Objective: To investigate if high glucose (HG) exacerbates Porphyromonas gingivalis (P.g) lipopolysaccharide (LPS)-induced inflammatory response in human gingival fibroblasts (HGFs) and to explore the underlying mechanisms. To provide a basis for the mechanism of diabetes aggravating periodontitis. Methods: HGFs were divided into four groups: the control group (basal medium), the LPS group (treated with 5 μg/mL P.g-LPS for 24 h), the HG group (treated with 25 mmol/L glucose for 24 h), and the HG+LPS group (treated with 25 mmol/L glucose + 5 μg/mL P.g-LPS for 24 h). After culturing for 24 h in the respective media, the cells were harvested for experiments. Intracellular reactive oxygen species (ROS) and mitochondrial reactive oxygen species (mtROS) were detected using 2 ', 7' - dichlorodihydrofluorescein diacetate (DCFH-DA) and MitoSOX Red staining, respectively. Fluorescence intensity was analyzed by confocal fluorescence microscopy and directly measured in cell suspension. Immunofluorescence was used to detect changes in mitochondrial DNA (mtDNA) content of HGFs. Real-time fluorescence quantitative PCR was used to detect the content of mtDNA in cytoplasm and cell supernatant. Protein expression of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway was assessed by western blot, while mRNA expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were detected by PCR. Results: Compared to the control group, both the LPS group and the HG group exhibited a significant increase in ROS and mtROS, with a more pronounced elevation in the HG+LPS group, demonstrating a synergistic effect (ROS: F = 396.5, P < 0.001; mtROS: F = 29.38, P < 0.001, CI < 1). The cytoplasmic mtDNA content was significantly elevated in the LPS group, with a more marked increase in the HG+LPS group (F = 27.85, P < 0.001). The supernatant mtDNA levels were significantly higher in both the LPS and HG groups, with a more pronounced elevation in the HG+LPS group (F = 15.26, P < 0.001). The phosphorylated proteins p-STING, p-TBK1, and p-P65 in the cGAS-STING pathway showed varying degrees of activation in the LPS and HG groups, reaching the highest levels in the HG+LPS group (p-STING: F = 52.67, P < 0.001; p-TBK1: F = 15.67, P = 0.001; p-P65: F = 9.83, P = 0.005), while p-IRF3 showed no significant differences among the groups (P = 0.072). Pro-inflammatory cytokine TNF-α was significantly higher in the HG+LPS group compared to the control group (F = 15.05, P < 0.001), and IL-1β increased in both the LPS and HG groups, with a more pronounced rise in the HG+LPS group (F = 30.98, P < 0.001). IL-6 showed no significant differences among the groups (P = 0.847). Conclusion High glucose and LPS act synergistically to enhance oxidative stress, accompanied by increased mtDNA release, which activates the cGAS-STING pathway, thereby amplifying the inflammatory response in HGFs.

Objective:By observing the effects of Calycosin on the proliferation and migration of human renal cancer 769-P cell, to explore the possible molecular mechanism of Calycosin against renal cancer.Methods:769-P cell were cultured with different concentrations of Calycosin [0, 12.5, 25, 50, 100, 200 μmol/L, dissolved in Dimethyl sulfoxide (DMSO)], and the effects of different concentrations of Calycosin on the viability of 769-P cell was detected by CCK8 method. The 769-P cell treated with 200 μmol/L Calycosin were used as the Calycosin group, and the 769-P cell treated with DMSO were used as the control group. The cell colony formation assay and cell scratch assay were used to detect the effects of Calycosin on the proliferation and migration of 769-P cell, respectively. Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the effect of Calycosin on the expression of miRNA-1246 and chemokine receptor-4 (CXCR4) in 769-P cell. Western blotting method was used to detect the effects of Calycosin on the expression of CXCR4 and extracellular signal-regulated kinase (ERK) pathway proteins in 769-P cell. Measurement data were expressed as mean ± standard deviation ( ± s), and one-way ANOVA was used for comparison between multiple groups, while t-test was used for comparison between two groups. Results:After cultured with 0, 12.5, 25, 50, 100, and 200 μmol/L of Calycosin, the absorbance values of renal cancer 769-P cell were 0.99 ± 0.06, 0.74 ± 0.07, 0.60 ± 0.03, 0.55 ± 0.05, 0.40 ± 0.06, 0.21 ± 0.04, respectively; compared with 0 μmol/L, the Calycosin could reduce the survival rate of 769-P cell ( P<0.05). The number of clones of 769-P cell in the control group and the Calycosin group was 109.80 ± 13.19 and 60.66 ± 11.22, respectively, and the number of clones of the 769-P cell in the Calycosin