Agrees with our experimental observation that BRE-silencing accelerated chondrogenic differentiation of HUCPV cells. Because actin and ANXA2 play a role in cell migration, we investigated the effect of BRE-silencing on cell movement. The HUCPV cells showed reduced ability to migrate after BREsilencing. The reduction is probably associated with the downregulation of actin protein which affected the cytoskeleton to change dynamically during movement �C since migration requires a synchronized interactions of actin and its interacting partners such as actin-binding proteins and integrins. ANXA2 has also been implicated in the regulation of HSC binding to osteoblasts and homing to the bone marrow niche. Further studies will be required to establish whether BRE has a role in cell homing. BRE-silencing could also suppress CALR, FUBP1 and PKM2 expression. In mESCs, down-regulation of CALR resulted in reduction of calcium ion level to enhance adipogenic differentiation. It has also been reported that CALR may be involved in the regulation of osteogenesis and chondrogenesis in MSCs. CALR expression is reduced in the early stage of osteoblast differentiation in MC-3T3-E1 cells. Overexpression of CALR inhibits both the basal and vitamin D-induced expression of osteocalcin and calcium ion accumulation in the extracellular matrix and mineralization of bone nodules in cultures. These findings may 4-(Benzyloxy)phenol explain our observation of why BRE-silencing resulted in enhanced osteogenic and chondrogenic differentiation in HUCPV cells. BRE-silencing also negatively regulates FUBP1 and PKM2. FUBP1 is present in undifferentiated cells but not in differentiated cells and regulates c-myc expression by binding to a single-stranded far-upstream element upstream of the c-myc promoter. Previous report showed that down-regulation of FUBP1 and subsequent down-regulation of c-myc were needed for lung cell differentiation in mice. This protein may act both as an activator and repressor of transcription. Likewise, PKM2 has been determined to stimulate Oct4-mediated transcriptional activation. Oct4 and c-myc constitute are two of the Yamanaka transcription factors crucial for maintaining pluripotency of stem cells. BRE-silencing resulted in decreased expression of pluripotency factors and may explain our observation of enhanced osteogenic and chondrogenic differentiation in HUCPV cells. Further studies are required to examine the effect of BRE-silencing on other mesenchymal Ginsenoside-F4 lineage differentiations. In sum, our findings suggest a multifunctional role for BRE in maintaining stemness and the cytoskeletal architecture of HUCPV cells. In addition, BRE expression can be manipulated to accelerate induced chondrogenic and osteogenic differentiation in HUCPV cells. Breast cancer is the most common malignant neoplasm and the second leading cause of death from cancer in women both in the USA and Europe. It is established that both adjuvant chemotherapy and hormonal therapy prolong disease-free and overall survival. Anthracyclines and taxanes are the two most commonly used classes of agents in this setting. However, despite the optimal management of patients with early-stage breast cancer, eventually approximately 30% of them suffer from disease relapse. Metastatic breast cancer is an incurable disease with few therapeutic options. With the increasing use of anthracyclines and taxanes in the adjuvant setting the number of available drugs for these patients is even more limited. Obviously, there is an unmet need for the introduction to the clinic of agents with novel modes of action, lack of cross-resistance with existing agents and promising activity in metastatic breast cancer.