http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
JCAD deficiency attenuates activation of hepatic stellate cells and cholestatic fibrosis
Li Xie,Hui Chen,Li Zhang,Yue Ma,Yuan Zhou,Yong-Yu Yang,Chang Liu,Yu-Li Wang,Ya-Jun Yan,Jia Ding,Xiao Teng,Qiang Yang,Xiu-Ping Liu,Jian Wu 대한간학회 2024 Clinical and Molecular Hepatology(대한간학회지) Vol.30 No.2
Background/Aims: Cholestatic liver diseases including primary biliary cholangitis (PBC) are associated with active hepatic fibrogenesis, which ultimately progresses to cirrhosis. Activated hepatic stellate cells (HSCs) are the main fibrogenic effectors in response to cholangiocyte damage. JCAD regulates cell proliferation and malignant transformation in nonalcoholic steatoheaptitis-associated hepatocellular carcinoma (NASH-HCC). However, its participation in cholestatic fibrosis has not been explored yet. Methods: Serial sections of liver tissue of PBC patients were stained with immunofluorescence. Hepatic fibrosis was induced by bile duct ligation (BDL) in wild-type (WT), global JCAD knockout mice (JCAD-KO) and HSC-specific JCAD knockout mice (HSC-JCAD-KO), and evaluated by histopathology and biochemical tests. In situ-activated HSCs isolated from BDL mice were used to determine effects of JCAD on HSC activation. Results: In consistence with staining of liver sections from PBC patients, immunofluorescent staining revealed that JCAD expression was identified in smooth muscle α-actin (α-SMA)-positive fibroblast-like cells and was significantly up-regulated in WT mice with BDL. JCAD deficiency remarkably ameliorated BDL-induced hepatic injury and fibrosis, as documented by liver hydroxyproline content, when compared to WT mice with BDL. Histopathologically, collagen deposition was dramatically reduced in both JCAD-KO and HSC-JCAD-KO mice compared to WT mice, as visualized by Trichrome staining and semi-quantitative scores. Moreover, JCAD deprivation significantly attenuated in situ HSC activation and reduced expression of fibrotic genes after BDL. Conclusions: JCAD deficiency effectively suppressed hepatic fibrosis induced by BDL in mice, and the underlying mechanisms are largely through suppressed Hippo-YAP signaling activity in HSCs.
Li, Ping,Xie, Xiao-Bing,Chen, Qian,Pang, Guo-Lian,Luo, Wan,Tu, Jian-Cheng,Zheng, Fang,Liu, Song-Mei,Han, Lu,Zhang, Jian-Kun,Luo, Xian-Yong,Zhou, Xin Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.16
Background: Recent studies have indicated that microRNA-15a (miR-15a) is dysregulated in breast cancer (BC). We aimed to evaluate the expression of miR-15a in BC tissues and corresponding para-carcinoma tissues. We also focused on effects of miR-15a on cellular behavior of MDA-MB-231 and expression of its target gene synuclein-${\gamma}$ (SNCG). Materials and Methods: The expression levels of miR-15a were analysed in BC formalin fixed paraffin embedded (FFPE) tissues by microarray and quantitative real-time PCR. CCK-8 assays, cell cycle and apoptosis assays were used to explore the potential functions of miR-15a in MDA-MB-231 human BC cells. A luciferase reporter assay confirmed direct targets. Results: Downregulation of miR-15a was detected in most primary BCs. Ectopic expression of miR-15a promoted proliferation and suppressed apoptosis in vivo. Further studies indicated that miR-15a may directly interact with the 3'-untranslated region (3'-UTR) of SNCG mRNA, downregulating its mRNA and protein expression levels. SNCG expression was negatively correlated with miR-15a expression. Conclusions: MiR-15a has a critical role in mediating cell cycle arrest and promoting cell apoptosis of BC, probably by directly targeting SNCG. Thus, it may be involved in development and progression of BC.