group was decreased, the difference was statistically significant ( t=5.67, P<0.01). The relative migration rates of 769-P cell in the control group and the Calycosin group were (43.13 ± 3.82)% and (14.27 ± 3.25)%, respectively, after the 769-P cell were treated with Calycosin, the cell migration ability was weakened ( t=5.71, P<0.05). The relative expression levels of miRNA-1246 in 769-P cell of the control group and the Calycosin group was 1.03 ± 0.12 and 6.99 ± 1.84, respectively, and the relative expression levels of CXCR4 mRNA was 7.17 ± 2.96 and 0.98 ± 0.06, respectively, showed that Calycosin can up-regulate the expression of miRNA-1246 in 769-P cell ( t=3.24, P<0.01), and down-regulate the expression of CXCR4 mRNA ( t=4.18, P<0.01). Compared with the control group, the Calycosin could down-regulate the expression of CXCR4 protein and ERK pathway protein in 769-P cell. Conclusion:Calycosin can inhibit the proliferation and migration of renal cancer 769-P cell, and its mechanism may be related to up-regulating the expression of miRNA-1246 and blocking the CXCR4/ERK pathway.

Objective:To explore the effect of long non-coding RNA (lncRNA) C10orf25 on the proliferation and invasion ability of prostate cancer cells and the possible role of miRNA-671-5p (miR-671-5p).Methods:Data from the Gene expression omnibus (GEO) database (data updated in January 2023) were used to analyze the differences in the expression levels of C10orf25 in 137 cases of prostate cancer tissues and paracancerous tissues. Prostate cancer C4-2B, DU-145, 22Rv1, PC-3, LNCaP cell lines and immortalized prostate epithelial RWPE-1 cell lines were selected, and then real-time quantitative fluorescence polymerase chain reaction (qRT-PCR) was used to detect the relative expression levels of C10orf25 in cell lines. The 22Rv1 cells with the lowest relative expression level of C10orf25 were selected and divided into the control group (transfected with negative plasmid) and the C10orf25 group (transfected with C10orf25 plasmid); the CCK-8 method was used to detect the proliferation activity of 22Rv1 cells in both groups at day 1, 2, 3, 4, 5 (expressed as absorbance value); the Transwell method was used to detect the invasion ability of 22Rv1 cells. Linc2GO software was used to predict miR-671-5p with binding sites for C10orf25. Dual luciferase reporter gene assay was used to verify the targeting relationship between C10orf25 and miR-671-5p. qRT-PCR was used to detect the relative expression levels of C10orf25 and miR-671-5p. Western blot was used to detect the expression of proteins related to the NF-κB signaling pathway of 22Rv1 cells in the both groups.Results:In the GEO database, the relative expression level of C10orf25 in prostate cancer tissues was lower than that in paracancerous tissues ( P < 0.01). The relative expression levels of C10orf25 in immortalized prostate epithelial cell line RWPE-1 and prostate cancer cell lines C4-2B, DU-145, 22Rv1, PC-3, and LNCaP were 1.00±0.05, 0.63±0.04, 0.42±0.03, 0.18±0.04, 0.81±0.02, 0.50±0.07, and the difference was statistically significant ( F = 43.29, P < 0.05). The proliferation ability of 22Rv1 cells in C10orf25 group was lower than that in the control group from the second day, and the differences were statistically significant (all P < 0.05). The number of invasive cells in the control group and C10orf25 group were (97±11) and (36±9), respectively, and the difference was statistically significant ( t = 4.15, P < 0.01). Linc2GO software prediction results showed that C10orf25 had a binding site for miR-671-5p. The dual luciferase reporter gene assay showed that the relative luciferase activity of miR-671-5p and C10orf25 wild plasmid co-transfecting 22Rv1 cells was lower than that of miR-NC and C10orf25 wild plasmid co-transfecting 22Rv1 cells, and the difference was statistically significant ( P < 0.01); when miR-671-5p or miR-NC was co-transfected with C10orf25 mutant plasmid, the difference in the luciferase activity of 22Rv1 cells was not statistically significant ( P > 0.05). The relative expression levels of miR-671-5p in 22Rv1 cells were 7.33±0.99 and 0.98±0.16, respectively in the control group and C10orf25 group, and the difference was statistically significant ( t = 6.32, P < 0.01). The results of Western blot showed that the expression levels of NF-κB signaling pathway protein p50, matrix metalloproteinase 9, c-myc, and vascular endothelial growth factor protein in 22Rv1 cells in C10orf25 group were lower than those in the control group. Conclusions:The overexpression of C10orf25 may inhibit the proliferation and invasion of prostate cancer cells through the miR-671-5p-NF-κB axis.

