Induction of resistance to murine tumor development is associated with alterations in the glycosylation of blood serum proteins

Autoren

Donenko

DOI

10.3892/mmr_00000126

ISSN

1791-2997

Zeitschrift

Molecular Medicine Reports

Datum der Veröffentlichung

2009

Status

Published

Herausgeber

Spandidos Publications

Herausgeber URL

http://dx.doi.org/10.3892/mmr_00000126

Datum der Datenerfassung

2017

Titel

Induction of resistance to murine tumor development is associated with alterations in the glycosylation of blood serum proteins

Data source: Crossref

Abstract

The phenomenon of accelerated metastatic tumor growth following the removal of the primary tumor is a major reason for cancer relapse, caused by underlying mechanisms that are not as yet understood. We hypothesized that a growth-stimulating factor is produced by the tumor-bearing host. This assumption was confirmed by an experiment involving the removal of a primary tumor (ascitic and solid Ehrlich carcinoma cells) from C57B1/6 mice, after which accelerated proliferation was observed in the remaining tumor cells. Peripheral blood leukocytes (PBLCs), spleen leukocytes (SLCs) and peritoneal cells (PCs) were transferred from donor animals with their tumors removed to healthy animals, along with tumor cells. This procedure suppressed tumor growth in 20-40% of the recipient animals when PBLCs, SLCs or PCs were collected 6-8 h after the removal of the tumor. In a second experiment, PBLCs, SLCs or PCs were injected into the mice, and the tumor cells were inoculated 14 days later. Resistance to tumor development occurred within the same time frame (6-8 h) but was more pronounced (60-80%) than in the previous experiment. Ehrlich carcinoma cells affected the binding of FITC-labeled blood serum glycoproteins in a time-dependent manner. Mass spectrometry revealed that the spectrum of glycopeptides in blood serum taken from control mice differed from the spectra of glycopeptides obtained from mice 8-24 h after the removal of Ehrlich carcinoma cells. Comparable effects were also observed with Cloudman S91 melanoma. In conclusion, the inhibition of tumor growth mediated by donor cells (PBLCs, SLCs and PCs) transferred from operated donor animals to recipient animals indicates the existence of a tumor-regulating factor in blood serum. This phenomenon is associated with characteristic alterations in the glycosylation of blood serum proteins.

Addresses

N.N. Blokhin Russian Cancer Research Center, Russian Academy of Medical Sciences, Moscow 115478, Russia. fedor.donenko@gmail.com.

Autoren

FV Donenko
RK Ziganshin
SM Sitdikova
BS Amandzholov
MV Kiselevskii
T Efferth

DOI

10.3892/mmr_00000126

eISSN

1791-3004

Externe Identifier

PubMed Identifier: 21475855

Open access

false

ISSN

1791-2997

Ausgabe der Veröffentlichung

3

Zeitschrift

Molecular medicine reports

Sprache

eng

Medium

Print

Paginierung

487 - 495

Datum der Veröffentlichung

2009

Status

Published

Datum der Datenerfassung

2011

Titel

Induction of resistance to murine tumor development is associated with alterations in the glycosylation of blood serum proteins.

Sub types

Journal Article

Ausgabe der Zeitschrift

2

Data source: Europe PubMed Central

Abstract

The phenomenon of accelerated metastatic tumor growth following the removal of the primary tumor is a major reason for cancer relapse, caused by underlying mechanisms that are not as yet understood. We hypothesized that a growth-stimulating factor is produced by the tumor-bearing host. This assumption was confirmed by an experiment involving the removal of a primary tumor (ascitic and solid Ehrlich carcinoma cells) from C57B1/6 mice, after which accelerated proliferation was observed in the remaining tumor cells. Peripheral blood leukocytes (PBLCs), spleen leukocytes (SLCs) and peritoneal cells (PCs) were transferred from donor animals with their tumors removed to healthy animals, along with tumor cells. This procedure suppressed tumor growth in 20-40% of the recipient animals when PBLCs, SLCs or PCs were collected 6-8 h after the removal of the tumor. In a second experiment, PBLCs, SLCs or PCs were injected into the mice, and the tumor cells were inoculated 14 days later. Resistance to tumor development occurred within the same time frame (6-8 h) but was more pronounced (60-80%) than in the previous experiment. Ehrlich carcinoma cells affected the binding of FITC-labeled blood serum glycoproteins in a time-dependent manner. Mass spectrometry revealed that the spectrum of glycopeptides in blood serum taken from control mice differed from the spectra of glycopeptides obtained from mice 8-24 h after the removal of Ehrlich carcinoma cells. Comparable effects were also observed with Cloudman S91 melanoma. In conclusion, the inhibition of tumor growth mediated by donor cells (PBLCs, SLCs and PCs) transferred from operated donor animals to recipient animals indicates the existence of a tumor-regulating factor in blood serum. This phenomenon is associated with characteristic alterations in the glycosylation of blood serum proteins.

Autoren

FV Donenko
RK Ziganshin
SM Sitdikova
BS Amandzholov
MV Kiselevskii
T Efferth

Autoren-URL

https://www.ncbi.nlm.nih.gov/pubmed/21475855

DOI

10.3892/mmr_00000126

eISSN

1791-3004

Ausgabe der Veröffentlichung

3

Zeitschrift

Mol Med Rep

Sprache

eng

Country

Greece

Paginierung

487 - 495

Datum der Veröffentlichung

2009

Status

Published

Datum, an dem der Datensatz öffentlich gemacht wurde

2012

Titel

Induction of resistance to murine tumor development is associated with alterations in the glycosylation of blood serum proteins.

Sub types

Journal Article

Ausgabe der Zeitschrift

2

Data source: PubMed

Induction of resistance to murine tumor development is associated with alterations in the glycosylation of blood serum proteins

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