scholarly journals Loss of large tumor suppressor 1 promotes growth and metastasis of gastric cancer cells through upregulation of the YAP signaling

Oncotarget ◽  
2016 ◽  
Vol 7 (13) ◽  
pp. 16180-16193 ◽  
Author(s):  
Jing Zhang ◽  
Ge Wang ◽  
Shao-Jun Chu ◽  
Jin-Shui Zhu ◽  
Rui Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Large Tumor ◽  
Large Tumor Suppressor

scholarly journals Context‐dependent activation of Wnt signaling by tumor suppressor RUNX 3 in gastric cancer cells

2014 ◽  
Vol 105 (4) ◽  
pp. 418-424 ◽  
Author(s):  
Xiaoli Ju ◽  
Tomo‐o Ishikawa ◽  
Kazuhito Naka ◽  
Kosei Ito ◽  
Yoshiaki Ito ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Wnt Signaling ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Context Dependent

scholarly journals Decreased RNA-binding motif 5 expression is associated with tumor progression in gastric cancer

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769454 ◽  
Author(s):  
Takahiko Kobayashi ◽  
Junich Ishida ◽  
Yuichi Shimizu ◽  
Hiroshi Kawakami ◽  
Goki Suda ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Growth ◽  
Tumor Suppressor ◽  
Protein Expression ◽  
Cancer Cells ◽  
Rna Binding ◽  
Suppressor Gene ◽  
Binding Motif ◽  
Gastric Cancer Cells ◽  
Rna Binding Motif 5

RNA-binding motif 5 is a putative tumor suppressor gene that modulates cell cycle arrest and apoptosis. We recently demonstrated that RNA-binding motif 5 inhibits cell growth through the p53 pathway. This study evaluated the clinical significance of RNA-binding motif 5 expression in gastric cancer and the effects of altered RNA-binding motif 5 expression on cancer biology in gastric cancer cells. RNA-binding motif 5 protein expression was evaluated by immunohistochemistry using the surgical specimens of 106 patients with gastric cancer. We analyzed the relationships of RNA-binding motif 5 expression with clinicopathological parameters and patient prognosis. We further explored the effects of RNA-binding motif 5 downregulation with short hairpin RNA on cell growth and p53 signaling in MKN45 gastric cancer cells. Immunohistochemistry revealed that RNA-binding motif 5 expression was decreased in 29 of 106 (27.4%) gastric cancer specimens. Decreased RNA-binding motif 5 expression was correlated with histological differentiation, depth of tumor infiltration, nodal metastasis, tumor–node–metastasis stage, and prognosis. RNA-binding motif 5 silencing enhanced gastric cancer cell proliferation and decreased p53 transcriptional activity in reporter gene assays. Conversely, restoration of RNA-binding motif 5 expression suppressed cell growth and recovered p53 transactivation in RNA-binding motif 5–silenced cells. Furthermore, RNA-binding motif 5 silencing reduced the messenger RNA and protein expression of the p53 target gene p21. Our results suggest that RNA-binding motif 5 downregulation is involved in gastric cancer progression and that RNA-binding motif 5 behaves as a tumor suppressor gene in gastric cancer.

scholarly journals MicroRNA-31 inhibits RhoA-mediated tumor invasion and chemotherapy resistance in MKN-45 gastric adenocarcinoma cells

2017 ◽  
Vol 242 (18) ◽  
pp. 1842-1847 ◽  
Author(s):  
Alireza Korourian ◽  
Raheleh Roudi ◽  
Ahmad Shariftabrizi ◽  
Zahra Madjd
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Vascular Invasion ◽  
Suppressor Gene ◽  
Small Gtpase ◽  
Gastric Cancer Cells ◽  
Increased Sensitivity ◽  
Rho Family

