miR-143-3p inhibits proliferation and invasion of hepatocellular carcinoma cells by regulating its target gene FGF1

Purpose To explore FGF1 and miR-143-3p expression in hepatocellular carcinoma (HCC) cells and its related mechanisms. Methods Eighty-two HCC patients treated at our hospital from January 2018 to January 2019 were enrolled as Group A, while further 80 healthy people undergoing physical examinations during the same time period were enrolled as Group B. HCC cells and normal human liver cells were purchased, with HepG2 and SMMC-7721 cells transfected with pcDNA3.1-FGF1, si-FGF1, NC, miR-143-3p-inhibitor and miR-143-3p-mimics. FGF1 and miR-143-3p expression was detected by qRT-PCR. The expression of N-cadherin, vimentin, Snail, Slug, E-cadherin and γ-catenin was detected by Western Blotting (WB). Cell proliferation was detected by MTT assay. Cell invasion was detected by Transwell. Cell apoptosis was detected by flow cytometry (FCM). Results FGF1 was highly expressed but miR-143-3p was poorly expressed in HCC cells. Areas under the curves (AUCs) of the two indicators were > 0.8. The indicators were correlated with the age, gender, tumor invasion, degree of differentiation, tumor location and TNM staging of the patients. Silencing FGF1 and overexpressing miR-143-3p could promote cell apoptosis, inhibit cell growth, cell epithelial-mesenchymal transition (EMT) and the expression of N-cadherin, vimentin, Snail and Slug, and increase the expression of E-cadherin and γ-catenin. Dual luciferase reporter gene assay (DLRGA) confirmed that FGF1 and miR-143-3p had a targeted relationship. The rescue experiment showed that the proliferation, invasion and apoptosis of HepG2 and SMMC-7721 cells in the miR-143-3p-mimics+pcDNA3.1-FGF1 and miR-143-3p-inhibitor+Si-FGF1 groups were not different from those in the miR-NC group. Conclusion Inhibiting FGF1 can upregulate miR-143-3p-mediated Hedgehog signaling pathway, and affect cells’ EMT, proliferation and invasion, so FGF1 is expected to become a potential therapeutic target for HCC (AU)

miR-143-3p inhibits proliferation and invasion of hepatocellular carcinoma cells by regulating its target gene FGF1.

PURPOSE: To explore FGF1 and miR-143-3p expression in hepatocellular carcinoma (HCC) cells and its related mechanisms. METHODS: Eighty-two HCC patients treated at our hospital from January 2018 to January 2019 were enrolled as Group A, while further 80 healthy people undergoing physical examinations during the same time period were enrolled as Group B. HCC cells and normal human liver cells were purchased, with HepG2 and SMMC-7721 cells transfected with pcDNA3.1-FGF1, si-FGF1, NC, miR-143-3p-inhibitor and miR-143-3p-mimics. FGF1 and miR-143-3p expression was detected by qRT-PCR. The expression of N-cadherin, vimentin, Snail, Slug, E-cadherin and γ-catenin was detected by Western Blotting (WB). Cell proliferation was detected by MTT assay. Cell invasion was detected by Transwell. Cell apoptosis was detected by flow cytometry (FCM). RESULTS: FGF1 was highly expressed but miR-143-3p was poorly expressed in HCC cells. Areas under the curves (AUCs) of the two indicators were > 0.8. The indicators were correlated with the age, gender, tumor invasion, degree of differentiation, tumor location and TNM staging of the patients. Silencing FGF1 and overexpressing miR-143-3p could promote cell apoptosis, inhibit cell growth, cell epithelial-mesenchymal transition (EMT) and the expression of N-cadherin, vimentin, Snail and Slug, and increase the expression of E-cadherin and γ-catenin. Dual luciferase reporter gene assay (DLRGA) confirmed that FGF1 and miR-143-3p had a targeted relationship. The rescue experiment showed that the proliferation, invasion and apoptosis of HepG2 and SMMC-7721 cells in the miR-143-3p-mimics+pcDNA3.1-FGF1 and miR-143-3p-inhibitor+Si-FGF1 groups were not different from those in the miR-NC group. CONCLUSION: Inhibiting FGF1 can upregulate miR-143-3p-mediated Hedgehog signaling pathway, and affect cells' EMT, proliferation and invasion, so FGF1 is expected to become a potential therapeutic target for HCC.

MiR-650 inhibits the progression of glioma by targeting FAM83F.

