High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells. / Topel, Hande; Bağırsakçı, Ezgi; Yılmaz, Yeliz; Güneş, Ayşim; Bağcı, Gülsün; Çömez, Dehan; Kahraman, Erkan; Korhan, Peyda; Atabey, Neşe.

In: Scientific Reports, Vol. 11, 11376, 2021.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Topel, H, Bağırsakçı, E, Yılmaz, Y, Güneş, A, Bağcı, G, Çömez, D, Kahraman, E, Korhan, P & Atabey, N 2021, 'High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells', Scientific Reports, vol. 11, 11376. https://doi.org/10.1038/s41598-021-89765-5

APA

Topel, H., Bağırsakçı, E., Yılmaz, Y., Güneş, A., Bağcı, G., Çömez, D., Kahraman, E., Korhan, P., & Atabey, N. (2021). High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells. Scientific Reports, 11, [11376]. https://doi.org/10.1038/s41598-021-89765-5

Vancouver

Topel H, Bağırsakçı E, Yılmaz Y, Güneş A, Bağcı G, Çömez D et al. High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells. Scientific Reports. 2021;11. 11376. https://doi.org/10.1038/s41598-021-89765-5

Author

Topel, Hande ; Bağırsakçı, Ezgi ; Yılmaz, Yeliz ; Güneş, Ayşim ; Bağcı, Gülsün ; Çömez, Dehan ; Kahraman, Erkan ; Korhan, Peyda ; Atabey, Neşe. / High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells. In: Scientific Reports. 2021 ; Vol. 11.

Bibtex

@article{2cc52903ca7e4b48ac1682325bfe0614,
title = "High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells",
abstract = "Hepatocellular carcinoma (HCC) is strongly associated with metabolic dysregulations/deregulations and hyperglycemia is a common metabolic disturbance in metabolic diseases. Hyperglycemia is defined to promote epithelial to mesenchymal transition (EMT) of cancer cells in various cancers but its molecular contribution to HCC progression and aggressiveness is relatively unclear. In this study, we analyzed the molecular mechanisms behind the hyperglycemia-induced EMT in HCC cell lines. Here, we report that high glucose promotes EMT through activating c-Met receptor tyrosine kinase via promoting its ligand-independent homodimerization. c-Met activation is critical for high glucose induced acquisition of mesenchymal phenotype, survival under high glucose stress and reprogramming of cellular metabolism by modulating glucose metabolism gene expression to promote aggressiveness in HCC cells. The crucial role of c-Met in high glucose induced EMT and aggressiveness may be the potential link between metabolic syndrome-related hepatocarcinogenesis and/or HCC progression. Considering c-Met inhibition in hyperglycemic patients would be an important complementary strategy for therapy that favors sensitization of HCC cells to therapeutics.",
keywords = "Carcinoma, Hepatocellular/genetics, Cell Line, Tumor, Cell Movement/drug effects, Dimerization, Epithelial-Mesenchymal Transition, Gene Expression Regulation, Neoplastic, Glucose/administration & dosage, Glycolysis, Humans, Liver Neoplasms/genetics, Neoplasm Invasiveness, Receptor Protein-Tyrosine Kinases/metabolism, Signal Transduction/drug effects",
author = "Hande Topel and Ezgi Bağırsak{\c c}ı and Yeliz Yılmaz and Ay{\c s}im G{\"u}ne{\c s} and G{\"u}ls{\"u}n Bağcı and Dehan {\c C}{\"o}mez and Erkan Kahraman and Peyda Korhan and Ne{\c s}e Atabey",
year = "2021",
doi = "10.1038/s41598-021-89765-5",
language = "English",
volume = "11",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells

AU - Topel, Hande

AU - Bağırsakçı, Ezgi

AU - Yılmaz, Yeliz

AU - Güneş, Ayşim

AU - Bağcı, Gülsün

AU - Çömez, Dehan

AU - Kahraman, Erkan

AU - Korhan, Peyda

AU - Atabey, Neşe

PY - 2021

Y1 - 2021

N2 - Hepatocellular carcinoma (HCC) is strongly associated with metabolic dysregulations/deregulations and hyperglycemia is a common metabolic disturbance in metabolic diseases. Hyperglycemia is defined to promote epithelial to mesenchymal transition (EMT) of cancer cells in various cancers but its molecular contribution to HCC progression and aggressiveness is relatively unclear. In this study, we analyzed the molecular mechanisms behind the hyperglycemia-induced EMT in HCC cell lines. Here, we report that high glucose promotes EMT through activating c-Met receptor tyrosine kinase via promoting its ligand-independent homodimerization. c-Met activation is critical for high glucose induced acquisition of mesenchymal phenotype, survival under high glucose stress and reprogramming of cellular metabolism by modulating glucose metabolism gene expression to promote aggressiveness in HCC cells. The crucial role of c-Met in high glucose induced EMT and aggressiveness may be the potential link between metabolic syndrome-related hepatocarcinogenesis and/or HCC progression. Considering c-Met inhibition in hyperglycemic patients would be an important complementary strategy for therapy that favors sensitization of HCC cells to therapeutics.

AB - Hepatocellular carcinoma (HCC) is strongly associated with metabolic dysregulations/deregulations and hyperglycemia is a common metabolic disturbance in metabolic diseases. Hyperglycemia is defined to promote epithelial to mesenchymal transition (EMT) of cancer cells in various cancers but its molecular contribution to HCC progression and aggressiveness is relatively unclear. In this study, we analyzed the molecular mechanisms behind the hyperglycemia-induced EMT in HCC cell lines. Here, we report that high glucose promotes EMT through activating c-Met receptor tyrosine kinase via promoting its ligand-independent homodimerization. c-Met activation is critical for high glucose induced acquisition of mesenchymal phenotype, survival under high glucose stress and reprogramming of cellular metabolism by modulating glucose metabolism gene expression to promote aggressiveness in HCC cells. The crucial role of c-Met in high glucose induced EMT and aggressiveness may be the potential link between metabolic syndrome-related hepatocarcinogenesis and/or HCC progression. Considering c-Met inhibition in hyperglycemic patients would be an important complementary strategy for therapy that favors sensitization of HCC cells to therapeutics.

KW - Carcinoma, Hepatocellular/genetics

KW - Cell Line, Tumor

KW - Cell Movement/drug effects

KW - Dimerization

KW - Epithelial-Mesenchymal Transition

KW - Gene Expression Regulation, Neoplastic

KW - Glucose/administration & dosage

KW - Glycolysis

KW - Humans

KW - Liver Neoplasms/genetics

KW - Neoplasm Invasiveness

KW - Receptor Protein-Tyrosine Kinases/metabolism

KW - Signal Transduction/drug effects

U2 - 10.1038/s41598-021-89765-5

DO - 10.1038/s41598-021-89765-5

M3 - Journal article

C2 - 34059694

VL - 11

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 11376

ER -

ID: 389913404