AIM: To compare the outcome of C3F8 versus silicone oil tamponade after pars plana vitrectomy(PPV)and inverted internal limiting membrane(ILM)for the treatment of highly myopic macular hole retinal detachment(MHRD).METHODS: Retrospective clinical study. Totally 45 patients(45 eyes)with highly myopic MHRD who visited our hospital between January 2019 and August 2022 were selected as the research subjects. The patients were divided into two groups according to different intraocular tamponade agents: C3F8(22 eyes)and silicone oil(23 eyes)groups. All patients underwent conventional three-incision PPV, ILM was tamped, a venous blood clot was placed on the tamped ILM, and 15% C3F8 and silicone oil were used as tamponade, respectively. The best corrected visual acuity(BCVA), multifocal electroretinogram(mfERG), the closure of the macular hole, retinal reattachment and the complications were observed.RESULTS: The macular hole closure rate was 77% in the C3F8 group and 83% in the silicone oil group, respectively(P>0.05), and retinal reattachment rates were 95% and 96%, respectively(P>0.05). The visual acuity of the two groups significantly improved, which was 0.99±0.34 and 1.22±0.37, respectively, and the C3F8 group was better than that of the silicone oil group(t=-2.156, P=0.037). After operation, the response density of the first ring of P1 wave in the first order kernel in mfERG was 114.27±26.37 nV/deg2 for the C3F8 group and 98.08±24.36 nV/deg2 for the silicone oil group, and the response density of the second ring of P1 wave was 80.45±14.94 nV/deg2 for the C3F8 group and 67.73±15.33 nV/deg2 for the silicone oil group, all of which were significantly higher compared to pre-operation [the response density of the first ring of P1 wave: 58.13±13.96 nV/deg2 for the C3F8 group and 55.30±10.48 nV/deg2 for the silicone oil group, the response density of the second ring of P1 wave: 51.18±8.19 nV/deg2 for the C3F8 group and 47.43±11.97 nV/deg2 for the silicone oil group](all P<0.05). It was found that the response density of the first ring of P1 wave was lower in the silicone oil group than in the C3F8 group(P<0.05). There was no statistically significant difference in the incidence of complications between the two groups(P>0.05).CONCLUSION: Silicone oil tamponade or C3F8 tamponade after PPV combined with ILM can both promote retinal reattachment and macular hole closure in patients with MHRD, and the C3F8 tamponade was superior to silicone oil in visual function recovery.

