R can promote

the growth of breast carcinoma cells, and it might be related to induction of tumor apoptosis and stimulation of an immune reaction to remove residual carcinoma cells [13]. Upon being combined with corresponding ligands, IGF-1R inactivates the BAD protein, a member of the bcl family, by activating the PI3K/Akt or Ras/Raf-1/MAPK family to avoid apoptosis. Meanwhile, IGF-1R can activate NF-κB viability and induce cell proliferation [14, 15]. PDGF is a group of peptide growth factors encoded by the primary mTOR inhibitor cancer gene c-sis. When PDGF combines with corresponding acceptors (PDGFR), it can phosphorylate cell membrane protein and induce cell malignant transformation. PDGFA/PDGFR-α

functions via autocrine and paracrine second signals to stimulate interstitial hyperplasia and indirectly promote tumor growth; in addition, it can promote cell proliferation by strengthening the response of IGF-1 [16, 17]. PDGF can improve PI3K activity, stimulate the phosphorylation of MAPK and AKT, increase degradation of extracellular proteins, upregulate MMP-2/9 expression, promote cell proliferation, and avoid apoptosis [18, 19]. NGF is a pluripotent polypeptide growth factor, strong mitogen related to the proliferation, invasion, and vascularization of breast carcinoma cells [20, 21]. Dolle et al. showed that breast carcinoma cells can produce and overexpress NGF [22]. Combined with acceptors in the breast carcinoma cell membrane, NGF can induce proliferation and inhibit apoptosis of breast carcinoma cells via a series of cascade reactions and signal transduction, then stimulate breast carcinoma cells to produce more NGF, forming a malignant autocrine loop.