Li, Jing-Ping,Cao, Nai-Xia,Jiang, Ri-Ting,He, Shao-Jian,Huang, Tian-Ming,Wu, Bo,Chen, De-Feng,Ma, Ping,Chen, Li,Zhou, Su-Fang,Xie, Xiao-Xun,Luo, Guo-Rong Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.6
Background: GC-binding factor 2 (GCF2) is a transcriptional regulator that represses transcriptional activity of the epidermal growth factor receptor (EGFR) by binding to a specific GC-rich sequence in the EGFR gene promoter. In addition to this function, GCF2 has also been identified as a tumor-associated antigen and regarded as a potentially valuable serum biomarker for early human hepatocellular carcinoma (HCC) diagnosis. GCF2 is high expressed in most HCC tissues and cell lines including HepG2. This study focused on the influence of GCF2 on cell proliferation and apoptosis in HepG2 cells. Materials and Methods: GCF2 expression at both mRNA and protein levels in HepG2 cells was detected with reverse transcription (RT) PCR and Western blotting, respectively. RNA interference (RNAi) technology was used to knock down GCF2 mRNA and protein expression. Afterwards, cell viability was analyzed with a Cell Counting Kit-8 (CCK-8), and cell apoptosis and caspase 3 activity by flow cytometry and with a Caspase 3 Activity Kit, respectively. Results: Specific down-regulation of GCF2 expression caused cell growth inhibition, and increased apoptosis and caspase 3 activity in HepG2 cells. Conclusions: These primary results suggest that GCF2 may influence cell proliferation and apoptosis in HepG2 cells, and also provides a molecular basis for further investigation into the possible mechanism at proliferation and apoptosis in HCC.
Implication of Polymorphisms in DNA Repair Genes in Prognosis of Hepatocellular Carcinoma
Yue, Ai-Min,Xie, Zhen-Bin,Guo, Shu-Ping,Wei, Qi-Dong,Yang, Xiao-Wei Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.1
XRCC1 genetic polymorphisms could be associated with increased risk of various cancer, including hepatocellular carcinoma (HCC), the fifth most common cancer. We here conducted a study to explore the role of selective SNPs of the XRCC1 and XPD genes in the prognosis of HCC. A total of 231 cases were collected, and genotyping of XRCC1 Arg194Trp, XRCC1 Arg399Gln, XPD Lys751Gln and XPD Asp312Asn was performed by duplex polymerase-chain-reaction with the confronting-two-pair primer method. Our findings indicated XRCC1 399Gln/Gln genotype was associated with a significant difference in the median survival time compared with patients carrying Arg/Trp and Arg/Arg genotypes, and individuals with XPD 751 Gln/ Gln genotype had a significantly greater survival time than patients carrying Lys/Lys and Lys/Gln genotypes. The Cox's regression analysis showed individuals carrying XRCC1 399Trp/Trp genotype had 0.55 fold risk of death from HCC than Arg/Arg genotype. Similarly, XPD 751Gln/Gln had a strong decreasein comparison to XPD Lys/Lys carriers with an HR of 0.34. These results suggest that polymorphisms in XRCC1 and XPD may have functional significance in the prognosis of HCC.
Insect-specific microRNA involved in the development of the silkworm Bombyx mori
Yong Zhang,Xue Zhou,Xie Ge,Jiang-Hao Jiang,Mu-Wang Li,Shi-Hai Jia,Xiao-Nan Yang,Yun-Chao Kan,Xue-Xia Miao,Guo-Ping Zhao,Fei Li,Yong-Ping Huang 한국응용곤충학회 2009 한국응용곤충학회 학술대회논문집 Vol.2009 No.10
MicroRNAs (miRNAs) are endogenous non-coding genes that participate in post-transcription regulation by either degrading mRNA or blocking its translation. It is considered to be very important in regulating insect development and metamorphosis. Insects are the largest group of animals and are extremely valuable in biological and agriculture research. Insects are also important pests to human health and agriculture, and efforts are necessary protect both humans and plants from disease and damage. Despite their importance, insects lag behind mammals, nematodes, and plants in miRNA research. At present, only 279 insect miRNAs have been identified from Drosophila melanogaster, Anopheles gambiae, Apis mellifera, Bombyx mori, and D. pseudoobscura in miRBase, and most of these miRNAs were computationally predicted without experimental validation. Functional analysis of insect miRNAs has only been conducted in D. melanogaster.