Objective:To explore the relationship between the relative expression of miRNA-676-3p and the survival of renal cancer patients, and its effect on the proliferation and invasion of renal cancer by targeting and regulating prefoldin 1 (PFDN1).Methods:OncoRank online software was selected to analyze the relationship between the relative expression of miRNA-676-3p and the survival rate of renal cancer patients. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the relative expression of miRNA-676-3p in renal cancer cell lines. Renal carcinoma CAKI1 cells were resuscitated, and the transfected miRNA-NC was used as the control group, and the transfected precursor miRNA-676-3p was used as the overexpression group. The relative expression of miRNA-676-3p was detected by RT-qPCR. The cell absorbance and invasion number of the two groups were measured by CCK-8 and Transwell invasion assays, respectively. The target gene of miRNA-676-3p was predicted and verified by referring to the TargetScan Release 8.0 website and dual-luciferase reporter gene experiment. The expression of PFDN1 gene and Wnt/β-catenin molecular pathway protein in the two groups of cells were determined by RT-qPCR and Western blotting, respectively. Measurement data were expressed as mean ± standard deviation ( ± s), t-test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:The survival rate of renal cancer patients with high expression of miRNA-676-3p was significantly higher than that of renal cancer patients with low expression of miRNA-676-3p, the difference was statistically significant ( P<0.01). The relative expression of miRNA-676-3p in renal cancer cell lines was significantly lower than that in normal renal tubular epithelial cells, the difference was statistically significant ( P<0.01), and the relative expression of miRNA-676-3p in CAKI1 cells was the lowest, the difference was statistically significant ( P<0.01). The relative expression levels of miRNA-676-3p in the control and overexpression groups were 1.04±0.59 and 15.90±1.70, respectively, and the overexpression group was significantly higher than the control group, the difference was statistically significant ( P<0.01). After 24, 48, 60, and 72 h of culture, the absorbance of cells in the overexpression group was lower than that in the control group, the difference was statistically significant ( P<0.05). The number of invasion cells in the control group and the overexpression group were (115.90 ± 24.73) and (43.83 ± 21.94) cells, respectively, and the number of cell invasion in the overexpression group was significantly lower than that in the control group, the difference was statistically significant ( P<0.01). PFDN1 was the downstream target gene of miRNA-676-3p ( P<0.01). The relative expression of PFDN1 gene in the overexpression group was significantly lower than that in the control group, the difference was statistically significant ( P<0.01). The expression of Wnt/β-catenin molecular pathway proteins in the overexpression group was lower than that in the control group. Conclusions:Renal cancer patients with high expression of miRNA-676-3p had a higher survival rate. miRNA-676-3p inhibited the proliferation and invasion of renal cancer CAKI1 cells by significantly down-regulating the expression of PFDN1, thereby inhibiting the development of renal cancer.

BACKGROUND: Vaccination has been shown effective in controlling the global coronavirus disease 2019 (COVID-19) pandemic and reducing severe cases. This study was to assess the flare and change in disease activity after COVID-19 vaccination in patients with stable rheumatoid arthritis (RA). METHODS: A prospective cohort of RA patients in remission or with low disease activity was divided into a vaccination group and a non-vaccination group based on their COVID-19 vaccination status. Each of them was examined every 3 to 6 months. In the vaccination group, disease activity was compared before and after vaccination. The rates of flare defined as disease activity scores based on 28-joint count (DAS28) >3.2 with ΔDAS28 ≥0.6 were compared between vaccination and non-vaccination groups. RESULTS: A total of 202 eligible RA patients were enrolled. Of these, 98 patients received no vaccine shot (non-vaccination group), and 104 patients received two doses of vaccine (vaccination group). The median time interval from pre-vaccination visit to the first immunization and from the second dose of vaccine to post-vaccination visit was 67 days and 83 days, respectively. The disease activity scores at pre-vaccination and post-vaccination visits in the vaccination group patients were similar. At enrollment, gender, RA disease course, seropositivity, and disease activity were comparable across the two groups. Flare was observed in five (4.8%) of the vaccination group patients and nine (9.2%) of the non-vaccination group patients at post-vaccination assessment ( P  = 0.221). In terms of safety, 29 (27.9%) patients experienced adverse events (AEs) after vaccination. No serious AEs occurred. CONCLUSIONS COVID-19 vaccinations had no significant effect on disease activity or risk of flare in RA patients in remission or with low disease activity. Patients with stable RA should be encouraged to receive the COVID-19 vaccination.