OBJECTIVE: The aim of this study was to explore whether miR-650 could inhibit the proliferation of glioma by regulating FAM83F and to investigate the specific role of miR-650 in glioma occurrence. PATIENTS AND METHODS: The expression of FAM83F in tumor or para-cancerous tissues of 24 glioma patients was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Meanwhile, FAM83F expression in 6 glioma cell lines (LN229, U87, U251, LN308, SNB19 and H4) was also detected. Subsequently, the proliferation of glioma cells transfected with miR-650 mimics was evaluated by cell counting kit-8 (CCK-8) and EDU (5-ethynyl-2'-deoxyuridine) assay, respectively. In addition, Luciferase reporter gene assay and rescue experiment were applied to verify the relationship between miR-650 and FAM83F. RESULTS: MiR-650 expression in glioma tissues was significantly decreased, while the expression of FAM83F was remarkably upregulated. This indicated that the level of miR-650 was negatively correlated with that of FAM83F. Similar results were obtained in glioma cells. We then transfected miR-650 mimics into LN229 and U251 cells, and found that the expression of miR-650 was significantly upregulated. Meanwhile, the viability of cells significantly decreased. In addition, the interaction between miR-650 and FAM83F was verified by Luciferase reporter gene assay. Rescue experiments showed that miR-650 could inhibit cell proliferation by targeting FAM83F. CONCLUSIONS: MiR-650 was lowly expressed in glioma tissues, which could promote cell proliferation through up-regulating the expression of FAM83F.

Overexpression of ezrin and galectin-3 as predictors of poor prognosis of cervical cancer.

The aim of this study was to explore the correlation of ezrin and galectin-3 expressions with prognosis in cervical cancer. The immunohistochemical method was applied to detect ezrin and galectin-3 expressions in normal cervix tissues (n=30), cervicitis tissues (n=28), cervical intraepithelial neoplasia (CIN) tissues (classified as I-III, n=89), and cervical carcinoma tissues (n=84). Follow-up was conducted for 5 to 78 months to analyze the correlation of protein expressions with prognosis. Ezrin and galectin-3 expressions in cervical cancer were significantly higher than in normal cervix, cervicitis and CIN (all P<0.05), and expressions in CIN were significantly higher than in normal cervix and cervicitis (both P<0.05). The expressions of ezrin and galectin-3 were both related with histological grade, deep myometrial invasion and lymph node metastasis (all P<0.05). Spearman analysis showed that ezrin expression was positively correlated with galectin-3 expression in cervical cancer (r=0.355, P<0.05). The survival rate of patients with high expressions of ezrin and galectin-3 was significantly lower than those with low expressions of proteins (both P<0.05). The expressions of ezrin and galectin-3, histological grade, depth of stromal invasion, and lymph node metastasis are risk factors affecting the survival rate of patients with cervical cancer. The expressions of ezrin and galectin-3 were correlated with the development of cervical cancer, and overexpressions of those proteins were indicative of poor prognosis in patients with cervical cancer.

[Clinical and experimental studies of zhenkeling oral liquor on treatment infantile cough].

One hundred and seventy children with cough were divied into two groups at random. 120 patient were treated with Zhenkeling oral liquor (ZKL group). The other 50 children were given pectoral syrup (control group). The results showed that the total effective rates of ZKL group and control group were 96.7% and 56.0% respectively, and the markedly effective rates were 80.8%, 18.0% respectively (P < 0.001). Animal experiments indicated Zhenkeling has the effect of relieving cough, reducing sputum and ameliorating asthma; their antibiotic and anti-inflammatory effects were discovered too. The dosage of Zhenkeling was 100 times as clinical dose in acute toxicity test and the dosage was 32, 16, 8 times as clinical dose in long term toxicity test respectively. No adverse action was found in these experiments.

[Clinical study on fungus lipid-reducing capsule in regulating lipometabolic disorder].

The patients with lipometabolic disorder were randomly divided into control group (70 cases), Fungus Lipid-reducing Capsule (FLC) treated group (70 cases), augmented treated group (90 cases). The results shown that: (1) TC and TG were reduced markedly in all three groups. The reducing extent in the treated group was greater than that in the control group (P < 0.01). HDL-C was increased markedly in all three group. The increasing extent in the treated group was greater than that in the control group (P < 0.05). These results indicated that the effectiveness of FLC was higher than that of control drug in the treatment of hyperlipidemia. (2) FLC had obvious effect in improving hemorheology indexes. (3) The therapeutic effect of TCM Syndrome-type indicated that FLC could activate the Spleen, remove Dampness and nourish the Liver and Kidney.