Objective:To investigate the effects and related mechanisms of long non-coding RNA (lncRNA) AC092295.2 expression on the proliferation and invasion abilities of endometrial cancer cells.Methods:The correlations between AC092295.2 expression level and overall survival (OS) and disease-free survival (DFS) of endometrial cancer patients (180 cases) were analyzed by cBioPortal database (updated in 2022). The miRNA with complementary nucleotide sequences to AC092295.2 was predicted by DIANA Tools sequencing tool. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression of AC092295.2 in human immortalised endometrial epithelial cell line hEEC and human endometrial cancer cell lines (KLE, AN3CA, Ishikawa, HEC-1A). Ishikawa cells with the lowest expression level of AC092295.2 were selected and divided into AC092295.2 overexpression group and control group, which were transfected with pGEX-AC092295.2 plasmid and pGEX-NC plasmid, respectively. qRT-PCR was used to detect the relative expression levels of AC092295.2 and miRNA-200c-3p (miR-200c-3p) in the two groups of cells. Methyl thiazol tetrazolium (MTT) method was used to detect cell viability. Transwell assay was used to detect cell invasion ability. Western blotting was used to detect the expression of proteins related to PTEN-AKT pathway. The dual luciferase reporter gene assay was used to verify the targeting relationship between AC092295.2 and miR-200c-3p.Results:The analysis results of cBioPortal database showed that the OS and DFS of endometrial cancer patients with high expression of AC092295.2 were better than those of patients with low expression (both P < 0.001); the expression levels of AC092295.2 and miR-200c-3p in endometrial cancer tissues were negatively correlated ( r = -0.846, P < 0.001). The results of qRT-PCR detection showed that the relative expression levels of AC092295.2 in endometrial cancer cell lines KLE, AN3CA, Ishikawa, HEC-1A and immortalized endometrial epithelial cell line hEEC were 0.56±0.09, 0.68±0.06, 0.17±0.07, 0.49±0.12 and 0.99±0.11, respectively, and the difference was statistically significant ( F = 35.10, P < 0.001); the relative expression levels of AC092295.2 in Ishikawa cells in the AC092295.2 overexpression group and the control group were 8.92±1.78 and 1.06±0.39, respectively, and the difference was statistically significant ( t = 4.31, P = 0.005). MTT assay results showed that the cell viability of Ishikawa cells in the AC092295.2 overexpression group was lower than that in the control group on days 2, 3, 4, and 5 (all P < 0.05). Transwell assay results showed that the number of invasive Ishikawa cells in the AC092295.2 overexpression group and the control group were 73±4 and 135±14, respectively, and the difference was statistically significant ( t = 4.25, P = 0.005). Western blotting results showed that the relative expression level of phosphatase and tensin homolog (PTEN) protein in Ishikawa cells in the AC092295.2 overexpression group was higher than that in the control group, while the relative expression levels of phosphorylated protein kinase B (p-AKT), Yes associated protein (YAP), murine double mimute 2 (MDM2), and bcl-2-associated death-promoting factor (BAD) proteins were lower than those in the control group. Dual luciferase reporter gene assay and qRT-PCR verified that AC092295.2 targeted negative regulation of miR-200c-3p expression. Conclusions:AC092295.2 is lowly expressed in endometrial cancer cells. Overexpression of AC092295.2 can inhibit the proliferation and invasion abilities of endometrial cancer cells, and its mechanism may be related to the expression of miR-200c-3p-PTEN-AKT signaling pathway.

