scholarly journals The essential role of TNIK gene amplification in gastric cancer growth

Oncogenesis ◽  
2014 ◽  
Vol 3 (2) ◽  
pp. e89-e89 ◽  
Author(s):  
D-H Yu ◽  
X Zhang ◽  
H Wang ◽  
L Zhang ◽  
H Chen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Gene Amplification ◽  
Essential Role ◽  
Cancer Growth

scholarly journals Erratum: The essential role of TNIK gene amplification in gastric cancer growth

Oncogenesis ◽  
2014 ◽  
Vol 3 (3) ◽  
pp. e93-e93 ◽  
Author(s):  
D-H Yu ◽  
X Zhang ◽  
H Wang ◽  
L Zhang ◽  
H Chen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Gene Amplification ◽  
Essential Role ◽  
Cancer Growth

Essential role of Her3 in two signaling transduction patterns: Her2/Her3 and MET/Her3 in proliferation of human gastric cancer

2014 ◽  
Vol 54 (12) ◽  
pp. 1700-1709 ◽  
Author(s):  
Chen Yun ◽  
Li Gang ◽  
Gu Rongmin ◽  
Wen Xu ◽  
Ming Xuezhi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Essential Role ◽  
Human Gastric Cancer ◽  
Signaling Transduction

scholarly journals Essential role of gastric gland mucin in preventing gastric cancer in mice

2012 ◽  
Vol 122 (3) ◽  
pp. 923-934 ◽  
Author(s):  
Fumitoshi Karasawa ◽  
Akira Shiota ◽  
Yukinobu Goso ◽  
Motohiro Kobayashi ◽  
Yoshiko Sato ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Essential Role ◽  
Gastric Gland

scholarly journals HOXA10 mediates epithelial-mesenchymal transition to promote gastric cancer metastasis partly via modulation of TGFB2/Smad/METTL3 signaling axis

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Chenlong Song ◽  
Chongzhi Zhou
Keyword(s):  
Gastric Cancer ◽  
Western Blot ◽  
Lung Metastasis ◽  
Essential Role ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Signaling Axis

Abstract Background Homeobox A10 (HOXA10) belongs to the HOX gene family, which plays an essential role in embryonic development and tumor progression. We previously demonstrated that HOXA10 was significantly upregulated in gastric cancer (GC) and promoted GC cell proliferation. This study was designed to investigate the role of HOXA10 in GC metastasis and explore the underlying mechanism. Methods Immunohistochemistry (IHC) was used to evaluate the expression of HOXA10 in GC. In vitro cell migration and invasion assays as well as in vivo mice metastatic models were utilized to investigate the effects of HOXA10 on GC metastasis. GSEA, western blot, qRT-PCR and confocal immunofluorescence experiments preliminarily analyzed the relationship between HOXA10 and EMT. ChIP-qPCR, dual-luciferase reporter (DLR), co-immunoprecipitation (CoIP), colorimetric m6A assay and mice lung metastasis rescue models were performed to explore the mechanism by which HOXA10 accelerated the EMT process in GC. Results In this study, we demonstrated HOXA10 was upregulated in GC patients and the difference was even more pronounced in patients with lymph node metastasis (LNM) than without. Functionally, HOXA10 promoted migration and invasion of GC cells in vitro and accelerated lung metastasis in vivo. EMT was an important mechanism responsible for HOXA10-involved metastasis. Mechanistically, we revealed HOXA10 enriched in the TGFB2 promoter region, promoted transcription, increased secretion, thus triggered the activation of TGFβ/Smad signaling with subsequent enhancement of Smad2/3 nuclear expression. Moreover, HOXA10 upregulation elevated m6A level and METTL3 expression in GC cells possible by regulating the TGFB2/Smad pathway. CoIP and ChIP-qPCR experiments demonstrated that Smad proteins played an important role in mediating METTL3 expression. Furthermore, we found HOXA10 and METTL3 were clinically relevant, and METTL3 was responsible for the HOXA10-mediated EMT process by performing rescue experiments with western blot and in vivo mice lung metastatic models. Conclusions Our findings indicated the essential role of the HOXA10/TGFB2/Smad/METTL3 signaling axis in GC progression and metastasis.

Extracellular matrix: the gatekeeper of tumor angiogenesis

2019 ◽  
Vol 47 (5) ◽  
pp. 1543-1555 ◽  
Author(s):  
Maurizio Mongiat ◽  
Simone Buraschi ◽  
Eva Andreuzzi ◽  
Thomas Neill ◽  
Renato V. Iozzo
Keyword(s):  
Extracellular Matrix ◽  
Tumor Angiogenesis ◽  
Signaling Cascades ◽  
Cancer Growth ◽  
Cell Behavior ◽  
Metastatic Progression ◽  
Surface Receptors ◽  
The Matrix ◽  
Multiple Signaling

Abstract The extracellular matrix is a network of secreted macromolecules that provides a harmonious meshwork for the growth and homeostatic development of organisms. It conveys multiple signaling cascades affecting specific surface receptors that impact cell behavior. During cancer growth, this bioactive meshwork is remodeled and enriched in newly formed blood vessels, which provide nutrients and oxygen to the growing tumor cells. Remodeling of the tumor microenvironment leads to the formation of bioactive fragments that may have a distinct function from their parent molecules, and the balance among these factors directly influence cell viability and metastatic progression. Indeed, the matrix acts as a gatekeeper by regulating the access of cancer cells to nutrients. Here, we will critically evaluate the role of selected matrix constituents in regulating tumor angiogenesis and provide up-to-date information concerning their primary mechanisms of action.

Sign in / Sign up

Export Citation Format

Share Document