CXCR4 knockdown inhibits the growth and invasion of nasopharyngeal cancer stem cells

Abstract

Nasopharyngeal cancer is a type of malignant tumor with a high rate of incidence. Cancer stem cells are regarded as one of the main causes for the formation and recurrence of nasopharyngeal cancer. CXC chemokine receptor type 4 (CXCR4) has been reported to perform an important role in cancer; however, the association between CXCR4 and nasopharyngeal cancer stem cells remains unclear. The present study explored the effect of CXCR4 on cellular viability, apoptosis and invasion of nasopharyngeal cancer stem cells. Results of the present study demonstrated that knockdown of CXCR4 inhibited the viability and invasion of nasopharyngeal cancer stem cells and promoted cellular apoptosis. Further studies have revealed that the anti-tumor effect of CXCR4 knockdown was associated with the inhibition of the protein kinase B signal. These results demonstrate that the knockdown of CXCR4 resulted in an anti-tumor effect in nasopharyngeal cancer stem cells. Therefore, CXCR4 may become a promising therapeutic target in the treatment of nasopharyngeal cancer.

Bioinformatics Studies Provide Insight into Possible Target and Mechanisms of Action of Nobiletin against Cancer Stem Cells

“…However, a recent study showed that tamoxifen-resistant cells exhibit increased stemness properties via activation of Wnt/ß-catenin signaling (Leung et al, 2017). The interaction of CXC chemokine receptor type 4 (CXCR4) with its ligand CXC motif ligand 12 (CXCL12) plays important roles in maintaining CSCs properties in tamoxifen-resistant breast cancer cells (Dubrovska et al, 2012), nasopharyngeal CSCs (Tian et al, 2017), esophageal CSCs (Wang et al, 2017b), and stimulates the angiogenesis in vascular endothelial cells through upregulation of the MAPK/ERK and PI3K/AKT and Wnt/β-catenin pathways. (Song et al, 2018).…”

Mechanisms on chemotherapy resistance of colorectal cancer stem cells and research progress of reverse transformation: A mini-review

“…When CSC is exposed to chemotherapeutic agents in vivo , some special regulatory mechanisms will be activated; pi3-K, MAPK and other pathways will be cascade-activated, and then the anti-apoptotic protein myeloid cell leukemia-1 (McL-1) will increase to inhibit the apoptosis of tumor cells ( 22 ). Many studies have suggested that inhibiting the activity of CSCs can increase the apoptosis of tumor cells ( 23 – 25 ). In another study by Zhang et al, CRCSCs were inhibited by pitavastatin, and the apoptosis of colon carcinoma cells was increased ( 26 ).…”