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Your search keyword '"Gao, Yongjian"' showing total 144 results
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144 results on '"Gao, Yongjian"'

23. sj-docx-1-npx-10.1177_1934578X221123698 - Supplemental material for Tanshinone IIA Inhibits Liver Fibrosis by Regulating COL1A1 Expression Through H19/let-7a in Mice

Author

Lin, Chao, Xing, Jianming, Jiang, Ziping, Sun, Liqun, Gao, Yongjian, Yang, Shuo, Wang, Dongxu, and Yin, Ning

Subjects
FOS: Clinical medicine, 111599 Pharmacology and Pharmaceutical Sciences not elsewhere classified
Abstract

Supplemental material, sj-docx-1-npx-10.1177_1934578X221123698 for Tanshinone IIA Inhibits Liver Fibrosis by Regulating COL1A1 Expression Through H19/let-7a in Mice by Chao Lin, Jianming Xing, Ziping Jiang, Liqun Sun, Yongjian Gao, Shuo Yang, Dongxu Wang and Ning Yin in Natural Product Communications

Published
2022
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27. Tanshinone IIA Inhibits Liver Fibrosis by Regulating COL1A1 Expression Through H19 / let-7a in Mice.

Author

Lin, Chao, Xing, Jianming, Jiang, Ziping, Sun, Liqun, Gao, Yongjian, Yang, Shuo, Wang, Dongxu, and Yin, Ning

Subjects
HEPATIC fibrosis, ASPARTATE aminotransferase, ENZYME-linked immunosorbent assay, POLYMERASE chain reaction, IMMUNOSTAINING, ALANINE aminotransferase
Abstract

Liver fibrosis is a serious health problem and may lead to advanced liver cirrhosis and hepatocellular carcinoma if left untreated. In this study, a mouse liver fibrosis model was established by the administration of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC), and tanshinone IIA. Salvia miltiorrhiza Bunge extract, shown to play a regulatory role in liver fibrosis, was administered to study its effect on the expression of COL1A1. Mice were divided into 3 groups, control (Con), model (DDC), and drug administration (DDC-Tan) groups, and were subjected to the respective treatment for 2 months. Following treatment, the degree of liver fibrosis in mice in each group was determined. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin, and albumin levels in mice were determined using enzyme-linked immunosorbent assay (ELISA). Mouse liver tissues were used for hematoxylin-eosin and immunohistochemical staining. ELISA results showed that treatment with tanshinone IIA inhibited the expression of ALT, AST, and bilirubin in the DDC-Tan group compared with the DDC group. Hematoxylin-eosin, Sirius red, and α-SMA staining showed that liver injury was delayed in the DDC-Tan group. Immunohistochemistry, quantitative polymerase chain reaction, and Western blot results showed that COL1A1 expression was reduced after tanshinone IIA treatment. Moreover, the bioinformatic analysis indicated that let-7a targets COL1A1, and H19 regulates let-7a expression. The quantitative polymerase chain reaction and Western blot results confirmed that the H19/let-7a axis regulates COL1A1 expression. Thus, tanshinone IIA inhibited liver fibrosis by regulating COL1A1 expression through the H19/let-7a axis in mice. [ABSTRACT FROM AUTHOR]

Published
2022
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38. miR-613 inhibits gastric cancer progression through repressing brain derived neurotrophic factor

Author

Ding, Dayong, Hou, Ruizhi, Gao, Yongjian, and Feng, Ye

Subjects
Articles
Abstract

MicroRNA (miR)-613 has been reported to function as a tumor suppressor in several types of cancer. However, the biological function and underlying mechanism in gastric cancer (GC) has remained elusive. Therefore, the aim of the present study was to assess the expression and biological role of miR-613 in GC tissues and cell lines. miR-613 expression was found to be downregulated in 38 GC tissue samples compared to that in their adjacent non-cancerous tissues, and low expression of miR-613 was associated with lymph node metastasis and advanced tumor-nodes-metastasis stage. A gain-of-function assay demonstrated that miR-613 overexpression reduced tumor cell proliferation, migration and invasion of SGC-7901 cells, as determined by MTT and Transwell assays. Furthermore, brain-derived neutrophic factor (BDNF) was identified as a direct target of miR-613 in GC cells by a luciferase reporter assay. BDNF expression was upregulated and inversely correlated with miR-613 levels in GC tissues. In addition, knockdown of BDNF expression mimicked the tumor suppressive effect of miR-613 in GC cells. In conclusion, these findings demonstrated that miR-613 functions as a tumor suppressor in GC by targeting BDNF. Thus, miR-613 is a potential therapeutic target for GC.