Ren Chen-Xi,Jin Xin,Xie Dan-Ping,Guo Xiao-Yu,Yu Li-Yun,Cui Yu-Dong,Kwon Taeho,Sun Hu-Nan 한국응용생명화학회 2021 Applied Biological Chemistry (Appl Biol Chem) Vol.64 No.5
Idiopathic pulmonary fibrosis (IPF) is a serious and irreversible chronic lung disease. Bleomycin (BLM) is an anticancer drug, which can cause severe lung toxicity. The main target of oxidative stress-induced lung injury is alveolar epithelial cells, which lead to interstitial fibrosis. The present study investigated whether hispidin (HP), which has excellent antioxidant activity, attenuates bleomycin-induced pulmonary fibrosis via anti-oxidative effects in A549 cells. We found that hispidin reduced bleomycin-induced fibrosis of A549 cells by reducing reactive oxygen species (ROS) levels and inhibiting epithelial-mesenchymal transition. Taken together, our data suggest that hispidin has therapeutic potential in preventing bleomycin-induced pulmonary fibrosis.
In Vitro Biological Characterization of DCUN1D5 in DNA Damage Response
Guo, Wei,Li, Guo-Jun,Xu, Hong-Bo,Xie, Jie-Shi,Shi, Tai-Ping,Zhang, Sheng-Zhong,Chen, Xiao-Hong,Huang, Zhi-Gang Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8
Background: Novel prognostic biomarkers or therapeutic molecular targets for laryngeal squamous cell carcinoma (LSCC) are an urgent priority. We here sought to identify multiple novel LSCC-associated genes. Methods: Using high-density microarray expression profiling, we identified multiple genes that were significantly altered between human LSCCs and paired normal tissues. Potential oncogenic functions of one such gene, DCUN1D5, were further characterized in vitro. Results: Our results demonstrated that DCUN1D5 was highly expressed in LSCCs. Overexpression of DCUN1D5 in vitro resulted in 2.7-fold increased cellular migration, 67.5% increased invasive capacity, and 2.6-fold increased proliferation. Endogenous DCUN1D5 expression was decreased in a time-dependent manner after genotoxic stress, and silencing of DCUN1D5 by siRNA decreased the number of cells in the S phase by 10.2% and increased apoptosis by 11.7%. Conclusion: Our data suggest that DCUN1D5 in vitro might have vital roles in DNA damage response, but further studies are warranted to assess its significance in vivo.
( Xiu Jing Zhang ),( Xue Lian Xiang ),( Lei Tu ),( Xiao Ping Xie ),( Xiao Hua Hou ) 대한소화기기능성질환·운동학회 2013 Journal of Neurogastroenterology and Motility (JNM Vol.19 No.4
Background/Aims Most recent studies using high-resolution manometry were based on supine liquid swallows. This study was to evaluate the differences in esophageal motility for liquid and solid swallows in the upright and supine positions, and to determine the percentages of motility abnormalities in different states. Methods Twenty-four asymptomatic volunteers and 26 patients with gastroesophageal reflux disease underwent high-resolution manometry using a 36-channel manometry catheter. The peristalses of 10 water and 10 steamed bread swallows were recorded in both supine and upright positions. Integrated relaxation pressure, contractile front velocity, distal latency (DL) and the distal contractile integral (DCI) were investigated and comparisons between postures and boluses were analyzed. Abnormal peristalsis of patients was assessed applying the corresponding normative values. Results In total, 829 swallows from healthy volunteers and 959 swallows from patients were included. (1) The upright position provided lower integrated relaxation pressure, shorter DL and weaker DCI than the supine position. (2) In the comparison of liquid swallows, the mean for contractile front velocity was obviously reduced while DL and DCI were increased in solid swallows. (3) The supine position detected more hypotensive peristalsis than the upright position. The upright position provided more rapid and premature contraction than the supine position but there was no statistically significant difference. Conclusions Supine solid swallows occur with more hypotensive peristalsis. Analysis should be based on normative values from the corresponding posture and bolus. (J Neurogastroenterol Motil 2013;19:467-472)