Publications by authors named "Tiangen Wu"

6 Publications

  • Page 1 of 1

Swertiamarin suppresses proliferation, migration, and invasion of hepatocellular carcinoma cells via negative regulation of FRAT1.

Eur J Histochem 2020 Oct 19;64(4). Epub 2020 Oct 19.

Department of Hepatobiliary Surgery, the Second Affiliated Hospital of Kunming Medical University, Kunming.

Studies have shown that swertiamarin (STM) has multiple biological activities, but its anti-tumour effects and molecular mechanisms are still unclear. The present research aimed to validate the STM's impacts on the proliferation, migration, and invasion of hepatocellular carcinoma (HCC) cells, and to study its potential mechanism. Two HCC cell lines were treated with STM. Tumour growth was observed by the mouse tumour xenografts model. HCC cell lines stably expressing T-cell lymphomas 1 (FRAT1) were generated by lentivirusmediated overexpression. Cell viability, proliferation, migration, and invasion were observed using Cell Counting Kit-8 (CCK8), the xCELLigence Real-Time Cell Analyzer system (RTCA), and transwell analysis, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used to observe the expression of FRAT1 and proteins related to the Wnt/β-catenin signalling pathway. Tumour growth was inhibited by STM in vivo. STM suppressed the proliferation, migration, and invasion of HCC cells. STM negatively regulated FRAT1 expression, whereas overexpressed FRAT1 blocked the anti-tumour function of STM. The results revealed that STM suppressed the FRAT1/Wnt/β-catenin signalling pathway. The findings of this study provide new insights into investigation of therapeutic strategies against HCC.
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http://dx.doi.org/10.4081/ejh.2020.3169DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7586251PMC
October 2020

Reduced glutathione ameliorates liver function, oxidative stress and inflammation after interventional therapy for hepatocellular carcinoma.

J BUON 2020 May-Jun;25(3):1361-1367

Department of Hepatobiliary Surgery, the Second Affiliated Hospital of Kunming Medical University, Kunming, China.

Purpose: To investigate the influence of reduced glutathione (GSH) in liver function, oxidative stress, inflammatory response, immune function and quality of life of patients after an interventional therapy for hepatocellular carcinoma.

Methods: 96 hepatocellular carcinoma patients undergoing hepatic arterial intervention chemotherapy were selected and randomly divided into the control group (n=48) and the observation group (n=48). The patients in the control group were given conventional treatment after operation, while those in the observation group were treated with GSH based on the treatment in the control group. The liver function, oxidative stress, inflammation, quality of life and adverse reactions were compared before and after treatment between the two groups.

Results: The levels of superoxide dismutase (SOD), cluster of differentiation (CD)3+, CD4+ and CD4+/CD8+ as well as physical, emotion and social function scores after treatment were higher in the observation group than in the control group. The observation group had lower levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin (TBiL), malondialdehyde (MDA), advanced oxidation protein product (AOPP), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and CD8+ as well as pain score than the control group (p<0.05). The total effective rate in the observation group was remarkably higher than in the control group (p<0.05), while there were no significant differences in disease control rate and clinical adverse reactions between the two groups (p>0.05).

Conclusions: GSH can evidently ameliorate the liver function and immune function, reduce oxidative stress and inflammatory response and improve the postoperative quality of life of the patients after the interventional therapy for hepatocellular carcinoma, with satisfactory clinical therapeutic effects, so it is worthy of further application and generalization.
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February 2021

Meta-analysis: The efficacy of metformin and other anti-hyperglycemic agents in prolonging the survival of hepatocellular carcinoma patients with type 2 diabetes.

Ann Hepatol 2020 May - Jun;19(3):320-328. Epub 2019 Dec 16.

Department of Hepatobiliary Surgery, the Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China; The Yunnan Provincial Clinical Center for Hepato-biliary-pancreatic Diseases, Kunming, Yunnan, China. Electronic address:

Introduction: This study aimed to compare the therapeutic efficacy of metformin and other anti-hyperglycemic agents in hepatocellular carcinoma (HCC) patients with type 2 diabetes (T2D).

Materials: A systematic electronic search on keywords including HCC and different anti-hyperglycemic agents was performed through electronic databases including Medline and EMBASE. The primary outcome was the overall survival (OS). The secondary outcomes were the recurrence-free survival (RFS) and progression-free survival (PFS).

Results: Six retrospective cohort studies were included for analysis: Four studies with curative treatment for HCC (618 patients with metformin and 532 patients with other anti-hyperglycemic agents) and two studies with non-curative treatment for HCC (92 patients with metformin and 57 patients with other anti-hyperglycemic agents). Treatment with metformin was associated with significantly longer OS (OR=2.62, 95%CI: 1.76-3.90; OR=3.14, 95%CI: 2.33-4.24; OR=3.31, 95%CI: 2.39-4.59, all P<0.00001) and RFS (OR=2.52, 95%CI: 1.84-3.44; OR=2.87, 95%CI: 2.15-3.84; all P<0.00001; and OR=2.26, 95%CI: 0.94-5.45, P=0.07) rates vs. those of other anti-hyperglycemic agents after curative therapies for HCC. However, both of the two studies reported that following non-curative HCC treatment, there were no significant differences in the OS and PFS rates between the metformin and non-metformin groups (I>50%).

