Cancer Research Meeting Calendar  EMT and Cancer Progression and Treatment
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 51, 3633-3638, July 15, 1991]
© 1991 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Clerc, P.
Right arrow Articles by Vaysse, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Clerc, P.
Right arrow Articles by Vaysse, N.

Lipid-dependent Proliferation of Pancreatic Cancer Cell Lines1

Pascal Clerc, Nacira Bensaadi, Pascale Pradel, Agnès Estival, François Clemente2 and Nicole Vaysse

INSERM U 151, CHU Rangueil, Bat L 3, 31054 Toulouse Cedex, France

Capan 1, a human pancreatic cancer cell line, is routinely grown in 10% fetal calf serum (FCS). In order to characterize the factors needed for its proliferation, FCS was replaced by a synthetic serum (Ultroser G). For Capan 1 proliferation we found that Ultroser G was as efficient as FCS. A subfraction of Ultroser G containing insulin, transferrin, and lipids was found to be responsible for that response since a combination of these compounds reproduced the growth observed with 10% FCS. Lipids stimulated cell proliferation even in the absence of other factors. Other human (MIA PaCa 2, AsPC1, Panc 1) or rat (AR4-2J) pancreatic cancer cell lines tested proliferated in the reconstituted medium containing insulin (100 ng/ml), transferrin (100 µg/ml), fatty acid-free albumin (1 mg/ml), and bovine serum lipids (0.7%), as in 10% FCS. Furthermore, the growth of nonpancreatic cell lines (HT29, A431, CREF) was not enhanced by lipids. Lipoproteins were found to be involved in the mitogenic response of pancreatic cells to lipids, whereas phosphatidylcholine and fatty acids were either inefficient or inhibitors (MIA PaCa 2 and AR4-2J). Alkaline phosphatase and amylase content, differentiation markers for Capan 1 and AR4-2J cells, respectively, were not modified by the reconstituted medium. These data suggest that lipids, insulin, and transferrin are the essential factors for the proliferation of pancreatic cancer cell lines, reproducing the growth effect of 10% FCS. Moreover, in the absence of most of the seric growth factors, pancreatic cells remained differentiated.

1 This study was supported by grants from Fédération Nationale des Centres de Lutte contre le Cancer and from ARC (Grant 6165).

2 To whom requests for reprints should be addressed.

Received 11/ 5/90. Accepted 4/30/91.




This article has been cited by other articles:


Home page
Clin. Cancer Res.Home page
W.-G. Tong, X.-Z. Ding, R. Hennig, R. C. Witt, J. Standop, P. M. Pour, and T. E. Adrian
Leukotriene B4 Receptor Antagonist LY293111 Inhibits Proliferation and Induces Apoptosis in Human Pancreatic Cancer Cells
Clin. Cancer Res., October 1, 2002; 8(10): 3232 - 3242.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1991 by the American Association for Cancer Research.