Published
2017

40. MicroRNA-370 inhibits the proliferation, invasion and EMT of gastric cancer cells by directly targeting PAQR4

Author

Feng, Ye, Sun, Tao, Yu, Yabo, Gao, Yongjian, Wang, Xuefeng, and Chen, Zhi

Abstract

It has been reported that PAQR4 (Progestin and AdipoQ Receptor 4) expression is closely associated with progression of many cancers and microRNA (miRNA) processing. However, the effects and its precise mechanisms of PAQR4 in gastric cancer (GC) have not been well clarified. Our study aimed to explore the interaction between PAQR4 and miR-370 in GC. In our study, we found that the miR-370 level was significantly down-regulated in GC tissues and cell lines, and the expression of PAQR4 was dramatically increased. Interestingly, the low miR-370 level was closely associated with up-regulated PAQR4 expression in GC tissues. Moreover, introduction of miR-370 dramatically suppressed proliferation, invasion and EMT of GC cells. Whereas, miR-370 knockdown increased the proliferation, invasion and EMT in GC cells. We demonstrated that miR-370 could directly target PAQR4 by using both bioinformatics analysis and luciferase reporter assay. In addition, PAQR4 silencing had the similar effects with miR-370 overexpression on GC cells. Overexpression of PAQR4 in GC cells partially reversed the inhibitory effects of miR-370 mimic. miR-370 inhibited cell proliferation, invasion and EMT of GC cells by directly down-regulating PAQR4 expression, and miR-370 targeting PAQR4 was responsible for inhibition of the proliferation, invasion and EMT of GC cells.

Published
2024
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41. MiR-135b-5p promotes viability, proliferation, migration and invasion of gastric cancer cells by targeting Krüppel-like factor 4 (KLF4).

Author

Zhi Chen, Yongjian Gao, Shuohui Gao, Defeng Song, Ye Feng, Chen, Zhi, Gao, Yongjian, Gao, Shuohui, Song, Defeng, and Feng, Ye

Subjects
STOMACH cancer, CANCER cells, CELL migration, EPITHELIAL cells, CELL survival
Abstract

Introduction: The expression of MiR-135b-5p was up-regulated while Krüppel-like factor 4 (KLF4) expression was extremely low in human gastric carcinoma (GC) tissues. This study aimed to explore the role of miR-135b-5p in GC cells and its influence on various cell capacity and viability by targeting KLF4.Material and Methods: The dual-luciferase reporter assay was first performed and the target relationship between miR-135b-5p and KLF4 was confirmed. Then three GC cell lines and the human normal gastric epithelial cell line (GES1) were analyzed for the expression level of miR-135b-5p and KLF4 mRNA by RT-qPCR. The BGC-823 GC cell line was chosen for subsequent assays.Results: The expression of miR-135b-5p and KLF4 was manipulated via transfection. The changes of proliferation, invasion, migration, viability, cycle and apoptosis of GC cells were evaluated by MTS, colony formation assay, transwell assay, wound healing assay and flow cytometry assay, respectively. Overexpression of MiR-135b-5p enhanced viability, proliferation, invasion and migration of GC cells, increased cell viability and reduced cell apoptosis. Replenishing of KLF4 functioned oppositely.Conclusions: The inhibitory effects of ectopic KLF4 could be attenuated by co-transfection of miR-135b-5p. Collective data suggested that miR-135b-5p has a tumor-promoting role in GC cells via downregulating KLF4. Hence, inhibition of miR-135b-5p could be valuable for treatment of gastric cancer. [ABSTRACT FROM AUTHOR]

Published
2020
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44. Correlation between microRNA-421 expression level and prognosis of gastric cancer

Author

Liu, Haiyan, Gao, Yongjian, Song, Defeng, Liu, Tong, and Feng, Ye

Subjects
Adult, Male, Kaplan-Meier Estimate, Adenocarcinoma, Middle Aged, Prognosis, Polymerase Chain Reaction, Gene Expression Regulation, Neoplastic, MicroRNAs, Stomach Neoplasms, Lymphatic Metastasis, Biomarkers, Tumor, Disease Progression, Humans, Original Article, Female, Aged
Abstract

