THE TUMOR-ASSOCIATED INFLAMMATION DETERMINES EMT-STEMNESS IN GLIOMA MALIGNANCY

Shvachko L. P.*, Gridina N. Ya., Draguncova N. G. and Veselova O. I.

ABSTRACT

Recent data have expanded the conception that cancer-related inflammation is a crucial component of tumor progression. Indeed, anti-inflammatory therapies have shown efficacy in cancer prevention and treatment. It`s becoming clear that blocking inflammation will play a major role in cancer outcome. Every tumor stage may be potentiated by the underlying inflammatory process. But an exact mechanism of tumor-associated inflammation in cancer metastatic progression is not clear. The investigation of the mechanisms of the relationship between cancer progression and inflammation remain elusive. In this study, we have focused on the causal interaction between tumor-associated inflammation and EMT-stemness stage during glioma malignancy. We found that verapamil Ca-blocking drug withaccumulating anti-inflammatory function in glioma therapies targeted EMT-inducer transcription factor Snail gene expression in malignancy glioma patients along with anti-inflammatory actions as increasing blood cells transmembrane potential (TMP) and decreasing lymphocytes blast transformation proliferation (LBTP) in the primary blood cell culture assay. On the date obtained we have proposed that glioma-related inflammation determines EMT-stemness phenotype development in glioma malignancy. In conclusion, our results have revealed that anti-inflammatory therapy as verapamil may be efficacy in the targeted EMT-stemness in cancer metastatic progression and combining current anti-inflammatory drugs with the targeting EMT-stemness pathway may emerging improve metastatic patient treatment and cure.

Keywords: Glioma Malignancy, Cancer-Related Inflammation, EMT-Stemness, Verapamil.