microRNAs are small single-stranded non-coding RNA molecules which modify gene expression by silencing potential target genes. The aberrant expression of RhoA, a small GTPase protein of Rho family, is involved in gastric cancer tumorigenesis. Since miR-31 is a pleomorphic molecule, we evaluated the miR-31/RhoA axis in inducing the malignant phenotype of gastric cancer cells MKN-45. Also, the clinicopathological significance of RhoA was investigated in a well-defined collection of gastric carcinomas which were embedded in tissue microarray blocks. Induction of miR-31 in MKN-45 followed by suppression of RhoA expression resulted in increased sensitivity to 5-fluorouracil, inhibition of cell proliferation, and invasion compared to the control groups. Immunohistochemical analysis in gastric adenocarcinoma patients’ samples showed significantly higher expression of RhoA in diffuse versus intestinal subtype tumors ( P = 0.009), poorly differentiated versus well and moderately differentiated tumors ( P = 0.03) and the presence of vascular invasion versus the absence of vascular invasion ( P = 0.04). Our findings suggest a critical role for miR-31, as a tumor suppressor gene, in gastric cancer tumorigenesis by targeting the RhoA. Impact statement Gastric cancer ranks as the third leading cause of cancer-associated deaths worldwide. The RhoA gene encodes a small GTPase protein of Rho family (RhoA) that its dysregulation is associated with cell motility and invasion. A strong line of evidence supports the regulation of RhoA by a number of miRs, including miR-31 in tumors. Our findings revealed that miR-31 is involved in gastric cancer tumorigenesis as a tumor suppressor gene. Through down-regulation of RhoA, miR-31 decreased cell proliferation, migration, and invasion in gastric cancer cells. In addition, induction of miR-31 increased sensitivity to 5-FU; thus, increasing its tissue concentrations could be a potential target for treatment of gastric cancer in the future.

scholarly journals Hypoxic silencing of tumor suppressor RUNX3 by histone modification in gastric cancer cells

Oncogene ◽  
2008 ◽  
Vol 28 (2) ◽  
pp. 184-194 ◽  
Author(s):  
S H Lee ◽  
J Kim ◽  
W-H Kim ◽  
Y M Lee
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Histone Modification ◽  
Cancer Cells ◽  
Gastric Cancer Cells

scholarly journals Galanin is an epigenetically silenced tumor suppressor gene in gastric cancer cells

PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0193275 ◽  
Author(s):  
Daseul Yoon ◽  
Kieun Bae ◽  
Min-Kyeong Lee ◽  
Jin Hee Kim ◽  
Kyong-Ah Yoon
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Gastric Cancer Cells

Genistein Induces G2/M Arrest in Gastric Cancer Cells by Increasing the Tumor Suppressor PTEN Expression

2013 ◽  
Vol 65 (7) ◽  
pp. 1034-1041 ◽  
Author(s):  
Yan-Long Liu ◽  
Guo-Qiang Zhang ◽  
Yue Yang ◽  
Chun-Yan Zhang ◽  
Rong-Xia Fu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Pten Expression ◽  
Gastric Cancer Cells

scholarly journals MiRNA-621 exerts tumor suppressor function in gastric adenocarcinoma by targeting AURKA/GSK-3β pathway

2021 ◽  
Author(s):  
Xiao Han ◽  
Hongxue Liu ◽  
Xiaojun Tang ◽  
Yao Zhao
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Gastric Adenocarcinoma ◽  
Molecular Mechanisms ◽  
Gastric Cancer Cells ◽  
Promising Target ◽  
Adenocarcinoma Cells ◽  
Gsk 3Β ◽  
Gastric Cancer Patients

Gastric adenocarcinoma is a major challenge to human health worldwide. Abnormal expression of miR-621 was found in many types of cancer. This research aimed to investigate the effects and detailed molecular mechanisms of miR-621 on gastric adenocarcinoma progression. The present study first showed that miR-621 was downregulated in gastric cancer patients, and its expression level was correlated with tumor size. MiR-621 overexpression inhibited viability, colony formation and proliferation of gastric cancer cells. AURKA was identified as a direct target of miR-621. AURKA knockdown induced decrease of p-GSK-3β/GSK-3β ratio and increase of p-β-catenin/β-catenin ratio which confirmed that AURKA positively regulated GSK-3β phosphorylation. AURKA knockdown also inhibited proliferation of gastric adenocarcinoma cells. AURKA expression was negatively correlated with miR-621 level. In addition, AURKA overexpression reversed the effect of miR-621 on the growth of cancer cells. Taken together, our results suggest that miR-621 is an important tumor suppressor in gastric cancer and could be a promising target for the cancer treatment.

Sign in / Sign up

Export Citation Format

Share Document