Humans ; Arthritis, Rheumatoid ; Cohort Studies ; COVID-19/prevention & control* ; COVID-19 Vaccines/adverse effects* ; East Asian People ; Prospective Studies ; Vaccination/adverse effects*

Objective : To investigate the expression of alpha-actinin-4 (ACTN4) and the effect on cell proliferation in esophageal squamous cell carcinoma (ESCC) ． Methods : The expression of ACTN4 in ESCC tissues and paired normal tissues was detected by immunohistochemistry，and the correlation between ACTN4 and the clinicopathologi- cal features was analyzed statistically．The ACTN 4 shRNA lentiviral plasmids were constructed ，and the stable ECA109 strain with ACTN4 shRNA knockdown was established using lentivirus packaging technology．The knock- down efficiency on protein level was checked by Western blot，and cell proliferation was detected by colony forma- tion assays．The downstream target proteins were validated in ESCC cell line ECA109 based on the previous pro- teomics analyses in melanoma cell line A375 with or without ACTN4 shRNA knockdown. Results : The expression of ACTN4 in ESCC tissues was significantly higher than that of normal tissues．ACTN4 shRNA stable knockdown ECA109 cell strains were successfully constructed． The results of colony formation assays showed that ACTN4 knockdown inhibited the cell proliferation and down-regulated NADH ∶ Ubiquinone oxidoreductase core subunit V1 ( NDUFV1) protein expression in ECA109 cells． Conclusion Upregulation of ACTN4 in ESCC cells promotes the cell proliferation and enhances the protein expression of NDUFV1 .

Objective:To observe the expression of microRNA (miRNA, miR) -7850 in renal cancer tissues, and to explore the effect of miR-7850 on the proliferation and migration of renal cancer cells and on the regulation of serine proteinase inhibitor B3 (SERPINB3) gene expression.Methods:Real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-7850 in renal cancer tissues and renal cancer cell lines. The renal cell carcinoma cell line with the lowest expression of miR-7850 was selected, and the negative control sequence (miR-NC) and miR-7850 mimics were transfected into renal cell carcinoma cells by Lipofectamine 2000 transfection reagent, respectively, which were defined as miR-NC group and miR-7850 group. qRT-PCR was used to detect the expression of miR-7850 in transfected renal cancer cells. The cell proliferation and migration ability after transfection were detected by cell counting kit-8 (CCK-8) method and transwell experiment. Bioinformatics prediction and dual luciferase reporter gene experiments were used to verify the target gene of miR-7850. qRT-PCR and Western blot were used to detect the expression of target genes in renal cancer cells after transfection.Results:Compared with adjacent tissues (5.95±0.44), the expression of miR-7850 in kidney cancer tissues (1.19±0.33) was lower ( P<0.01). Compared with immortalized proximal renal tubular epithelial cells (1.01±0.07), the expression of miR-7850 was lower in renal cancer cell lines ( P<0.05), and the lowest in A498 cells (0.13±0.01) ( P<0.01). The expression of miR-7850 in the miR-7850 group (7.46±0.93) was significantly higher than that in the miR-NC group (1.01±0.08) ( P<0.01), indicating successful transfection. Compared with the miR-NC group, the cell proliferation ability of the miR-7850 group was significantly reduced ( P<0.05). The number of migrating cells in miR-NC group and miR-7850 group were (139.50±12.31) and (75.09±16.05) cells, respectively, and the cell migration ability in miR-7850 group decreased significantly ( P<0.01). Bioinformatics technology shows that the target gene of miR-7850 was SERPINB3. The dual luciferase reporter gene experiment confirmed that miR-7850 can target the SERPINB3 gene ( P<0.05). Compared with the miR-NC group, the expression of SERPINB3 in cells of miR-7850 group was significantly reduced ( P<0.05), as well as the CDK4, CyclinD, Snail and Vimentin. Conclusions:miR-7850 is lowly expressed in renal cancer tissues and cell lines. miR-7850 can inhibit the proliferation and migration of renal cancer A498 cells, which may be related to its inhibition of SERPINB3 gene expression.

