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Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells

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Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells. / Mehta, Kosha; Sharp, Paul.

In: Scientific Reports, Vol. 10, No. 1, 14.12.2020, p. 21926.

Research output: Contribution to journalArticlepeer-review

Harvard

Mehta, K & Sharp, P 2020, 'Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells', Scientific Reports, vol. 10, no. 1, pp. 21926. https://doi.org/10.1038/s41598-020-78348-5

APA

Mehta, K., & Sharp, P. (2020). Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells. Scientific Reports, 10(1), 21926. https://doi.org/10.1038/s41598-020-78348-5

Vancouver

Mehta K, Sharp P. Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells. Scientific Reports. 2020 Dec 14;10(1):21926. https://doi.org/10.1038/s41598-020-78348-5

Author

Mehta, Kosha ; Sharp, Paul. / Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells. In: Scientific Reports. 2020 ; Vol. 10, No. 1. pp. 21926.

Bibtex Download

@article{2639f25a9744412e8d96876151bef83b,
title = "Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells",
abstract = "Liver iron excess is observed in several chronic liver diseases and is associated with the development of hepatocellular carcinoma (HCC). However, apart from oxidative stress, other cellular mechanisms by which excess iron may mediate/increase HCC predisposition/progression are not known. HCC pathology involves epithelial to mesenchymal transition (EMT), the basis of cancer phenotype acquisition. Here, the effect of excess iron (holo-transferrin 0-2 g/L for 24 and 48 h) on EMT biomarkers in the liver-derived HepG2 cells was investigated. Holo-transferrin substantially increased intracellular iron. Unexpectedly, mRNA and protein expression of the epithelial marker E-cadherin either remained unaltered or increased. The mRNA and protein levels of metastasis marker N-cadherin and mesenchymal marker vimentin increased significantly. While the mRNA expression of EMT transcription factors SNAI1 and SNAI2 increased and decreased, respectively after 24 h, both factors increased after 48 h. The mRNA expression of TGF-β (EMT-inducer) showed no significant alterations. In conclusion, data showed direct link between iron and EMT. Iron elevated mesenchymal and metastatic biomarkers in HepG2 cells without concomitant decrement in the epithelial marker E-cadherin and altered the expression of the key EMT-mediating transcription factors. Such studies can help identify molecular targets to devise iron-related adjunctive therapies to ameliorate HCC pathophysiology.",
keywords = "Iron, Liver, epitheliam mesenchymal transition",
author = "Kosha Mehta and Paul Sharp",
year = "2020",
month = dec,
day = "14",
doi = "10.1038/s41598-020-78348-5",
language = "English",
volume = "10",
pages = "21926",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells

AU - Mehta, Kosha

AU - Sharp, Paul

PY - 2020/12/14

Y1 - 2020/12/14

N2 - Liver iron excess is observed in several chronic liver diseases and is associated with the development of hepatocellular carcinoma (HCC). However, apart from oxidative stress, other cellular mechanisms by which excess iron may mediate/increase HCC predisposition/progression are not known. HCC pathology involves epithelial to mesenchymal transition (EMT), the basis of cancer phenotype acquisition. Here, the effect of excess iron (holo-transferrin 0-2 g/L for 24 and 48 h) on EMT biomarkers in the liver-derived HepG2 cells was investigated. Holo-transferrin substantially increased intracellular iron. Unexpectedly, mRNA and protein expression of the epithelial marker E-cadherin either remained unaltered or increased. The mRNA and protein levels of metastasis marker N-cadherin and mesenchymal marker vimentin increased significantly. While the mRNA expression of EMT transcription factors SNAI1 and SNAI2 increased and decreased, respectively after 24 h, both factors increased after 48 h. The mRNA expression of TGF-β (EMT-inducer) showed no significant alterations. In conclusion, data showed direct link between iron and EMT. Iron elevated mesenchymal and metastatic biomarkers in HepG2 cells without concomitant decrement in the epithelial marker E-cadherin and altered the expression of the key EMT-mediating transcription factors. Such studies can help identify molecular targets to devise iron-related adjunctive therapies to ameliorate HCC pathophysiology.

AB - Liver iron excess is observed in several chronic liver diseases and is associated with the development of hepatocellular carcinoma (HCC). However, apart from oxidative stress, other cellular mechanisms by which excess iron may mediate/increase HCC predisposition/progression are not known. HCC pathology involves epithelial to mesenchymal transition (EMT), the basis of cancer phenotype acquisition. Here, the effect of excess iron (holo-transferrin 0-2 g/L for 24 and 48 h) on EMT biomarkers in the liver-derived HepG2 cells was investigated. Holo-transferrin substantially increased intracellular iron. Unexpectedly, mRNA and protein expression of the epithelial marker E-cadherin either remained unaltered or increased. The mRNA and protein levels of metastasis marker N-cadherin and mesenchymal marker vimentin increased significantly. While the mRNA expression of EMT transcription factors SNAI1 and SNAI2 increased and decreased, respectively after 24 h, both factors increased after 48 h. The mRNA expression of TGF-β (EMT-inducer) showed no significant alterations. In conclusion, data showed direct link between iron and EMT. Iron elevated mesenchymal and metastatic biomarkers in HepG2 cells without concomitant decrement in the epithelial marker E-cadherin and altered the expression of the key EMT-mediating transcription factors. Such studies can help identify molecular targets to devise iron-related adjunctive therapies to ameliorate HCC pathophysiology.

KW - Iron, Liver, epitheliam mesenchymal transition

UR - http://www.scopus.com/inward/record.url?scp=85098476299&partnerID=8YFLogxK

U2 - 10.1038/s41598-020-78348-5

DO - 10.1038/s41598-020-78348-5

M3 - Article

VL - 10

SP - 21926

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

ER -

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