ABSTRACT
Transcription factor forkhead box Q1 (FOXQ1) is a member of forkhead box (FOX) superfamily, which exists widely in a variety of tissues and organs of human body. FOXQ1 protein affects the genesis, progression, invasion and metastasis of tumor by promoting epithelial-mesenchymal transition (EMT) and activating multiple cell signal transduction pathways. In recent years, studies have found that FOXQ1 is abnormally expressed in a variety of digestive tract tumors. In-depth study on the expression and mechanism of FOXQ1 in digestive tract tumor is of great significance for early diagnosis and specific molecular therapy of digestive tract tumors. This article reviewed the latest literatures related to FOXQ1 and digestive tract tumors, and expounding its mechanism in the progression of different digestive tract tumors, in order to provide theoretical basis and reference for the research and development of new chemotherapy drugs.
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Objective:To observe the effect of polyphyllin Ⅰ on the expressions of forkhead box Q1（FOXQ1）and epithelial-mesenchymal transition (EMT)-related factors, in order to explore the possible mechanism of polyphyllin Ⅰ in inhibiting the metastasis of colon cancer. Method:After the treatment with 1.25，2.50 μmol·L-1 polyphyllin Ⅰ on HCT116 cells, Western blot and Real-time PCR were used to detect the expressions of FOXQ1，E-cadherin，Vimentin protein and mRNA. Result:Compared with the blank group, relative expressions of FOXQ1 protein and mRNA in low-concentration polyphyllin Ⅰ group were decreased, while relative expression of E-cadherin mRNA was increased, the differences were not statistically significant, and relative expressions of Vimentin protein and mRNA in low-concentration polyphyllin Ⅰ group were decreased (P<0.05)， and relative expression of E-cadherin protein in low-concentration polyphyllin Ⅰ group was increased (P<0.01). Compared with the blank group, relative expressions of FOXQ1, Vimentin protein and mRNA in high-concentration polyphyllin Ⅰ group were decreased，while relative expressions of E-cadherin protein and mRNA were increased (P<0.05, P<0.01). Compared with low-concentration polyphyllin Ⅰ group, relative expressions of Vimentin protein and mRNA in high-concentration polyphyllin Ⅰ group were decreased, but the difference was not statistically significant, relative expressions of E-cadherin protein and mRNA in high-concentration polyphyllin Ⅰ group were increased, whereas relative expressions of FOXQ1 protein and mRNA were decreased (P<0.05, P<0.01). Conclusion:Mechanism of polyphyllin Ⅰ inhibiting the metastasis of colon cancer may be related to the decrease of FOXQ1 and Vimentin expressions, and the up-regulation of E-cadherin.
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Objective@#To investigate the role of microRNA-96-5p in the proliferation and invasion of gastric cancer cells and its molecular mechanism.@*Methods@#From June 2015 to January 2017, 53 resected specimens were collected. The transcriptional levels of microRNA-96-5p and forkhead box Q1 (FoxQ1) in gastric cancer tissues and the matched para-cancerous tissues were quantified by quantitative real-time PCR (qRT-PCR). The expression of FoxQ1 protein was also detected by immunohistochemistry (IHC). The relationship between microRNA-96-5p expression and the clinicopathological features of gastric cancer and its correlation with FoxQ1 expression were analyzed. The expressions of miRNA-96-5p in gastric cancer tissue and adjacent normal tissue were detected by qRT-PCR. miRNA-96-5p mimics was transfected to BGC-823 gastric cancer cells. The effects of miRNA-96-5p on cell proliferation and invasion were detected by cell counting kit-8 (CCK-8) assay and Transwell assay, respectively. The protein expressions of FoxQ1, E-cadherin and vimentin were determined by western blot. The relationship between FoxQ1 and miRNA-96-5p expressed in BGC-823 cells was detected by dual-luciferase reporter assay.@*Results@#The median expression of miRNA-96-5p in gastric cancer tissue was 1.05, significantly lower than 3.23 of para-cancerous tissues (P<0.05). The positive rate of FoxQ1 expression in gastric cancer tissue was 71.7%, significantly higher than 28.3% of para-cancerous tissues (P<0.05). The expression of FoxQ1 was negatively corelated with the level of miRNA-96-5p (r=-0.613, P=0.006). The expression of miRNA-96-5p in gastric cancer cell BGC-823 was significantly decreased compared with normal gastric epithelial cell (0.96±0.08 vs 2.84±0.15, P<0.05). The results of CCK-8 assay and Transwell assay showed that overexpression of miRNA-96-5p significantly reduced the proliferation and invasion abilities of gastric cancer cells (P<0.05). Overexpression of miRNA-96-5p decreased the protein level of FoxQ1. Moreover, it upregulated the expression of E-cadherin and downregulated the expression of vimentin. The result of dual-luciferase-3′-UTR reporter assay confirmed that miRNA-96-5p binds to the 3′UTR of FoxQ1.@*Conclusion@#miRNA-96-5p may suppress the proliferation, migration and epithelial-mesenchymal transition (EMT) of gastric cancer cell by down-regulation of FoxQ1.
ABSTRACT
Forkhead box Q1 (FoxQ1) is a transcription factor protein with the function of cell differentiation regulation.Recently,increasing evidence has demonstrated that FoxQ1 is significantly associated with pathogenesis of digestive system tumors.This article systematically reviewed the expression and the role of FoxQ1 in the pathogenesis of digestive system tumors.Potential therapeutic target of FoxQ1 was discussed as well.
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Objective To investigate the expression levels and clinical significance of (forkhead box Q1) FOXQ1 and E-cadherin in esophageal squamous cell carcinoma (ESCC). Methods Expression levels of FOXQ1 and E-cadherin were in ESCC tissues (ESCC group, n=42) and adjacent normal esophageal tissues (control group, n=42) were detected using im?munohistochemistry. Correlations of FOXQ1 and E-cadherin expressions with clinical pathological parameters and progno?sis were analyzed between two groups. Results The expression level of FOXQ1 was significantly higher in ESCC group than that in control group(64.29% vs 28.57%,χ2=5.384,P<0.05). The expression level of E-cadherin was significantly lower in ESCC group than that incontrol group(52.38%vs 90.48%,χ2=7.691,P<0.05). There were significant differences in FOXQ1 expressions between different TNM stages and whether lymph node metastasis is involved within ESCC group. There were significant differences in expression of E-cadherin between different tumor differentiation, depth of invasion, TNM stage and whether lymph node metastasis is involved within ESCC group. The expression of FOXQ1 was negatively cor?related with E-cadherin in ESCC (r=-0.412, P<0.05). The 5-year survival rates were significantly lower with high expres?sion of FOXQ1 or with low expression of FOXQ1(18.52%vs 66.67%,χ2=9.737,P<0.05). The 5-year survival rates were significantly higher with high expression of E-cadherinor low expression of E-cadherin(59.09%vs 10.00%,χ2=10.996,P<0.05). A multivariate Cox's proportional hazard regression analysis indicated that high FOXQ1 expression, low E-cadherin expression and lymph node metastasis were independent prognostic factors for ESCC. Conclusion The expression of FOXQ1 and E-cadherin showed a good correlation with ESCC. And examining expressions of both FOXQ1 and E-cadherin in ESCC may have practical values in estimating the prognosis of ESCC and directing future treatment .