[Abstract] Objective: To investigate the effect of lncRNA SNHG15 targeting miR-153 on cell viability and apoptosis of breast cancer cells and its apoptotic mechanism. Methods:The expression of SNHG15 in breast cancer cell lines(MDA-MB-231, BT-549 and MCF-7) were detected by Real-time fluorescent quantitative PCR (qPCR). MDA-MB-231 cells were divided into control (Ctrl) group, si-NC group, si-SNHG15 group, si-SNHG15+anti-NC group and si-SNHG15+anti-miR-153 group. Cell viability and apoptosis rate were detected by MTT and Flow cytometry, respectively. The targeting relationship between SNHG15 and miR-153 was verified by Dual luciferase report gene system. Mitochondrial membrane potential fluorescent probe (JC-1) staining method was used to detect cell mitochondrial membrane potential. The expressions of mitochondrial apoptosis-related proteins (Bcl-2, Bax, caspase3, cleaved caspase3 [c-caspase3] and Cyt-C）were detected by Western blotting. Results: The expression of SNHG15 in breast cancer cells was significantly higher than that in human normal mammary epithelial MCF10A cells (P<0.01). There was a targeting relationship between SNHG15 and miR-153. Compared with the control group, the cell viability and mitochondrial membrane potential of MDA-MB-231 cells in si-SNHG15 group were decreased, while apoptosis rate was increased (all P<0.01); the expressions of Bcl-2 and caspase3 were decreased while expressions of Bax, c-caspase3 and Cyt-C were increased (all P<0.01). However, co-transfection of si-SNHG15 and anti-miR-153 significantly attenuated the effects of si-SNHG15 on cell viability, apoptosis, mitochondrial membrane potential and expressions of Bcl-2, Bax, caspase3, c-caspase3 and Cyt-C (all P<0.01). Conclusion: lncRNA SNHG15 can target miR-153 to induce apoptosis of MDA-MB-231 cells, and the mechanism may be related to the regulation of apoptosis of mitochondrial pathway.

Objective:To understand the clinical characteristics of human immunodeficiency virus (HIV) infection/acquired immunodeficiency syndrome (AIDS) patients with renal injury after antiviral therapy in Henan Province, and to explore the risk factors of renal injury.Methods:A cross-sectional study was conducted to investigate HIV infection/AIDS patients receiving antiviral therapy in Zhengzhou Sixth People′s Hospital, Anyang Fifth People′s Hospital, Hebi Third People′s Hospital, Luo Yang Zhoushan Hospital and Lankao Central Hospital in Henan Province from April 1 to September 30, 2023. The clinical information including basic data, antiviral therapy regimens and comorbidities, and laboratory test results (blood urea nitrogen, serum creatinine, blood uric acid, urine routine, urine microalbumin, urine α 1-microglobulin (α 1-MG), urine β 2-microglobulin (β 2-MG), urine retinol binding protein (RBP), urine creatinine, HIV viral load, CD4 + T lymphocyte count) were collected. Multivariate binary logistic regression was used to analyze independent risk factors for renal injury. Results:A total of 2 526 HIV infection/AIDS patients were included, with the age of (45.52±14.28) years and 2 156 (85.4%) males. The main route of transmission was sexual transmission (91.6%, 2 314/2 526). The duration of antiviral therapy was 5.00(2.92, 8.00) years. Tenofovir (TDF)+ lamivudine (3TC)+ non-nucleoside reverse transcriptase inhibitors (NNRTI) accounted for 55.3%(1 396/2 526) of the current antiviral therapy regimen. The percentage of HIV viral load <50 copies/mL was 93.0%(2 350/2 526). The CD4 + T lymphocyte count was 476(337, 645)/μL. There were 156 patients (6.2%) complicated with hepatitis B and/or hepatitis C, 205 patients (8.1%) with diabetes, 379 patients (15.0%) with hyperlipidemia, and 189 patients (7.5%) with hyperuricemia. A total of 1 040 patients (41.2%) with renal injury were found through renal function test, including 355 cases (14.1%) with estimated glomerular filtration rate (eGFR) <60 mL/(min·1.73 m 2) or urine protein positive or urine albumin creatine ratio (UACR) ≥30 mg/g, 682 patients (27.0%) with pure tubular injury presented with only positive for urinary α 1-MG, urinary β 2-MG, or urinary RBP. eGFR< 60 mL/(min·1.73 m 2) was found in 71 cases (2.8%), eGFR from 60 to 89 mL/(min·1.73 m 2) was found in 509 cases (20.2%), and eGFR≥90 mL/(min·1.73 m 2) was found in 1 946 cases (77.0%). A total of 138 patients (5.5%) were identified as having combined chronic kidney disease (CKD). Among them, 110 patients (79.7%) were in CKD stages 1 to 2, and 117 patients (84.8%) were in urinary albumin A2 grade. Multivariate analysis of 355 patients with renal injury who had eGFR<60 mL/(min·1.73 m 2) or positive urine protein in urine routine or UACR ≥30 mg/g showed that ages of 50 to 69 years old (odds ratio( OR)=2.189, 95% confidence interval ( CI) 1.333 to 3.596, P=0.002)), ≥70 years old ( OR=5.190, 95% CI 2.912 to 9.248, P<0.001), female ( OR=1.685, 95% CI 1.241 to 2.286, P=0.001), combined opportunistic infection ( OR=2.521, 95% CI 1.567 to 4.056, P<0.001), combined hepatitis B ( OR=1.962, 95% CI 1.110 to 3.467, P=0.020), combined hepatitis C ( OR=1.883, 95% CI 1.043 to 3.400, P=0.036), combined diabetes ( OR=2.703, 95% CI 1.911 to 3.821, P<0.001), using TDF for two to four years ( OR=1.674, 95% CI 1.103 to 2.459, P=0.015), using TDF for greater than or equal to five years ( OR=1.880, 95% CI 1.287 to 2.746, P=0.001), using TDF combined with lopinavir/ritonavir (LPV/r) ( OR=3.610, 95% CI 2.273 to 5.734, P<0.001) and using TDF combined with non-LPV/r ( OR=1.495, 95% CI 1.036 to 2.157, P=0.031) were the risk factors of renal injury. Conclusions:There is a high proportion of renal injury among HIV infection/AIDS patients after antiviral therapy in Henan Province, including CKD and simple renal tubular injury. Older age, female, comorbidities, and long-term use of TDF are risk factors for renal injury.