Conclusions: Metformin significantly prolonged the survival of HCC patients with T2D after the curative treatment of HCC. However, the efficacy of metformin needs to be further determined after non-curative therapies for HCC patients with T2D.
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http://dx.doi.org/10.1016/j.aohep.2019.11.008DOI Listing
December 2019

Bioinformatics analysis of differentially expressed genes in hepatocellular carcinoma cells exposed to Swertiamarin.

J Cancer 2019 21;10(26):6526-6534. Epub 2019 Oct 21.

State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650201, PR China.

: To explore gene expression profiling in hepatocellular carcinoma (HCC) cells exposed to swertiamarin. : Cell viability, apoptosis and invasion were examined in HepG2 cells after swertiamarin treatment. Tumor growth of SK-Hep-1 cells xenografted in nude mice was monitored after swertiamarin treatment. Total RNA was isolated from HepG2 cells treated with swertiamarin for microarray analysis. The data of microarray were analyzed by bioinformatics. : Swertiamarin treatment decreased the viability and invasion while increased the apoptosis of HepG2 cells, and significantly inhibited the growth of SK-Hep-1 cells xenografted in nude mice. Pathway and biological process analysis of differentially expressed genes (DEGs) in swertiamarin treated HepG2 cells showed that PI3k-Akt was the most significant regulated pathway. 47 targets of swertiamarin were predicted by CGBVS while 21 targets were predicted by 3NN. Notably, 8 targets were predicted as the targets of swertiamarin by both programs, including two prominent targets JUN and STAT3. A large range of DEGs induced by swertiamarin could be regulated by JUN and STAT3. : Swertiamarin treatment led to significant changes in the expression of a variety of genes that modulate cell survival, cell cycle progression, apoptosis, and invasion. Moreover, most of these genes can be clustered into pathway networks such as PI3K, JUN, STAT3, which are predicted targets of swertiamarin. Further confirmation of these targets will reveal the anti-tumor mechanisms of swertiamarin and facilitate the development of swertiamarin as a novel agent for cancer prevention and treatment.
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http://dx.doi.org/10.7150/jca.33666DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856900PMC
October 2019

Long non-coding RNA snaR is involved in the metastasis of liver cancer possibly through TGF-β1.

Oncol Lett 2019 Jun 16;17(6):5565-5571. Epub 2019 Apr 16.

Department of Hepatopancreatobiliary Surgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.

It was previously demonstrated that the long non-coding RNA (lncRNA) small NF90-associated RNA (snaR) served an oncogenic role in human colon cancer, although its roles in other types of cancer remain unknown. To investigate the potential involvement of lncRNA snaR in hepatocellular carcinoma (HCC), expression of snaR in liver biopsies and plasma of patients with HCC and healthy controls was detected by reverse transcription-quantitative polymerase chain reaction. ELISA was used to determine the protein expression levels of transforming growth factor-β1 (TGF-β1). A snaR expression vector was transfected into HCC cells, and the effects on cell migration and invasion were analyzed by Transwell migration and Matrigel invasion assays, respectively. The protein expression levels of TGF-β1 in HCC cells were detected by western blotting. The expression of snaR and TGF-β1 was significantly increased in the patients with HCC compared with the healthy controls. The plasma expression levels of snaR and TGF-β1 were positively correlated in patients with HCC; however, not in healthy controls. snaR overexpression significantly promoted cancer cell migration and invasion, and additionally increased TGF-β1 expression. Treatment with TGF-β1 did not significantly affect snaR expression. A TGF-β1 inhibitor attenuated the effects of snaR overexpression in cancer cell migration and invasion. snaR may promote the metastasis of liver cancer through TGF-β1.
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http://dx.doi.org/10.3892/ol.2019.10258DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6507301PMC
June 2019

The BBZDR/Wor rat model for investigating the complications of type 2 diabetes mellitus.

ILAR J 2004 ;45(3):292-302

Biomedical Research Models, Worcester, MA, USA.

Congenic and inbred strains of rats offer researchers invaluable insight into the etiopathogenesis of diabetes and associated complications. The inbred Bio-Breeding Zucker diabetic rat (BBZDR)/Wor rat strain is a relatively new and emerging model of type 2 diabetes. This strain was created by classical breeding methods used to introgress the defective leptin receptor gene (Lepr(fa)) from insulin-resistant Zucker fatty rats into the inbred BBDR/Wor strain background. The diabetic male BBZDR/Wor rat is homozygous for the fatty mutation and shares the genetic background of the original BB strain. Although lean littermates are phenotypically normal, obese juvenile BBZDR/Wor rats are hyperlipidemic and hyperleptinemic, become insulin resistant, and ultimately develop hyperglycemia. Furthermore, the BBZDR/Wor rat is immune competent and does not develop autoimmunity. Similar to patients with clinical diabetes, the BBZDR/Wor rat develops complications associated with hyperglycemia. The BBZDR/Wor rat is a model system that fully encompasses the ability to study the complications that affect human type 2 diabetic patients. In this review, recent work that has evaluated type 2 diabetic complications in BBZDR/Wor rats is discussed, including the authors' preliminary unpublished studies on cardiovascular disease.
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http://dx.doi.org/10.1093/ilar.45.3.292DOI Listing
July 2005