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.

BACKGROUND:Traditional core decompression and al ograft fibula supporting can reduce the stress load within femoral head and improve mechanical properties of femoral head. However, it cannot provide supports for maintaining the stability of five pathological areas fol owing femoral head necrosis. OBJECTIVE:To observe the clinical effect of fan-shaped decompression and al ograft fibula supporting internal fixation in treatment of early femoral head necrosis in adults, taking al ograft fibula grants as the control. METHODS:Forty patients with early femoral head necrosis were randomly divided into treatment group and control group, receiving fan-shaped decompression plus al ograft fibula supporting internal fixation and traditional decompression plus al ograft fibula grafting, respectively. The therapeutic effects in two groups were observed and compared. After treatment, patients were detected by bilateral hip anteroposterior films, Harris scoring and X-ray ARCO staging to evaluate the col apse severity and restoration of necrosis. RESULTS AND CONCLUSION:At the last fol ow-up, Harris scores in the treatment group were significantly higher and the repairing effect was better than control group (P<0.05). In treatment group, 18 hips restored wel (72%) and 7 hips delayed or failed to restore (28%);in control group, 9 hips restored wel (60%) and 6 hips delayed or failed to restore (40%). Our findings indicate that, fan-shaped decompression plus al ograft fibula supporting internal fixation yields a more complete decompression, a higher stability of femoral head and a more reliable supporting, compared with traditional decompression plus al ograft fibula grafting.