RESUMO
Natural killer (NK) cells are innate immune cells with cytotoxic potentials to kill cancerous cells in several mechanisms, which could be implied for cancer therapy. While potent, their antitumor activities specially for solid tumors impaired by inadequate tumor infiltration, suppressive tumor microenvironment, cancer-associated stroma cells, and tumor-supportive immune cells. Therefore, manipulating or reprogramming these barriers by prospective strategies might improve current immunotherapies in the clinic or introduce novel NK-based immunotherapies. NK-based immunotherapy could be developed in monotherapy or in combination with other therapeutic regimens such as oncolytic virus therapy and immune checkpoint blockade, as presented in this review.
Assuntos
Antineoplásicos , Neoplasias , Humanos , Estudos Prospectivos , Imunoterapia , Células Matadoras Naturais , Neoplasias/terapia , Microambiente Tumoral , Imunoterapia AdotivaRESUMO
INTRODUCTION: This paper sought to scrutinize the role of microRNA-32 (miR-32) on the growth and migration as well as on the expression of metastatic genes in PC3 cells of prostate cancer in vitro. METHODS: Subsequent transfection of cells with miR-32 mimics, miR-32 inhibitor, negative control (NC), cell proliferation using MTT, and apoptosis by ELISA were performed. Furthermore, qRT-PCR was directed to measure the expression levels of matrix metalloproteinase 2 (MMP2) and vascular endothelial growth factors (VEGF) as metastatic and angiogenesis genes in the progression of PC3. RESULTS: miR-32 was overexpressed in PC3 cells compared to normal cells (P<0.001). Down-regulation of miR-32 obstructs in vitro proliferation and migration while intensifying the apoptosis rate in PC3 cells. Also, we found that miR-32 negatively modulates the expression of VEGF and MMP2 in PC3 cells. CONCLUSION: These results indicate that the suppression of miR-32 might offer an auxiliary treatment procedure for addressing the invasion, progression, and metastasis in PCa patients by improving cell apoptosis.