scholarly journals HHIP Overexpression Suppresses Human Gastric Cancer Progression and Metastasis by Reducing Its CpG Island Methylation

2020 ◽  
Vol 10 ◽  
Author(s):  
Yu Song ◽  
Jianchen Tu ◽  
Yanan Cheng ◽  
Fang Zhou ◽  
Peilin Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Promoter Methylation ◽  
De Novo ◽  
Cpg Island ◽  
Negative Regulator ◽  
Cancer Tissue ◽  
Human Gastric Cancer ◽  
Ags Cells ◽  
Gastric Cancer Progression

Human hedgehog-interacting protein (HHIP), a negative regulator of hedgehog (HH) signaling pathway, has been reported to be dysregulated in many types of cancer, including gastric cancer. However, the inhibitory role of HHIP as well as the underlying molecular mechanism of HHIP regulation in gastric cancer haven’t been fully elucidated yet. In this study, we demonstrated that HHIP overexpression significantly suppressed the proliferation and invasion of AGS cells evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and transwell assays, respectively. Interestingly, methylation-specific polymerase chain reaction (MS-PCR, MSP) showed that HHIP overexpression dramatically decreased its de novo promoter methylation levels in AGS cells. Furthermore, HHIP expression was higher in adjacent non-cancerous tissue compared to matched gastric cancer tissue. High HHIP level was negatively correlated with metastasis (p = 0.035) but not local recurrence (p = 0.58). Taken together, our study suggested that HHIP can modulate gastric cancer progression and metastasis via regulation of its de novo promoter methylation levels in a feedback manner. Lower HHIP levels is positively associated with gastric cancer metastasis, which not only indicates HHIP could be served as a protective marker for gastric cancer, but also suggests restoring HHIP expression might be a potential therapeutic strategy for clinical treatment.

scholarly journals Inhibition of the miR-192/215–Rab11-FIP2 axis suppresses human gastric cancer progression

2018 ◽  
Vol 9 (7) ◽  
Author(s):  
Xiaojing Zhang ◽  
Yin Peng ◽  
Yong Huang ◽  
Shiqi Deng ◽  
Xianling Feng ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Human Gastric Cancer ◽  
Gastric Cancer Progression

scholarly journals 1,25-Dihydroxyvitamin D3 affects gastric cancer progression by repressing BMP3 promoter methylation

2019 ◽  
Vol Volume 12 ◽  
pp. 2343-2353 ◽  
Author(s):  
Ye Zhao ◽  
Liang-Liang Cai ◽  
Hui-Ling Wang ◽  
Xiao-Juan Shi ◽  
Hui-Ming Ye ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Promoter Methylation ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Gastric Cancer Progression

Augmented gp130-mediated cytokine signalling accompanies human gastric cancer progression

2007 ◽  
Vol 213 (2) ◽  
pp. 140-151 ◽  
Author(s):  
CB Jackson ◽  
LM Judd ◽  
TR Menheniott ◽  
I Kronborg ◽  
C Dow ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Human Gastric Cancer ◽  
Gastric Cancer Progression

scholarly journals Glycogen synthase kinase 3 beta inhibits microRNA-183-96-182 cluster via the β-Catenin/TCF/LEF-1 pathway in gastric cancer cells

2013 ◽  
Vol 42 (5) ◽  
pp. 2988-2998 ◽  
Author(s):  
Xiaoli Tang ◽  
Dong Zheng ◽  
Ping Hu ◽  
Zongyue Zeng ◽  
Ming Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3 ◽  
Cancer Tissue ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
Cell Functions