The expression of microRNA-421 (miR-421) is significantly elevated in gastric carcinoma cells, thus may play an important role in tumor occurrence. This study thus aimed to further illustrate the correlation between miR-421 expression level and the progression and prognosis of gastric carcinoma. A total of 96 gastric carcinoma tissue samples were quantified for miR-421 expression level using quantitative PCR (qPCR) method. Kaplan-Meier survival curve was further deployed to analyze the postoperative survival of all patients. No significant correlation existed between miR-421 level and general information of patients such as age, sex, tumor size, location, invasion depth, TNM stage, differentiation stage and metastasis. However, miR-421 was significantly up-regulated in those tumors with lymph node metastasis (P0.05). These results suggested the correlation between miR-421 up-regulation and lymph node metastasis. Those patients with high miR-421 expression had significantly shorter survival time compared to normal miR-421 patients (median: 37.34 months vs. 54.23 months, P

Published
2015

45. Hydroxyflavanone inhibits gastric carcinoma MGC-803 cell proliferation

Author

Zhang, Haiyan, Zhan, Zhuo, Cui, Mingfu, Gao, Yongjian, Wang, Dayu, and Feng, Ye

Subjects
Original Article
Abstract

Gastric carcinoma (GC) is the most common primary malignancy of the digestive tract, with increasing incidence in many countries. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to assess inhibition of HepG2 cell proliferation by 2'-hydroxyflavanone. The STAT3 pathway was performed. 2'-hydroxyflavanone reduced inhibitory effects on MGC-803 cell proliferation. 2'-hydroxyflavanone exhibited the highest inhibition rate. Treatment of MGC-803 cells with 400, 200, and 100 μg/ml 2'-hydroxyflavanone resulted in 88.9±0.7%, 81.2±0.5%, 68.4±0.5% decrease in cell viability, respectively, indicating an IC50 of 9.3 μg/ml. The 100 μg/ml 2'-hydroxyflavanone can significantly inhibit the STAT3 pathway activation. 2'-hydroxyflavanone inhibits MGC-803 cell proliferation by inhibiting STAT3 pathway activation. This extract is therefore a potential drug candidate for treatment of liver cancer.

Published
2015

50. miR‐375‐3p/YWHAZ/β‐catenin axis regulates migration, invasion, EMT in gastric cancer cells.

Author

Guo, Feng, Gao, Yongjian, Sui, Guoqing, Jiao, Dan, Sun, Lina, Fu, Qingfeng, and Jin, Chunxiang

Subjects
*CATENINS, *CANCER cells, *CELL proliferation, *STOMACH cancer, *MESENCHYMAL stem cells, *GENE expression, *WNT genes
Abstract

Summary: YWHAZ (14‐3‐3ζ) plays crucial roles in regulating proliferation, apoptosis, migration, and invasion of gastric cancer (GC) cells. However, its extensive roles and potential mechanisms in GC cells remain unknown, and need to be researched deeply. In this study, we focus on the role of miR‐375/YWHAZ axis in migration, invasion and epithelial‐to‐mesenchymal transition (EMT) of GC cells. YWHAZ level was assessed by western blot and qPCR assays in GC cells. Scratch and transwell assays were used to determine the migration and invasion of GC cells. The protein levels of correlative molecules were detected by western blot. The regulation of miR‐375 on the expression of its target gene YWHAZ was verified by dual‐luciferase report system. According to the results, knockdown of YWHAZ inhibited the migration, invasion and EMT of GC cells. Moreover, silencing of YWHAZ restrained the activation of wnt/β‐catenin signalling pathway. YWHAZ was confirmed to be a target gene of miR‐375, and its expression was regulated by miR‐375 in GC cells. Transfection of miR‐375 inhibitor promoted the migration, invasion, EMT and activation of wnt/β‐catenin pathway in GC cells, which was suppressed by inhibition of YWHAZ. Taken together, this study suggests that miR‐375/YWHAZ axis may be served as a novel therapeutic target for GC patients. [ABSTRACT FROM AUTHOR]

Published
2019
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