Objective To analyze the expression of long non-coding RNA(lncRNA)ABHD11-AS1 in clear cell renal cell carcinoma(ccRCC)and renal cancer cell lines,and explore its potential functions and mechanisms of action.Methods The bioinformatics tool GEPIA2 software was used to analyze The Cancer Genome Atlas(TCGA)database and compare the expression levels of ABHD11-AS1 in ccRCC and normal kidney tissues.Real-time quantitative PCR was performed to assess ABHD11-AS1 expression in ccRCC tissues,normal kidney tissues,and renal cancer cell lines.Subcellular localization experiments were performed to determine the subcellular locali-zation of ABHD11-AS1 in renal cancer cells.The MTT assay,Transwell assay,real-time quantitative PCR,and Western blotting were used to detect the effects of ABHD11-AS1 and miR-133a-3p on the proliferation,invasion,and expression of SLC6A1 in renal cancer cells.A dual-luciferase reporter gene experiments was performed to validate the binding effect of ABHD11-AS1 to miR-133a-3p and the effect of miR-133a-3p on SLC6A1.Results GEPIA2 software and real-time quantitative PCR analyses indicated that ABHD11-AS1 was highly expressed in ccRCC tissues compared to normal kidney tissues(P＜0.05).Compared to the immortalized renal tubular epithelial cell line HK-2 cells,the expression of ABHD11-AS1 was significantly upregulated in the ACHN,786-O,and SN12-PM6 cells,with the highest expression observed in 786-O cells.The results of the subcellular localization experiments indicated that ABHD11-AS1 was primarily distributed in the cytoplasm of 786-O cells.ABHD11-AS1 knockdown reduced the proliferative and invasive abilities of 786-O cells and decreased SLC6A1 mRNA and protein expression(P＜0.05).Dual-luciferase reporter gene experiments demonstrated that ABHD11-AS1 targets and binds to miR-133a-3p,which in turn binds to SLC6A1.Overexpression of miR-133a-3p reduced the mRNA and protein levels of SLC6A1 in 786-O cells,whereas downregulation of miR-133a-3p had the opposite effect.Downregulation of miR-133a-3p enhanced the proliferation and invasion of 786-O cells,while knockdown of SLC6A1 partially reversed the promoting effect of miR-133a-3p downreg-ulation on the proliferation and invasion of 786-O cells(P＜0.05).Simultaneously,downregulation of miR-133a-3p could also partially reverse the inhibitory effects of ABHD11-AS1 knockdown on 786-O cell proliferation,invasion,and SLC6A1 expression(P＜0.05).Con-clusion ABHD11-AS1 exerts a pro-cancer effect on ccRCC by regulating the miR-133a-3p/SLC6A1 axis,which influences the prolifera-tion and invasion of renal cancer cells.

Objective To analyze the expression of long non-coding RNA(lncRNA)ABHD11-AS1 in clear cell renal cell carcinoma(ccRCC)and renal cancer cell lines,and explore its potential functions and mechanisms of action.Methods The bioinformatics tool GEPIA2 software was used to analyze The Cancer Genome Atlas(TCGA)database and compare the expression levels of ABHD11-AS1 in ccRCC and normal kidney tissues.Real-time quantitative PCR was performed to assess ABHD11-AS1 expression in ccRCC tissues,normal kidney tissues,and renal cancer cell lines.Subcellular localization experiments were performed to determine the subcellular locali-zation of ABHD11-AS1 in renal cancer cells.The MTT assay,Transwell assay,real-time quantitative PCR,and Western blotting were used to detect the effects of ABHD11-AS1 and miR-133a-3p on the proliferation,invasion,and expression of SLC6A1 in renal cancer cells.A dual-luciferase reporter gene experiments was performed to validate the binding effect of ABHD11-AS1 to miR-133a-3p and the effect of miR-133a-3p on SLC6A1.Results GEPIA2 software and real-time quantitative PCR analyses indicated that ABHD11-AS1 was highly expressed in ccRCC tissues compared to normal kidney tissues(P＜0.05).Compared to the immortalized renal tubular epithelial cell line HK-2 cells,the expression of ABHD11-AS1 was significantly upregulated in the ACHN,786-O,and SN12-PM6 cells,with the highest expression observed in 786-O cells.The results of the subcellular localization experiments indicated that ABHD11-AS1 was primarily distributed in the cytoplasm of 786-O cells.ABHD11-AS1 knockdown reduced the proliferative and invasive abilities of 786-O cells and decreased SLC6A1 mRNA and protein expression(P＜0.05).Dual-luciferase reporter gene experiments demonstrated that ABHD11-AS1 targets and binds to miR-133a-3p,which in turn binds to SLC6A1.Overexpression of miR-133a-3p reduced the mRNA and protein levels of SLC6A1 in 786-O cells,whereas downregulation of miR-133a-3p had the opposite effect.Downregulation of miR-133a-3p enhanced the proliferation and invasion of 786-O cells,while knockdown of SLC6A1 partially reversed the promoting effect of miR-133a-3p downreg-ulation on the proliferation and invasion of 786-O cells(P＜0.05).Simultaneously,downregulation of miR-133a-3p could also partially reverse the inhibitory effects of ABHD11-AS1 knockdown on 786-O cell proliferation,invasion,and SLC6A1 expression(P＜0.05).Con-clusion ABHD11-AS1 exerts a pro-cancer effect on ccRCC by regulating the miR-133a-3p/SLC6A1 axis,which influences the prolifera-tion and invasion of renal cancer cells.

