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.

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

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

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 ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis

2021 ◽  
Author(s):  
Xiaqiong Mao ◽  
Tao Ji ◽  
Aiguo Liu ◽  
Yunqi Weng
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Tumor Suppressor Genes ◽  
Luciferase Reporter ◽  
Diagnosis And Prognosis ◽  
Reporter Assays ◽  
Non Coding Rnas ◽  
Gastric Cancer Progression ◽  
Proliferation And Invasion

Abstract Background Long non-coding RNAs (lncRNAs) play important regulatory roles in the initiation and progression of various cancers. However, the biological roles and the potential mechanisms of lncRNAs in gastric cancers remain unclear. Methods The expression of SNHG22 in gastric cancer was analyzed in public databases (TCGA) and validated via qRT-PCR. SNHG22 knockdown cell lines were construced, and cell proliferation and invasion were analyzed. CHIP and luciferase reporter assays were performed to clarify the transcriptional role of ELK4. RNA pull-down followed MS and RIP assays were employed to identify the interaction between SNHG22 and EZH2. Luciferase reporter assays and RIP assays were used to confirm the regulation of SNHG22 on Notch1 by sponging miR-2003-3p. Results Knockdown of SNHG22 inhibited the proliferation and invasion ability of GC cells. Moreover, we identified that the transcriptional factor, ELK4, could promote SNHG22 expression in GC cells. In addition, using RNA pull-down followed MS assay, we found that SNHG22 directly bound to EZH2 to suppress the expression of tumor suppressor genes. At the same time, SNHG22 sponged miR-200c-3p to increase Notch1 expression. Conclusions Taken together, our findings demonstrated the role of SNHG22 on promoting proliferation and invasion of GC cells. And we revealed a new regulatory mechanism of SNHG22 in GC cells. SNHG22 is a promising lncRNA biomarker for diagnosis and prognosis and a potential target for GC treatment.

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

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 microRNA arm-imbalance in part from complementary targets mediated decay promotes gastric cancer progression

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhengyi Zhang ◽  
Jingnan Pi ◽  
Dongling Zou ◽  
Xiaoshuang Wang ◽  
Jiayue Xu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Mature Mirnas ◽  
Gastric Carcinogenesis ◽  
Tissue Formation ◽  
Pathological Effect ◽  
Promising Strategy ◽  
Dynamic Expression ◽  
Gastric Cancer Patients ◽  
Gastric Cancer Progression

Abstract Strand-selection is the final step of microRNA biogenesis in which functional mature miRNAs are generated from one or both arms of precursor. The preference of strand-selection is diverse during development and tissue formation, however, its pathological effect is still unknown. Here we find that two miRNA arms from the same precursor, miR-574-5p and miR-574-3p, are inversely expressed and play exactly opposite roles in gastric cancer progression. Higher-5p with lower-3p expression pattern is significantly correlated with higher TNM stages and poor prognosis of gastric cancer patients. The increase of miR-574-5p/-3p ratio, named miR-574 arm-imbalance is partially due to the dynamic expression of their highly complementary targets in gastric carcinogenesis, moreover, the arm-imbalance of miR-574 is in turn involved and further promotes gastric cancer progression. Our results indicate that miR-574 arm-imbalance contribute to gastric cancer progression and re-modification of the miR-574-targets homeostasis may represent a promising strategy for gastric cancer therapy.

scholarly journals Decreased IFIT2 Expression Promotes Gastric Cancer Progression and Predicts Poor Prognosis of the Patients

2017 ◽  
Vol 45 (1) ◽  
pp. 15-25 ◽  
Author(s):  
Lujun Chen ◽  
Wensi Zhai ◽  
Xiao Zheng ◽  
Quanqin Xie ◽  
Qi Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Gastric Cancer Cell ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cell Lines ◽  
Cancer Tissues ◽  
Gastric Cancer Progression

Background/Aims: The status of interferon (IFN) signaling pathway has been shown to be closely associated with the response of immune checkpoint blockade therapy against advanced human cancers. IFN-induced protein with tetratricopeptide repeats 2 (IFIT2), also known as IFN-stimulated gene 54 (ISG54), is one of the most highly responsive ISGs, which can inhibit the proliferation and migration of cancer cells, and regulate viral replication, resulting in anti-cancer and anti-viral effects. In the present study, we aimed to investigate the role of IFIT2 in human gastric cancer. Methods: Immunohistochemistry assay was used to investigate the correlation between the IFIT2 expression in cancer tissues and clinical parameters of gastric cancer patients. Knockdown of IFIT2 was performed using RNAi to assess the role of IFIT2 in the regulation of biological behaviors in human gastric cancer cell lines. Results: IFIT2 expression in gastric cancer tissues was significantly associated with tumor stage and postoperative prognoses of the patients. Moreover, decreased IFIT2 expression in human gastric cancer cell lines SGC-7901 and AGS significantly increased the cell viability, cell migration and the ratios of cells in S phase. Conclusion: Our present study demonstrated that the decreased IFIT2 expression could promote the gastric cancer progression and predict poor therapeutic outcomes of the patients.

Sign in / Sign up

Export Citation Format

Share Document