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Moreover, the expression of MET was high and significantly correlated with the low expression of miR-802 in OSCC tissues. Overexpression of MET in Tca8113 and SCC9 cells reduced the tumor-suppressive effects, which was induced by miR-802 overexpression. CONCLUSIONS MiR-802 suppresses the malignant biological behavior of OSCC by targeting proto-oncogene MET. This work provides a new potential molecular target for treating OSCC.OBJECTIVE Previous studies have found that IPO5 is a cancer-promoting gene. However, the role of IPO5 in esophageal cancer has not been reported. This study aims to investigate the expression characteristics of IPO5 in esophageal cancer, and to further analyze its relationship with clinical parameters and prognosis of esophageal cancer. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression of matrix metalloproteinase 7 (MMP7) in 45 pairs of tumor tissue specimens and adjacent normal ones collected from esophageal cancer patients. The correlation between IPO5 expression and clinical indicators and prognosis of esophageal cancer patients was analyzed. Meanwhile, IPO5 expression in esophageal cancer cell lines was also detected using qRT-PCR. In addition, the influence of IPO5 on esophageal cancer cell functions was analyzed using cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assays. Finally, Dual-Luciferase reporter assay and ceon significantly increased in esophageal cancer tissues, which was associated with pathological staging and poor prognosis of esophageal cancer patients. IPO5 may promote malignant progression of esophageal cancer through the regulation of MMP7.OBJECTIVE Growing evidence has shown that long non-coding RNAs (lncRNAs) can serve as prospective markers for survival in patients with gastric cancer (GC). In this study, we mainly focused on the potential roles of LINC00511 in the development process of GC. PATIENTS AND METHODS RT-PCR was used to detect the expressions of LINC00511 and miR-124-3p in GC tumor tissues, adjacent tissues and GC cell lines. Furthermore, correlations between LINC00511 with miR-124-3p, and miR-124-3p with EZH2, were analyzed by Correlation analysis. Moreover, the overall survival (OS) of patients was analyzed using Kaplan-Meier method. Additionally, proliferation ability was measured by CCK-8 assay and invasion ability of GC cell line was detected by transwell assay. Besides, Western blot was performed to measure protein levels of GC tissues and GC cell lines. Finally, Dual-Luciferase reporter assay was performed to prove the potential binding sites between LINC00511 and miR-124-3p, miR-124-3p and EZH2. RESULTS We found that LINC0sults, we found that LINC00511 was increased in GC tissues, which was associated with the poor OS in patients with GC. We uncovered a previously unappreciated LINC00511/miR-124-3p/EZH2 signaling axis in promoting cell proliferation and invasion in GC patients and GC cell lines, which suggested that it might be a potential target for treating human GC.OBJECTIVE This study aims to investigate the expression characteristics of Krüppel-like factor 5 (KLF5) in gastric cancer (GC) and its potential correlation to pathological indexes in GC patients. Molecular mechanisms underlying the regulatory effect of KLF5 on GC progression are explored. PATIENTS AND METHODS KLF5 expressions in GC tissues were analyzed through GEPIA dataset and those collected in our hospital. By analyzing the clinical data of GC patients, the correlation between KLF5 level and pathological characteristics of GC was determined. The regulatory effects of KLF5 on proliferative ability and cell cycle progression of SGC7901 and MGC803 cells were assessed by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) assay, and flow cytometry. Zasocitinib cost The regulation of KLF5 on expression levels of p21 and CDK4 in GC cells was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. RESULTS KLF5 was markedly upregulated in GC tissues. KLF5 level was positively correlated to TNM staging, tumor size, and metastasis of GC. Meanwhile, high level of KLF5 predicted poor prognosis in GC patients. The knockdown of KLF5 in SGC7901 and MGC803 cells attenuated proliferative ability and arrested cell cycle in G0/G1 phase. Both mRNA and the protein levels of p21 were upregulated, and CDK4 levels were downregulated in SGC7901 and MGC803 cells transfected with si-KLF5. CONCLUSIONS KLF5 is upregulated in GC and closely linked to pathological characteristics of GC patients. High level of KLF5 indicates poor prognosis of GC. It is believed that KLF5 may be a potential therapeutic target for GC.OBJECTIVE MicroRNA493-5p (miR-493-5p) appears to have an essential role in the abnormal cell proliferation and migration observed in the development and progression of various cancers. However, the function and mechanism of action of miR-493-5p in colorectal cancer (CRC) is unclear. PATIENTS AND METHODS MiR-493-5p expression was analyzed in CRC patient tissue samples and cell lines by fluorescence quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). SW480 and Caco-2 cells were transfected with miR-493-5p mimics or treated with the phosphoinositide 3-kinase (PI3K) agonist 740Y-P. Cell proliferation was determined by colony formation and cell proliferation assays and cell migration and invasion by transwell migration and wound-healing assays. The Luciferase reporter assay was used to verify the association between the expression of miR-493-5p and PI3K activity. Expression levels of PI3K, protein kinase B(Akt), and forkhead box O 3a (FoxO3a) proteins were measured by Western blot analysis and immunofluorescence assay. RESULTS MiR-493-5p expression was significantly downregulated in CRC tissue samples and cell lines which was associated with progression of CRC. The proliferation, migration, and invasion of CRC cells were inhibited by miR-493-5p overexpression. The finding that miR-493-5p upregulation decreased PI3K, Akt, and FoxO3a protein expression revealed that it directly targets PI3K. Additionally, the miR-493-5p-mediated suppression of CRC cell proliferation, migration and invasion was counteracted by the PI3K agonist, indicating that miR-493-5p suppresses CRC progression by inhibiting the PI3K-Akt-FoxO3a signaling pathway. CONCLUSIONS MiR-493-5p suppresses the proliferation, migration, invasion, and progression of CRC via the PI3K-Akt-FoxO3a signaling pathway.
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