Anti-HSP70 alleviates cell migration and proliferation in colorectal cancer cells (CRC) by targeting CXCR4 (in vitro study).

Colorectal cancer (CRC), the third most common cancer in men and women, accounts for 8% of new cancer cases in the US and 8 to 9% of the nation's anticipated cancer mortality in 2014. In the pathophysiology of colon cancer, heat shock protein 70 (HSP70) and CXCR4 are essential. In this research, we concentrated on the connection between CXCR4 expression and HSP70 inhibitor activity in the development of colorectal cancer. The HSP70 inhibitor's effect on cell proliferation was also evaluated. Samples were obtained from patients with CRC; the surrounding marginal tissues were considered healthy. The One CRC cell lines (HCA-7) were divided into two groups based on untreated and treated with anti-HSP70. HSP70 and CXCR4 mRNA expression and migration (Wound healing assay) were measured in these groups. Also, we evaluated the expression levels of HSP70 and CXCR4 in thirty CRC and healthy non-cancerous samples (Using Real-time PCR and Western Blotting). Moreover, we examined the viability of CRC cells in untreated and treated groups with anti-HSP70. Higher expression levels of CXCR4 (p < 0.0001) and HSP70 (p = 0.002) mRNA were observed in patients who had CRC. In contrast, lower mRNA expressions of HSP70 (p < 0.0001) and CXCR4 (P < 0.0001) were detected in the CRC cell line (HCA-7) after being treated with anti-HSP70. Moreover, the viability and migration of cancer cells were remarkably reduced in CRC cells treated with anti-HSP70. Our study's innovation was the in vitro demonstration of inhibiting HSP70 in the CRC cancer cell line drastically reduced CXCR4 expression, viability, and cancer cell migration. These findings may pave the way for additional studies on CRC cancer treatment and be examined in vivo in studies, given that the primary goal of therapy is to decrease the viability and spread of cancer cells.