Objective:To explore the effect of microRNA (miRNA)-3126-5p on the proliferation and migration of colorectal cancer cells by inhibiting the expression of LIM and SH3 protein 1 ( LASP1). Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-3126-5p in colorectal cancer cell lines (HT-29, HCT116, LoVo, SW480) and normal intestinal mucosal epithelial cells (HIEC). The cell line with the lowest expression level was selected as the experimental object. The experiment was divided into 2 groups: the negative control group (transfected with miR-NC) and the miR-3126-5p group (transfected with miR-3126-5p). Cells of each group were collected 48h after transfection. qRT-PCR method was used to detect the expression level of miR-3126-5p in each group. The MTS method and the scratch healing experiment were used to detect the proliferation level and migration ability of the cells in each group. The bioinformatics software microRNA.org and the dual-luciferase reporter gene experiment were used to predict and verify the target genes of miR-3126-5p, respectively. qRT-PCR and Western blot were used to detect the expression levels of target genes in each group of cells. Measurement data were expressed as mean±standard deviation ( Mean± SD), t test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:Compared with normal intestinal mucosal epithelial cells (HIEC), the expression level of colorectal cancer cell line miR-3126-5p was significantly reduced ( P<0.05), and the cell line with the lowest expression level was HCT116 cells ( P<0.01). The expression of miR-3126-5p in HCT116 cells in the negative control group and miR-3126-5p group were (1.05±0.16) and (7.91±1.26) respectively, and the difference was statistically significant ( t=5.40, P<0.01). Compared with the negative control group, the proliferation ability of HCT116 cells in the miR-3126-5p group was significantly reduced ( t=4.52, P<0.05), and the migration ability was significantly reduced ( P<0.01). microRNA.org shows that miR-3126-5p has complementary binding sites with LIM and SH3 protein 1 ( LASP1) gene mRNA. miR-3126-5p can target LASP1 mRNA ( P<0.01). Compared with the negative control group, the expression of LASP1 gene in HCT116 cells of the miR-3126-5p group was significantly reduced ( t=4.56, P<0.01). Conclusion:The expression of miR-3126-5p in colorectal cancer cell lines is low, and miR-3126-5p can reduce the proliferation and migration ability of colorectal cancer HCT116 cells by inhibiting the expression of the target gene LASP1.

Objective:To investigate the effect of long non-coding RNA (lncRNA) HAGLR on the proliferation and migration of gastric cancer cells by inhibiting the expression of microRNA (miRNA, miR)-93-5p.Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of HAGLR in gastric cancer cell lines (HS-746T, BGC823, SGC7901, MGC803) and normal gastric mucosal epithelial cells (GES-1). Selected the cell line with the lowest HAGLR expression and transfected with the negative control plasmid (negative control group) or HAGLR-high-expression plasmid (HAGLR group) respectively. The MTS method and the scratch healing test were used to detect the proliferation and migration ability of the cells after transfection. The bioinformatics software miRcode database was used to predict the target gene of HAGLR, and the dual luciferase reporter gene experiment was used to verify the binding of HAGLR to the target gene. qRT-PCR was used to detect the expression of the target gene. Western blot was used to detect the expression of Hippo signaling pathway. The software SPSS 21.0 was used to conduct statistical analysis. The t test was used for comparison between two groups, and the one-way analysis of variance was used for comparison between multiple groups. Results:Compared with GES-1 cells, the expression level of HAGLR in gastric cancer cell lines was lower (all P<0.05), and the cell line with the lowest HAGLR expression was SGC7901 cells ( P<0.01). The HAGLR expression in SGC7901 cells in the HAGLR group and the negative control group were 1.03±0.13 and 9.75±1.10, respectively. The expression level of HAGLR in the negative control group was significantly lower than that in the HAGLR group ( t=7.87, P<0.01). Compared with the negative control group, the absorbance of SGC7901 cells in the HAGLR group was significantly reduced ( P<0.05), and the scratch healing rate was significantly reduced ( P<0.01). The miRcode database showd that HAGLR and miR-93-5p have complementary binding sites. The dual luciferase reporter gene experiment showed that HAGLR can complement miR-93-5p ( P<0.01). Compared with the negative control group, the expression of miR-93-5p in SGC7901 cells in the HAGLR group was significantly reduced ( P<0.01), and the expression of Hippo signaling pathway protein was significantly reduced (all P<0.01). Conclusions:HAGLR is low expressed in gastric cancer cell lines. HAGLR inhibits the proliferation and migration of gastric cancer SGC7901 cells by negatively regulating miR-93-5p.