Objective To explore the saffety and efficacy of super-selective prostate artery embolization (PAE) combined with TURP (transurethral resection of prostate) as an alternative method for patients with severe large BPH (＞ 80 ml).Methods From March 2015 to June 2017,a total of 40 patients with large benign prostatic hyperplasia who failed in medical treatment were selected for PAE combined with TURP (18 cases)and TURP (22 cases).In the PAE combined with TURP group,the mean age was (75.0±8.7) years (ranging60-88 years) and the mean prostatic volume was (111.0 ±23.3) ml,ranged from 83 to 145 ml).The international prostate symptom score (IPSS),quality of life (QOL),maximal t rine flow rate (Qmax) and postvoid residual urine(PVR) were(25.2 ±3.6),(5.1 ± 1.0),(6.4 ± 2.3) ml/s and (107.7 ± 32.6) ml,respectively.In the TURP group,the mean age was (76.0 ± 6.9) years (ranging 62-85 years) and the mean prostatic volume was (107.5 ±27.4) ml,ranged from 80 to 150 ml).The IPSS,QOL,Q andPVRwere(24.3±4.2),(4.9 ±0.9),(6.7±2.2)ml/s and (106.6±32.2)ml,respectively.Clinical data of all of patients were analyzed retrospectively,including operative time,estimate blood loss,weight and efficacy of resected tissue,time of continuous bladder irrigation and catheterization,IPSS,QOL,PVR,Q and postoperative complications.Results There were significant differences in the operative time [(75.8 ± 25.1) min vs.(103.2 ± 27.7) min],estimate blood loss [(122.8 ± 33.9) ml vs.(447.6 ± 36.0) ml],weight of resected tissue [(99.9 ± 24.2) g vs.(82.9 ± 15.5) g],efficacy of resected tissue [(76.9 ± 20.7) g/h vs.(41.7 ± 14.2) g/h],continuous bladder irrigation time [(1.4 ± 0.5) d vs.(2.4 ± 0.8) d] and catheterization time [(2.2 ± 0.4) d vs.(3.4 ± 0.6) d] between PAE combined TURP group and TURP group (P ＜ 0.05).The postoperative complications of PAE combined TURP group and TURP group were included secondary hemorrhage (0 case vs.3 cases),secondary TURP (0 case vs.3 cases),temporary urinary incontinence (2 case vs.4 case),urinary tract infection (1 case vs.2 case).After 1-year follow up,the IPSS,QOL,Qmax and PVR of PAE combined TURP group and TURP group were (6.7 ±1.5)and(6.9± 1.5),(2.3 ±0.5) and(2.3 ±0.6),(15.6 ±2.3) ml/s and(15.0 ±2.1) ml/s,(32.8±6.5) ml and(32.3± 8.4)ml,respectively.Both goups were found to have significantly improved in IPSS,QOL,Q and PVR,as compared with preoperative indexes,respectively (P ＜ 0.05).However,there was no significant difference in those indexes between two groups (P ＞ O.05).Conclusions PAE combined TURP could be used a safe and effective therapy for treating patients with LUTS due to large volume (＞ 80 ml) BPH.It has been a priority in less blood,more efficient of resected tissue and less postoperative complications.