scholarly journals TGF-β1 induces epigenetic silence of TIP30 to promote tumor metastasis in esophageal carcinoma

Oncotarget ◽  
2014 ◽  
Vol 6 (4) ◽  
pp. 2120-2133 ◽  
Author(s):  
Fangfang Bu ◽  
Xing Liu ◽  
Jingjing Li ◽  
Shukun Chen ◽  
Xin Tong ◽  
...  
Keyword(s):  
Esophageal Carcinoma ◽  
Tumor Metastasis ◽  
Epigenetic Silence ◽  
Tgf Β1

scholarly journals MiR-23a promotes TGF-β1-induced EMT and tumor metastasis in breast cancer cells by directly targeting CDH1 and activating Wnt/β-catenin signaling

Oncotarget ◽  
2017 ◽  
Vol 8 (41) ◽  
pp. 69538-69550 ◽  
Author(s):  
Fei Ma ◽  
Wenjie Li ◽  
Chunxiao Liu ◽  
Wei Li ◽  
Haining Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tumor Metastasis ◽  
Tgf Β1

scholarly journals Activation of Slit2/Robo1 Signaling Promotes Tumor Metastasis in Colorectal Carcinoma through Activation of the TGF-β/Smads Pathway

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 635 ◽  
Author(s):  
Yuying Yao ◽  
Zijun Zhou ◽  
Liuyou Li ◽  
Junchen Li ◽  
Lixun Huang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Tumor Metastasis ◽  
Transforming Growth Factor ◽  
Serum Levels ◽  
Transforming Growth Factor Β1 ◽  
Migration And Invasion ◽  
Tumor Cell Migration ◽  
Pathological Stages ◽  
Tgf Β1

Slit2 (slit guidance ligand 2), a ligand of the Roundabout1 (Robo1) transmembrane receptor, is often overexpressed in colorectal carcinomas (CRCs). In this study, we performed data mining in the Metabolic gEne RApid Visualizer (MERAV) database and found that Slit2 and TGF-β1 (Transforming growth factor-β1) are highly expressed in carcinomas relative to those in tumor-free tissues from healthy volunteers or wild type mice. Furthermore, expression of Slit2 and TGF-β1 in CRCs increases with pathological stages. Serum levels of Slit2 in patients with CRC and in ApcMin/+ mice with spontaneous intestinal adenoma were significantly increased compared with those in healthy controls. Specific blockage of Slit2 binding to Robo1 inactivated TGF-β/Smads signaling and inhibited tumor cell migration and metastasis, which can be partially restored by treatment with TGF-β1. However, specific inhibition of TGF-β1/Smads signaling reduced CRC tumor cell migration and invasion without affecting cell proliferation. This study suggests that activation of Slit2/Robo1 signaling in CRC induces tumor metastasis partially through activation of the TGF-β/Smads pathway.

Tumor-to-tumor metastasis: esophageal carcinoma metastatic to an intracranial paraganglioma

2009 ◽  
Vol 110 (4) ◽  
pp. 744-748 ◽  
Author(s):  
Jian-Qiang Lu ◽  
Moosa Khalil ◽  
William Hu ◽  
Garnette R. Sutherland ◽  
Arthur W. Clark
Keyword(s):  
Esophageal Carcinoma ◽  
Tumor Metastasis ◽  
Histopathological Examination ◽  
Unique Case ◽  
Blurred Vision ◽  
Poorly Differentiated Carcinoma ◽  
History Of ◽  
Poorly Differentiated ◽  
Tumor To Tumor Metastasis ◽  
Upper Gastrointestinal

Tumor-to-tumor metastasis (TTM) is a relatively rare but well-documented phenomenon. The authors report a unique case of esophageal carcinoma metastatic to an intracranial paraganglioma. A sellar and suprasellar tumor was found using MR imaging in an 81-year-old man who presented with a 3-week history of progressive headache and blurred vision. A subtotal excision of the tumor was achieved. Histopathological examination of the tumor disclosed a neoplasm with two distinct components: one showing the classic Zellballen pattern of a paraganglioma, the other exhibiting malignant features leading to the diagnosis of a poorly differentiated carcinoma metastatic to a sellar/suprasellar paraganglioma. The primary esophageal carcinoma was not uncovered until 2 months later, after the patient presented with upper gastrointestinal bleeding. The patient died 4 months after initial presentation. This case expands the spectrum of TTM, and emphasizes the importance of TTM in the practice of pathology.