Objective:To observe the expression of long non-coding RNA (lncRNA) PP7080 in gastric cancer tissues and cell lines, and clarify its effect on the migration and proliferation of gastric cancer cell MGC803 and its molecular mechanism.Methods:Real-time PCR was used to detect the expression of lncRNA PP7080 in gastric cancer tissues and adjacent tissues, gastric cancer cell lines and immortalized normal gastric mucosal epithelial cell lines. The gastric cancer cell line with the least expression was selected, and the expression plasmid of lncRNA PP7080 and the negative control plasmid were transfected into gastric cancer cells, respectively, and named as lncRNA PP7080 group and NC group. Real-time PCR to verify the effect of transfection. Cell scratch test and CCK-8 test were used to detect the regulation of lncRNA PP7080 on the migration and proliferation of gastric cancer cells.The statistical saftware SPSS 20.0 was used for statistical analysis, the measurement data of normal distribution were expressed as ( Mean± SD). Real-time PCR and Western blot were used to detect the expression of tumor metastasis suppressor gene 1 ( TMSG-1) in the transfected cells. The t test was used for comparison between groups. Results:The expression of lncRNA PP7080 in gastric cancer tissue was less than that in adjacent tissues [(0.85±0.34) vs (5.33 ± 0.76), P<0.01]. The expression of lncRNA PP7080 in gastric cancer cell lines is less than that of immortalized normal gastric mucosal epithelial cells ( P<0.05), and the least expression in MGC803 cells ( P<0.01). The expression of lncRNA PP7080 in the lncRNA PP7080 group was significantly higher than that in the NC group, and the difference was statistically significant ( P<0.01). The cell migration rates of NC group and lncRNA PP7080 group were (72.67±6.39)% and (26.45±6.63)%, respectively, and the cell migration ability of lncRNA PP7080 group was significantly reduced ( P<0.01). Compared with the NC group, the cell proliferation ability of the lncRNA PP7080 group was significantly reduced ( P<0.05). Compared with the NC group, the expression of TMSG-1 in MGC803 cells of the lncRNA PP7080 group was significantly reduced ( P<0.01). Conclusion:lncRNA PP7080 is lowly expressed in gastric cancer tissues and cell lines. lncRNA PP7080 can inhibit the migration and proliferation of gastric cancer cell MGC803 by promoting the expression of TMSG-1 gene.

Objective To explore the clinical efficacy of Shenkang Injection and its influence on C-reactive protein (CRP)and interleukin-6 (IL-6)levels in patients with diabetic nephropathy (DN).Methods A total of 120 patients with type 2 diabetes mellitus combined with DN admitted in our hospital from Jan.2012 to Jan.2014 were randomly divided into observation group and con-trol group,60 cases for each.Control group was treated with high-quality protein diets and insulin to control blood glucose and pressure,on which basis observation group was added with intravenous injection of Shenkang Injection.Clinical efficacy,fasting blood glucose (FBG),Triglyceride (TG), total cholesterol (TC),serum creatinine (SCr),24 h urinary protein (24 hUpro),CRP and IL-6 level changes before and after treatment in both groups were observed.Results Clinical efficacy was 90.00% in observation group,evidently higher than 75.00% in control group (P <0.05). Aboveindexeswere all improvedobviously after treatment than treatment before (P < 0 .0 5 ,P <0.01)and were markedly lower in observation group than in control group (P <0.01).Conclusion Shenkang Injection can effectively reduce IL-6 and CRP levels and decrease blood glucose and pressure,prolong disease progression and improve prognosis in DN patients.

Objective To explore the clinical efficacy of Shenkang Injection and its influence on C-reactive protein (CRP)and interleukin-6 (IL-6)levels in patients with diabetic nephropathy (DN).Methods A total of 120 patients with type 2 diabetes mellitus combined with DN admitted in our hospital from Jan.2012 to Jan.2014 were randomly divided into observation group and con-trol group,60 cases for each.Control group was treated with high-quality protein diets and insulin to control blood glucose and pressure,on which basis observation group was added with intravenous injection of Shenkang Injection.Clinical efficacy,fasting blood glucose (FBG),Triglyceride (TG), total cholesterol (TC),serum creatinine (SCr),24 h urinary protein (24 hUpro),CRP and IL-6 level changes before and after treatment in both groups were observed.Results Clinical efficacy was 90.00% in observation group,evidently higher than 75.00% in control group (P <0.05). Aboveindexeswere all improvedobviously after treatment than treatment before (P < 0 .0 5 ,P <0.01)and were markedly lower in observation group than in control group (P <0.01).Conclusion Shenkang Injection can effectively reduce IL-6 and CRP levels and decrease blood glucose and pressure,prolong disease progression and improve prognosis in DN patients.

