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Blood, Vol. 93 No. 4 (February 15), 1999:
pp. 1287-1298
Muc-1 Core Protein Is Expressed on Multiple Myeloma Cells and Is
Induced by Dexamethasone
Steven P. Treon,
Joseph A. Mollick,
Mitsuyoshi Urashima,
Gerrard Teoh,
Dharminder Chauhan,
Atsushi Ogata,
Noopur Raje,
Joseph H.M. Hilgers,
Lee Nadler,
Andrew R. Belch,
Linda M. Pilarski, and
Kenneth
C. Anderson
From the Department of Adult Oncology, Dana Farber Cancer Institute,
and Department of Medicine, Harvard Medical School, Boston, MA; the
Division of Hematology and Oncology, Massachusetts General Hospital,
Boston, MA; the Department of Haematology, Singapore General Hospital,
Singapore; the Academisch Ziekenhuis, Vrije Universiteit, Amsterdam,
The Netherlands; and the Cross Cancer Institute, University of Alberta,
Edmonton, Alberta, Canada.
Monoclonal antibodies (MoAbs) that selectively identify Muc-1 core
protein (MoAbs DF3-P, VU-4H5) determinants were used to identify the
Muc-1 glycoform present on 7 multiple myeloma (MM) cell lines, 5 MM
patient plasma cells, 12 MM patient B cells, as well as 32 non-MM cell
lines and normal hematopoietic cells. Flow cytometry studies
demonstrated that all MM cell lines, MM patient plasma cells, and MM
patient B cells expressed Muc-1 core protein epitopes. Circulating B
cells from 4 normal donors also expressed Muc-1 core protein. In
contrast, Muc-1 core protein was absent on 28 of 32 non-MM neoplastic
cell lines, 17 of which expressed Muc-1. Splenic and tonsillar B cells,
CD34+ stem cells, resting T cells, and bone marrow plasma
cells obtained from normal donors both lacked Muc-1 glycoforms. We next
studied the effects of estrogen, progesterone, and glucocorticoid
receptor agonists and antagonists on Muc-1 expression, because
consensus sequences for the response elements of these steroids are
present on the Muc-1 gene promoter. These studies showed that
dexamethasone (Dex) induced Muc-1 expression on MM cell lines, as
determined by both flow cytometry and Western blot analyses. Dex also
induced upregulation of Muc-1 on prostate and ovarian cancer cell
lines. Time and dose-response studies demonstrated that Dex induced
maximal cell surface Muc-1 expression by 24 hours at concentrations of 10 8 mol/L. Dex induced Muc-1 upregulation could be
blocked with a 10-fold excess of the glucocorticoid receptor antagonist
RU486, confirming that Dex was acting via the glucocorticoid receptor. No changes in Muc-1 expression were observed on MM cells treated with
estrogen and progesterone receptor agonists and antagonists or with
RU486. These studies provide the framework for targeting Muc-1 core
protein in vaccination and serotherapy trials in MM. In addition, the
finding that Muc-1 expression on MM cells can be augmented by Dex at
pharmacologically achievable levels suggests their potential utility in
enhancing treatments targeting Muc-1 in MM.
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