Objective:To investigate the effects and related mechanisms of long non-coding RNA (lncRNA) AC092295.2 expression on the proliferation and invasion abilities of endometrial cancer cells.Methods:The correlations between AC092295.2 expression level and overall survival (OS) and disease-free survival (DFS) of endometrial cancer patients (180 cases) were analyzed by cBioPortal database (updated in 2022). The miRNA with complementary nucleotide sequences to AC092295.2 was predicted by DIANA Tools sequencing tool. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression of AC092295.2 in human immortalised endometrial epithelial cell line hEEC and human endometrial cancer cell lines (KLE, AN3CA, Ishikawa, HEC-1A). Ishikawa cells with the lowest expression level of AC092295.2 were selected and divided into AC092295.2 overexpression group and control group, which were transfected with pGEX-AC092295.2 plasmid and pGEX-NC plasmid, respectively. qRT-PCR was used to detect the relative expression levels of AC092295.2 and miRNA-200c-3p (miR-200c-3p) in the two groups of cells. Methyl thiazol tetrazolium (MTT) method was used to detect cell viability. Transwell assay was used to detect cell invasion ability. Western blotting was used to detect the expression of proteins related to PTEN-AKT pathway. The dual luciferase reporter gene assay was used to verify the targeting relationship between AC092295.2 and miR-200c-3p.Results:The analysis results of cBioPortal database showed that the OS and DFS of endometrial cancer patients with high expression of AC092295.2 were better than those of patients with low expression (both P < 0.001); the expression levels of AC092295.2 and miR-200c-3p in endometrial cancer tissues were negatively correlated ( r = -0.846, P < 0.001). The results of qRT-PCR detection showed that the relative expression levels of AC092295.2 in endometrial cancer cell lines KLE, AN3CA, Ishikawa, HEC-1A and immortalized endometrial epithelial cell line hEEC were 0.56±0.09, 0.68±0.06, 0.17±0.07, 0.49±0.12 and 0.99±0.11, respectively, and the difference was statistically significant ( F = 35.10, P < 0.001); the relative expression levels of AC092295.2 in Ishikawa cells in the AC092295.2 overexpression group and the control group were 8.92±1.78 and 1.06±0.39, respectively, and the difference was statistically significant ( t = 4.31, P = 0.005). MTT assay results showed that the cell viability of Ishikawa cells in the AC092295.2 overexpression group was lower than that in the control group on days 2, 3, 4, and 5 (all P < 0.05). Transwell assay results showed that the number of invasive Ishikawa cells in the AC092295.2 overexpression group and the control group were 73±4 and 135±14, respectively, and the difference was statistically significant ( t = 4.25, P = 0.005). Western blotting results showed that the relative expression level of phosphatase and tensin homolog (PTEN) protein in Ishikawa cells in the AC092295.2 overexpression group was higher than that in the control group, while the relative expression levels of phosphorylated protein kinase B (p-AKT), Yes associated protein (YAP), murine double mimute 2 (MDM2), and bcl-2-associated death-promoting factor (BAD) proteins were lower than those in the control group. Dual luciferase reporter gene assay and qRT-PCR verified that AC092295.2 targeted negative regulation of miR-200c-3p expression. Conclusions:AC092295.2 is lowly expressed in endometrial cancer cells. Overexpression of AC092295.2 can inhibit the proliferation and invasion abilities of endometrial cancer cells, and its mechanism may be related to the expression of miR-200c-3p-PTEN-AKT signaling pathway.

Objective:To investigate the effects of long non-coding RNA (lncRNA) RP11-1212A22.4 on the cell viability and invasive ability of esophageal cancer cell lines by targeting miRNA-483-5p (miR-483-5p).Methods:The expression of RP11-1212A22.4 in esophageal cancer tissues was analyzed by using GEPIA online database. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of RP11-1212A22.4 in human esophageal cancer cell lines EC9706, KYSE30, TE-13, Eca109 and normal esophageal epithelial cell line HET-1A. The lowest expression level of EC9706 cell line in RP11-1212A22.4 was divided into RP11-1212A22.4 group (transfected with pcDNA-RP11-1212A22.4 plasmid) and the control group (transfected with pcDNA-NC plasmid). The cell viability of EC9706 cell was analyzed by using methyl thiazolyl tetrazolium (MTT) method, and the invasion ability of EC9706 cell was detected by using Transwell assay. The targeting relationship between RP11-1212A22.4 and miR-483-5p was verified by using StarBase database prediction and dual luciferase reporter assay. The relative expression level of miR-483-5p of EC9706 cell in two groups was detected by using qRT-PCR. Western blot was used to detect the expressions of