Objective:To explore the expression of long non-coding RNA LINC00630 in bladder cancer cell lines, and to explore the effect of interference with its expression in vitro on the proliferation and migration of bladder cancer cells.Methods:Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of LINC00630 in bladder cancer cell lines 5637, BIU-87, T24, J82 and normal bladder epithelial cell line SV-HUC-1. The bladder cancer cell line with the highest LINC00630 expression was selected for follow-up experiments, then the cell line infected with the control lentivirus was used as the control group, and the cell line infected with the lentivirus that could interfere with the expression of LINC00630 was used as the experimental group. qRT-PCR was used to detect the expression of LINC00630 in the two groups of cells. MTS method and cell scratch test were used to detect the proliferation and migration abilities of cells in the two groups. qRT-PCR was used to detect the expression of neuregulin 1 (NRG1) mRNA in the two groups of cells, and Western blot was used to detect the expressions of NRG1 protein, cell proliferation-related proteins (cyclin D3 and CDK2) and cell migration-related proteins (Vimentin and N-cadherin) in the two groups of cells.Results:Compared with SV-HUC-1 cells (1.05±0.17), the expression of LINC00630 was significantly increased in all bladder cancer cell lines (all P < 0.01), and the expression was highest in J82 cells (relative expression 5.83±0.42). Compared with J82 cells of the control group, the expression of LINC00630 in J82 cells of the experimental group decreased (0.18±0.02 vs. 1.00±0.05, t=14.36, P < 0.01); from day 2 of transfection, the cell proliferation activity of the experimental group was lower than that of the control group (all P < 0.05). The cell scratch closure rate of the experimental group was lower than that of the control group [(27.4±7.1)% vs. (66.0±5.4)%, t = 4.31, P < 0.01]. Therelative expression of NRG1 mRNA in the experimental group was lower than that in the control group (0.34±0.03 vs. 1.07±0.24, t = 2.99, P < 0.05). Compared with the control group, the expressions of NRG1 protein, cell proliferation-related proteins and cell migration-related proteins in the experimental group were reduced. Conclusions:LINC00630 is up-regulated in bladder cancer cell lines, and interference with LINC00630 may inhibit the proliferation and migration of J82 cells by down-regulating the expression of NRG1 gene. LINC00630 may be a new molecular target for the treatment of bladder cancer.

Objective:To explore the molecular mechanism of microRNA (miRNA, miR)-1914-3p regulating the expression of ARL4C and affecting the invasion and proliferation of renal cancer cells.Methods:Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of miR-1914-3p in tumor tissues and adjacent tissues of 53 renal cancer patients, 4 types of renal cancer cell lines (ACHN, OS-RC-2, 786-O, A498) and normal proximal renal tubular epithelial cell line (HK-2). The nonsense sequence (NC) and miR-1914-3p mimic were transiently transfected into renal cancer cells with the lowest miR-1914-3p expression by liposome method, namely the NC group and miR-1914-3p group. qRT-PCR was used to detect the expression level of miR-1914-3p in transfected cells. Transwell invasion test and cell counting kit-8 (CCK-8) were used to detect the invasion and proliferation ability of each group of cells. Bioinformatics software and dual luciferase gene report experiment were used to predict and test the targeted regulation mechanism of miR-1914-3p on target genes. qRT-PCR and Western blot was conducted to analyze the target gene expression level in cells of each group.Results:The expression level of miR-1914-3p in renal cancer tissue was significantly lower than that in adjacent tissues ( P<0.01). The expression level of miR-1914-3p in renal cancer cell lines was significantly lower than that in HK-2 cell lines ( P<0.01), and the expression of miR-1914-3p in OS-RC-2 cells was the lowest ( P<0.01). The expression of miR-1914-3p in the NC group and the miR-1914-3p group were (1.04±0.17) and (11.40±0.91), respectively. The expression level of miR-1914-3p in the miR-1914-3p group was significantly increased ( P<0.01), indicating that the transfection was successful. Overexpression of miR-1914-3p can significantly inhibit the invasion ( P<0.01) and proliferation ( P<0.05) of renal cancer OS-RC-2 cells. Dual luciferase gene report experiment indicated that the target gene of miR-1914-3p may be ADP-ribosylation factor-like 4C (ARL4C); miR-1914-3p can significantly inhibit the luciferase activity of wild-type ARL4C-3′UTR ( P<0.01). Overexpression of miR-1914-3p decreased the expression of ARL4C mRNA and protein in OS-RC-2 cells ( P<0.01), and decreased the expression of cell invasion phenotype proteins (Snail, Slug) and cell proliferation phenotype proteins (Mcm2, Mcm7) ( P<0.01). Conclusions:miR-1914-3p is low-expressed in renal cell carcinoma. It inhibits the invasion and proliferation of renal cell carcinoma OS-RC-2 cells through targeted interference with the expression of the oncogene ARL4C, and participates in the occurrence and development of renal cell carcinoma.