Effects of miR-103a-3p Targeted Regulation of TRIM66 Axis on Docetaxel Resistance and Glycolysis in Prostate Cancer Cells

Objective: We aimed to study the expressions of miR-103a-3p and TRIM66 in prostate cancer (PCa) cells, explore the direct target genes of miR-103a-3p, and analyze the effects of miR-103a-3p targeted regulation of the TRIM66 axis on docetaxel (DTX) resistance and glycolysis of PCa cells. Methods: Human normal prostate cells and PCa cells were used to detect the expressions of miR-103a-3p and TRIM66 and analyze their relationship. DTX-resistant (DR) PCa cells were established and transfected with miR-103a-3p and TRIM66 plasmids. The MTT assay, the plate cloning assay, the wound healing assay, and the Transwell assay were used to detect cell viability, colony formation, cell migration, and cell invasion, respectively. Cell glycolysis was analyzed using a cell glycolysis kit. Results: The expression of miR-103a-3p was low and that of TRIM66 was high in PCa cells. MiR-103a-3p had a binding site with TRIM66, and the double luciferase report confirmed that they had a targeting relationship. Compared with the PCa group cells, the DTX-resistant group cells showed increased resistance to DTX. The resistance index was 13.33, and the doubling time of the DTX-resistant group cells was significantly longer than that of the PCa group cells. The DTX-resistant group showed more obvious low expression of miR-103a-3p and high expression of TRIM66. After the DTX-resistant group cells were transfected with miR-103a-3p and TRIM66 plasmids, the expression of miR-103a-3p increased significantly and that of TRIM66 decreased significantly. Upregulation of miR-103a-3p and interference with TRIM66 can inhibit the proliferation, metastasis, and glycolysis of DTX-resistant cells. Conclusion: The expression of miR-103a-3p was downregulated and that of TRIM66 was upregulated in the malignant progression of PCa, especially during DTX resistance. Upregulation of miR-103a-3p and interference with TRIM66 can inhibit DTX resistance and glycolysis of PCa cells. Targeting TRIM66 may provide potential application value in molecular therapy for PCa.