Research Paper Volume 13, Issue 19 pp 23096—23107

Figure 5. Qi Ling inhibited docetaxel resistance and glycolysis through SNHG10/miR-1271-5p/TRIM66 axis in CRPC cells. (A–I) PC3-DR and DU145-DR cells were transfected with empty vector and cultured in normal media (ctrl + vector), transfected with empty vector and cultured in media supplement with Qi Ling (QL-treatment + vector) or transfected with SNHG10 overexpression plasmid and cultured in media supplement with Qi Ling (QL-treatment + SNHG10-OE). (A and B) RNA levels of SNHG10, miR-1271-5p and TRIM66 were examined by qRT-PCR. (C) Protein level of TRIM66 was determined by Western blot. (D–G) Cell viability and IC50 value of docetaxel were determined by CCK-8 assay and colony formation assay. (H and I) Cell apoptosis was measured by Caspase-3 activity assay and DNA fragmentation assay. (J–N) PC3 and DU145 cells were transfected with empty vector and cultured in normal media (ctrl + vector), transfected with empty vector and cultured in media supplement with Qi Ling (QL-treatment + vector) or transfected with SNHG10 overexpression plasmid and cultured in media supplement with Qi Ling (QL-treatment + SNHG10-OE). Relative glucose consumption (J), pyruvate concentration (K), and lactate production (L) were assessed in PC3 and DU145 cells (M and N) mRNA levels of glycolytic components (SLC2A1, PFKP, PKM and LDHA) in PC3 and DU145 cells were examined by qRT-PCR. Values are mean ± SD. ^*P < 0.05; ^**P < 0.01; ^***P < 0.001.