Objective:This study investigates the influence of the apolipoprotein E ε4(APOE ε4)genotype on the relationship between glucose-lipid metabolism disorders and diabetes-related cognitive impairment(DCI).Methods:A case-control study was conducted involving 891 patients with type 2 diabetes mellitus(T2DM)with a mean age of(62.1±13.8)years, all of whom underwent elective surgery at the First Hospital of Shanxi Medical University between January 2017 and December 2022.Among these participants, 229 were diagnosed with DCI(case group), while 662 were cognitively normal(control group).Routine clinical information was collected, and peripheral venous blood samples were analyzed for glycated hemoglobin(HbA1c)and blood lipid levels.The single nucleotide polymorphisms rs429358 and rs7412 were analyzed to determine the presence of the APOE ε4 genotype.Stepwise Logistic regression was employed to identify independent risk factors for DCI, and subgroup analyses were performed to evaluate the effect of the APOE ε4 genotype on the relationship between HbA1c and blood lipid levels in relation to DCI risk. Results:Among all patients, female gender( OR=1.915, 95% CI: 1.393-2.631, P<0.001), longer duration of T2DM( OR=1.169, 95% CI: 1.087-1.257, P<0.001), elevated triglycerides( OR=1.161, 95% CI: 1.041-1.294, P=0.007), and being an APOE ε4 carrier( OR=1.638, 95% CI: 1.115-2.405, P=0.012)were identified as independent risk factors for developing DCI.High levels of low-density lipoprotein(LDL)were found to be independently associated with an increased risk of DCI specifically in APOE ε4 carriers( OR=1.408, 95% CI: 1.060-1.870, P=0.018), but not in non-APOE ε4 carriers( P>0.05).In contrast, elevated HbA1c was independently associated with a higher risk of DCI in non-APOE ε4 carriers( OR=1.220, 95% CI: 1.040-1.430, P=0.014), but not in APOE ε4 carriers( P>0.05).Additionally, elevated triglycerides were independently linked to an increased risk of DCI across the entire sample and within each APOE ε4 genotype subgroup. Conclusions:The APOE genotype plays a significant role in modulating the relationship between dyslipidemia and the risk of developing DCI.This highlights the critical importance of lipid metabolism disorders and APOE risk genes in both the development and progression of DCI.These findings offer valuable insights for future clinical and mechanistic studies focused on DCI.

Objective:To explore the effect of down-regulation of long non-coding RNA (lncRNA) CTB-191K22.5 on the proliferation and invasion of colorectal cancer SW480 cells and the molecular mechanism.Methods:The TCGA database was used to analyze the expression differences of CTB-191K22.5 in colorectal cancer tissues and normal tissues. The CTB-191K22.5 inhibitor (Anti-CTB-191K22.5) and negative inhibitor (Control) were transfected into colorectal cancer SW480 cells, denoted as Observation group and Control group, real-time quantitative polymerase chain reaction (qRT) -PCR) was used to evaluate the inhibitory effect. MTT method and Transwell chamber method were used to evaluate the proliferation and invasion of SW480 cells. Western blot was used to evaluate the protein levels of PI 3K/AKT/mTOR signaling pathway in SW480 cells. The bioinformatics software starBase v2.0 was used to predict the target genes of CTB-191K22.5. qRT-PCR was used to evaluate the expression of CTB-191K22.5 target gene in SW480 cells. Measurement data were expressed as Mean±SD, and t-test was used for comparison between two groups. Results:Compared with normal tissues, the expression of CTB-191K22.5 in colorectal cancer tissues was significantly increased ( P<0.01). The expression of CTB-191K22.5 in SW480 cells of the Control group and Observation group were 6.60±0.85 and 1.08±0.21, respectively. The expression level of CTB-191K22.5 decreased after transfection with Anti-CTB-191K22.5 ( P<0.01). Compared with the Control group, the SW480 cell proliferation ability of the Observation group decreased ( P<0.01). The invasion numbers of SW480 cells in the Control group and Observation group were (135.4 ± 16.29) and (42.24±14.59), respectively. The invasion ability of SW480 cells decreased after transfection with Anti-CTB-191K22.5 ( P<0.01). Compared with the Control group, the expression levels of PI 3K/AKT/mTOR signaling pathway protein in SW480 cells in the Observation group decreased. miR-326 may be the target gene of CTB-191K22.5. Compared with the Control group, transfection with Anti-CTB-191K22.5 significantly increased the expression level of miR-326 in SW480 cells ( P<0.01). Conclusion:CTB-191K22.5 is highly expressed in colorectal cancer tissues, and down-regulation of CTB-191K22.5 may inhibit the proliferation and invasion of colorectal cancer SW480 cells by targeting miR-326.