scholarly journals RNF144A-AS1, a TGF-β1- and hypoxia-inducible gene that promotes tumor metastasis and proliferation via targeting the miR-30c-2-3p/LOX axis in gastric cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zengliang Li ◽  
Liang Shi ◽  
Xiangwei Li ◽  
Xiaopeng Wang ◽  
Haixiao Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Noncoding Rna ◽  
Tumor Metastasis ◽  
Cellular Localization ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Gene Set Enrichment Analysis ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Tgf Β1

Abstract Background Although recent molecular analyses have improved our knowledge regarding gastric cancer (GC) biology, the molecular mechanisms that confer metastatic potential to GC remain poorly understood. In this study, we intend to explore the function and characterize the underlying mechanism of long noncoding RNA RNF144A-AS1 in GC metastasis and outgrowth. Methods The expression of RNF144A-AS1, miR-30c-2-3p, and Lysyl oxidase (LOX) was detected by quantitative real-time PCR assay. Fluorescence in situ hybridization and subcellular fractionation assay determined the cellular localization of RNF144A-AS1. Cell counting kit 8 assay, transwell assay, and tube formation assay were performed to detect the effect on cell proliferation, migration, invasion, and angiogenesis, respectively. Animal models were also applied to verify the effect on tumor metastasis, outgrowth, and angiogenesis. Bioinformatic analysis, luciferase reporter assay, and RNA immunoprecipitation (RIP) assay explored the interactions among RNF144A-AS1, miR-30c-2-3p, and LOX. Gene regulation was further validated by knockdown of Dicer or mutating the miRNA binding sites on RNF144A-AS1 and LOX 3ʹUTR. Cells were treated with recombinant human TGF-β1 (Transforming Growth Factor β1) to explore the effect of TGF-β1 on RNF144A-AS1. Western blot and immunohistochemistry were used to detect protein expression. Results The expression of RNF144A-AS1 was significantly upregulated in GC tissues and was associated with poor prognosis and later-stage diseases. Hypoxia stimulated the expression of RNF144A-AS1 in a HIF-1α-independent manner. Additionally, RNF144A-AS1 was also induced by TGF-β1. Loss and gain of function assays revealed that RNF144A-AS1 promoted tumor metastasis, angiogenesis, and proliferation. Mechanism exploration indicated RNF144A-AS1 served as a microRNA decoy of miR-30c-2-3p to release LOX. Gene Set Enrichment Analysis further suggested LOX and RNF144A-AS1 were enriched in the same gene sets, emphasizing the internal mechanism connection between these two genes. Conclusions TGF-β1- and hypoxia-inducible RNF144A-AS1 promoted tumor metastasis, angiogenesis, and proliferation through targeting the miR-30c-2-3p/LOX axis in GC, highlighting the value of the RNF144A-AS1/miR-30c-2-3p/LOX axis in therapeutic interventions of GC.

Reduced expression of TMEM166 is associated with esophageal carcinoma and gastric cancer

2010 ◽  
Vol 34 (8) ◽  
pp. S54-S54
Author(s):  
Dong Xu ◽  
Ying Chang ◽  
Huiying He ◽  
Yingyu Chen
Keyword(s):  
Gastric Cancer ◽  
Esophageal Carcinoma

Thrombin induced TGF-β1 pathway: a cause of communicating hydrocephalus post subarachnoid hemorrhage

2010 ◽  
Vol 34 (8) ◽  
pp. S19-S19
Author(s):  
Tong Li ◽  
Peng Zhang ◽  
Bin Yuan ◽  
Dongliang Zhao ◽  
Yueqin Chen ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Communicating Hydrocephalus ◽  
Tgf Β1

Genomic alterations of micrometastatic tumor cells in patients with operable esophageal carcinoma

2001 ◽  
Vol 120 (5) ◽  
pp. A344-A344
Author(s):  
N STOECKLEIN ◽  
M PETRONIO ◽  
T BLANKENSTEIN ◽  
S HOSCH ◽  
A ERBERSDOBLER ◽  
...  
Keyword(s):  
Esophageal Carcinoma ◽  
Tumor Cells ◽  
Genomic Alterations
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