Abstract Glycogen synthase kinase 3 beta (GSK3β) is a critical protein kinase that phosphorylates numerous proteins in cells and thereby impacts multiple pathways including the β-Catenin/TCF/LEF-1 pathway. MicroRNAs (miRs) are a class of noncoding small RNAs of ∼22 nucleotides in length. Both GSK3β and miR play myriad roles in cell functions including stem cell development, apoptosis, embryogenesis and tumorigenesis. Here we show that GSK3β inhibits the expression of miR-96, miR-182 and miR-183 through the β-Catenin/TCF/LEF-1 pathway. Knockout of GSK3β in mouse embryonic fibroblast cells increases expression of miR-96, miR-182 and miR-183, coinciding with increases in the protein level and nuclear translocation of β-Catenin. In addition, overexpression of β-Catenin enhances the expression of miR-96, miR-182 and miR-183 in human gastric cancer AGS cells. GSK3β protein levels are decreased in human gastric cancer tissue compared with surrounding normal gastric tissue, coinciding with increases of β-Catenin protein, miR-96, miR-182, miR-183 and primary miR-183-96-182 cluster (pri-miR-183). Furthermore, suppression of miR-183-96-182 cluster with miRCURY LNA miR inhibitors decreases the proliferation and migration of AGS cells. Knockdown of GSK3β with siRNA increases the proliferation of AGS cells. Mechanistically, we show that β-Catenin/TCF/LEF-1 binds to the promoter of miR-183-96-182 cluster gene and thereby activates the transcription of the cluster. In summary, our findings identify a novel role for GSK3β in the regulation of miR-183-96-182 biogenesis through β-Catenin/TCF/LEF-1 pathway in gastric cancer cells.

scholarly journals Overexpression of SULT2B1b Promotes Angiogenesis in Human Gastric Cancer

2016 ◽  
Vol 38 (3) ◽  
pp. 1040-1054 ◽  
Author(s):  
Wen Chen ◽  
Haiyu Zhou ◽  
Lei Ye ◽  
Baogen Zhan
Keyword(s):  
Gastric Cancer ◽  
Hepatocellular Carcinoma ◽  
Endothelial Cells ◽  
Cancer Progression ◽  
Human Gastric Cancer ◽  
Qrt Pcr ◽  
Diagnosis And Prognosis ◽  
Promising Strategy ◽  
Oncogenic Protein ◽  
Gastric Cancer Progression

Background/Aims: Overexpression of cytosolic sulfotransferase 2B1b (SULT2B1b) has been commonly found in colorectal and hepatocellular carcinoma, suggesting that SULT2B1b might act as a potential oncogenic protein. However, its clinical significance and biological role in gastric cancer progression remain largely unknown. Methods: Expressions of SULT2B1b in clinical gastric cancer (GC) samples were examined using qRT-PCR and Western blot. Results: SULT2B1b was markedly overexpressed in human GC samples, and positively correlated with vessel density and associated with poor clinical features. We also demonstrated that overexpression of SULT2B1b resulted in increased tumor angiogenesis and tumor growth in mouse GC models. In addition, ablation of SULT2B1b in human GC cells lines BGC823 and MKN45 decreased the capability of the cells to recruit endothelial cells. Moreover, depletion of SULT2B1b in GC cells reduced VEGF-A expression by downregulating SP1 and AP2. Conclusion: Our results suggested that the SULT2B1b-mediated angiogenic pathway could serve as biomarkers for GC diagnosis and prognosis, and suppressing SULT2B1b-mediated angiogenic signaling might be a promising strategy for developing novel GC treatment.

Role of hMLH1 and E-Cadherin Promoter Methylation in Gastric Cancer Progression

2013 ◽  
Vol 45 (1) ◽  
pp. 40-47 ◽  
Author(s):  
Meysam Moghbeli ◽  
Omeed Moaven ◽  
Bahram Memar ◽  
Hamid Reza Raziei ◽  
Azadeh Aarabi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Promoter Methylation ◽  
Gastric Cancer Progression ◽  
E Cadherin

Targeting IGF-I Receptor Has Therapeutic Utility of Prevention of Human Gastric Cancer Progression

2011 ◽  
Vol 140 (5) ◽  
pp. S-684
Author(s):  
Yasushi Adachi ◽  
Yasutaka Sukawa ◽  
Hiroyuki Yamamoto ◽  
Katsuhiko Nosho ◽  
Chie Miyamoto ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Human Gastric Cancer ◽  
Igf I ◽  
Gastric Cancer Progression ◽  
Therapeutic Utility

scholarly journals Differential Expression and Function of Caveolin-1 in Human Gastric Cancer Progression

2007 ◽  
Vol 67 (18) ◽  
pp. 8519-8526 ◽  
Author(s):  
Elke Burgermeister ◽  
Xiangbin Xing ◽  
Christoph Röcken ◽  
Mark Juhasz ◽  
Jie Chen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Differential Expression ◽  
Cancer Progression ◽  
Human Gastric Cancer ◽  
Caveolin 1 ◽  
And Function ◽  
Gastric Cancer Progression
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