Cargando…
Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells
Albumin is the most abundant plasma protein and functions as a transport molecule that continuously interacts with various cell types. Because of these properties, albumin has been exploited by the pharmaceutical industry to improve drug delivery into target cells. The immediate effects of albumin o...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
PeerJ Inc.
2020
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060934/ https://www.ncbi.nlm.nih.gov/pubmed/32185103 http://dx.doi.org/10.7717/peerj.8568 |
_version_ | 1783504316591505408 |
---|---|
author | Ibrahim, Badr Stange, Jan Dominik, Adrian Sauer, Martin Doss, Sandra Eggert, Martin |
author_facet | Ibrahim, Badr Stange, Jan Dominik, Adrian Sauer, Martin Doss, Sandra Eggert, Martin |
author_sort | Ibrahim, Badr |
collection | PubMed |
description | Albumin is the most abundant plasma protein and functions as a transport molecule that continuously interacts with various cell types. Because of these properties, albumin has been exploited by the pharmaceutical industry to improve drug delivery into target cells. The immediate effects of albumin on cells, however, require further understanding. The cell interacting properties and pharmaceutical applications of albumin incentivises continual research into the immediate effects of albumin on cells. The HepG2/C3A hepatocellular carcinoma cell line is used as a model for studying cancer pathology as well as liver biosynthesis and cellular responses to drugs. Here we investigated the direct effect of purified albumin on HepG2/C3A cell proliferation in the absence of serum, growth factors and other serum originating albumin bound molecules. We observed that the reduced cell counts in serum starved HepG2/C3A cultures were increased by the inclusion of albumin. Cell cycle analysis demonstrated that the percentage of cells in G1 phase during serum starvation was reduced from 86.4 ± 2.3% to 78.3 ± 3.2% by the inclusion of albumin whereas the percentage of cells in S phase was increased from 6.5 ± 1.5% to 14.3 ± 3.6%. A significant reduction in the cell cycle inhibitor protein, P21, accompanied the changes in the proportions of cell cycle phases upon treatment with albumin. We have also observed that the levels of dead cells determined by DNA fragmentation and membrane permeabilization caused by serum starvation (TUNEL: 16.6 ± 7.2%, ethidium bromide: 13.8 ± 4.8%) were not significantly altered by the inclusion of albumin (11.6 ± 10.2%, ethidium bromide: 16.9 ± 8.9%). Therefore, the increase in cell number was mainly caused by albumin promoting proliferation rather than protection against cell death. These primary findings demonstrate that albumin has immediate effects on HepG2/C3A hepatocellular carcinoma cells. These effects should be taken into consideration when studying the effects of albumin bound drugs or pathological ligands bound to albumin on HepG2/C3A cells. |
format | Online Article Text |
id | pubmed-7060934 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | PeerJ Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-70609342020-03-17 Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells Ibrahim, Badr Stange, Jan Dominik, Adrian Sauer, Martin Doss, Sandra Eggert, Martin PeerJ Biochemistry Albumin is the most abundant plasma protein and functions as a transport molecule that continuously interacts with various cell types. Because of these properties, albumin has been exploited by the pharmaceutical industry to improve drug delivery into target cells. The immediate effects of albumin on cells, however, require further understanding. The cell interacting properties and pharmaceutical applications of albumin incentivises continual research into the immediate effects of albumin on cells. The HepG2/C3A hepatocellular carcinoma cell line is used as a model for studying cancer pathology as well as liver biosynthesis and cellular responses to drugs. Here we investigated the direct effect of purified albumin on HepG2/C3A cell proliferation in the absence of serum, growth factors and other serum originating albumin bound molecules. We observed that the reduced cell counts in serum starved HepG2/C3A cultures were increased by the inclusion of albumin. Cell cycle analysis demonstrated that the percentage of cells in G1 phase during serum starvation was reduced from 86.4 ± 2.3% to 78.3 ± 3.2% by the inclusion of albumin whereas the percentage of cells in S phase was increased from 6.5 ± 1.5% to 14.3 ± 3.6%. A significant reduction in the cell cycle inhibitor protein, P21, accompanied the changes in the proportions of cell cycle phases upon treatment with albumin. We have also observed that the levels of dead cells determined by DNA fragmentation and membrane permeabilization caused by serum starvation (TUNEL: 16.6 ± 7.2%, ethidium bromide: 13.8 ± 4.8%) were not significantly altered by the inclusion of albumin (11.6 ± 10.2%, ethidium bromide: 16.9 ± 8.9%). Therefore, the increase in cell number was mainly caused by albumin promoting proliferation rather than protection against cell death. These primary findings demonstrate that albumin has immediate effects on HepG2/C3A hepatocellular carcinoma cells. These effects should be taken into consideration when studying the effects of albumin bound drugs or pathological ligands bound to albumin on HepG2/C3A cells. PeerJ Inc. 2020-03-05 /pmc/articles/PMC7060934/ /pubmed/32185103 http://dx.doi.org/10.7717/peerj.8568 Text en ©2020 Ibrahim et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited. |
spellingShingle | Biochemistry Ibrahim, Badr Stange, Jan Dominik, Adrian Sauer, Martin Doss, Sandra Eggert, Martin Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells |
title | Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells |
title_full | Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells |
title_fullStr | Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells |
title_full_unstemmed | Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells |
title_short | Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells |
title_sort | albumin promotes proliferation of g1 arrested serum starved hepatocellular carcinoma cells |
topic | Biochemistry |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060934/ https://www.ncbi.nlm.nih.gov/pubmed/32185103 http://dx.doi.org/10.7717/peerj.8568 |
work_keys_str_mv | AT ibrahimbadr albuminpromotesproliferationofg1arrestedserumstarvedhepatocellularcarcinomacells AT stangejan albuminpromotesproliferationofg1arrestedserumstarvedhepatocellularcarcinomacells AT dominikadrian albuminpromotesproliferationofg1arrestedserumstarvedhepatocellularcarcinomacells AT sauermartin albuminpromotesproliferationofg1arrestedserumstarvedhepatocellularcarcinomacells AT dosssandra albuminpromotesproliferationofg1arrestedserumstarvedhepatocellularcarcinomacells AT eggertmartin albuminpromotesproliferationofg1arrestedserumstarvedhepatocellularcarcinomacells |