cyclin-dependent kinase 6 (CDK6), matrix metalloproteinase 2 (MMP-2), cyclin-dependent kinase 4 (CDK4), and matrix metalloproteinase 9 (MMP-9) proteins in two groups.Results:In GEPIA online database, compared with adjacent tissues, the relative expression level of RP11-1212A22.4 in esophageal cancer tissues was decreased, and the difference was statistically significant ( P < 0.001). The relative expression levels of RP11-1212A22.4 in esophageal cancer cell lines EC9706, KYSE30, TE-13, Eca109 and normal esophageal mucosal epithelial cell line HET-1A were 0.11±0.08, 0.32±0.09, 0.72±0.09, 0.59±0.13 and 0.97±0.12, and the difference was statistically significant ( F = 40.42, P < 0.001). The relative expression levels of RP11-1212A22.4 in EC9706 cells of RP11-1212A22.4 group and the control group were 11.9±2.4 and 1.0±0.3, respectively, and the difference was statistically significant ( t = 8.89, P < 0.001). Compared with the control group, the cell viability of EC9706 cell in RP11-1212A22.4 group was decreased (all P < 0.05). The number of invasive cells in RP11-1212A22.4 group was lower than that in the control group (48±12 vs. 106±22, t = 4.63, P < 0.001). StarBase database prediction and dual luciferase reporter assay both showed that RP11-1212A22.4 targeted miR-483-5p. The relative expression level of miR-483-5p in RP11-1212A22.4 group was lower than that in the control group (0.24±0.11 vs. 1.02±0.23, t = 5.98, P = 0.001). Compared with the control group, the expressions of CDK6, MMP-2, CDK4 and MMP-9 proteins in the RP11-1212A22.4 group were decreased. Conclusions:RP11-1212A22.4 is lowly expressed in esophageal cancer tissues and cell lines, and it inhibits the cell viability and invasive ability of esophageal cancer cells by targeting miR-483-5p.

Objective To evaluate the effect of iodine contrast agent on the biological responses of CT examination. Methods A total of sixty patients with suspected urinary tract disease who underwent computed tomography urography ( CTU ) examination were randomly divided into control group and experimental group. The control group was treated with routine CTU, where only CT scan was performed on the first day. CTU was added after 3 days. The test group was treated with fractional injection CTU and injected with enhanced scanning agent on the first day. Before and after CT examination, the patients′peripheral blood was collected and the number of γ-H2AX foci in lymphocytes ( mononuclear cells) was measured by immunofluorescence, and the differences of DNA damage in these two groups were observed. Results Before and after CT examination, the number ofγ-H2AX foci was 0. 06 ± 0. 02 and 1. 06 ± 0. 27 in the lymphocytes of control group,0. 06 ± 0. 03 and 1. 42 ± 0. 50 in the test group, respectively. Hence, the number ofγ-H2AX foci in the test group was increased by 38. 14%. Moreover, the change ofγ-H2AX foci in these two groups was not influenced by gender, but correlated with ages( between≤50 years old and>50 years old) in control group (t= -4. 76, P<0. 05) and in test group(t= -8. 16, P <0. 05). Conclusions The iodine contrast agent can increase DNA damage of CT examination, and therefore the use of iodine contrast agent in CT should be reduced as much as possible in clinical work.

Objective To observe the effects of eluting stents coated with arsenic trioxide(As2O3)and suspended in poly-L-lactic acid(PLLA)on expression of monocyte chemoattractant protein-1 (MCP-1)and interleukin-6(IL-6)and to assess the effects of As2O3 eluting stents on local inflammatory reaction in injured coronary arteries in pigs. Methods Bare metal stents,rapamycin eluting stents and As2O3-eluting stents were randomly and double-blindly implanted into the anterior descending branches,circumflex branches and right coronary arteries in eight pigs.Animals were sacrificed and coronary arteries were isolated 7 days after stents implantation.The expression levels of protein and mRNA of MCP-1 and IL-6 were determined by Western blot analysis and reverse transcription polymerase chain reaction(RT-PCR),and the inflammatory cell infiltration was observed by HE staining and immunohistochemistry. Results Compared to bare metal stents,As2O3-eluting stents and rapamycin-eluting stents identically and markedly inhibited the protein expression level of MCP-1(0.421±0.055 and 0.406±0.042 vs.0.857±0.053,P＜0.01)and IL-6(0.151±0.032 and 0.146±0.051 vs.0.551±0.032,P＜0.01)and correspondingly lowered the mRNA expression level of MCP-1(0.338±0.047 and 0.327±0.051 vs.0.724±0.027,P＜0.01)and IL-6(0.531±0.052 and 0.523±0.061 vs.1.015±0.041,P＜0.01),and significantly reduced the inflammatory cell infiltration of injured coronary arteries in pigs. Conclusions As2O3-eluting stents can effectively inhibit the expressions of MCp-1 and IL-6 and reduce the inflammatory cell infiltration of injured coronary arteries in pigs.