# STUDIES OF REGULATION IN E.COLI EXTENDED TO LYMPHOMAS

> **NIH NIH R01** · SALK INSTITUTE FOR BIOLOGICAL STUDIES · 1988 · $331,010

## Abstract

The aim of our project remains to understand effects of glucocorticoid
hormones on gene expression.  We are investigating two responses:  the
lysis of T-lymphoma cells and the induction of fibronectin in a
fibrosarcoma cell line.

Our studies of glucocorticoid-induced lymphocytolysis have been done so far
with murine lymphoid cell lines.  In recent months we have extended our
work to the human acute lymphoblastic leukemic cell line CEM.  We have
examined the basis for glucocorticoid resistance in a subclone of that
line, CEM-C1, known to contain functional glucocorticoid receptor.
Treatment of CEM-C1 cells with the DNA-demethylating agent 5-aza-2'
deoxycytidine yielded glucocorticoid-sensitive subclones at high frequency
(approximately 10%).  This indicates that DNA methylation is responsible
for inactivating the expression of a "lytic" function required for
glucocorticoid-sensitivity in these cells.

We have followed up on our observation that glucocorticoids increase 10-\to
20-fold the rate of fibronectin biosynthesis in HT1080 fibrosarcoma cells.
Using a human fibronectin cDNA clone to probe Northern blots, we found that
this probe hybridizes with a high molecular weight mRNA from
dexamethasone-treated HT1080.  This mRNA is present at a much lower level
in untreated HT1080 cells and is undetectable in CEM cells, which do not
produce fibronectin.  By "slot" blot analysis of total cellular RNA, we
found a 16-\to 32-fold increase in fibronectin RNA level after hormone
treatment.  Moreover, this induction is inhibited by a glucocorticoid
antagonist, RU486.  This study demonstrates that the dexamethasone-induced
stimulation of fibronectin biosynthesis is the result of an increase in
accumulated fibronectin mRNA mediated by the glucocorticoid receptor.
Studies are currently in progress to examine whether this effect is due to
an increased rate of transcription.  (D)

## Key facts

- **NIH application ID:** 3173654
- **Project number:** 5R01CA036146-15
- **Recipient organization:** SALK INSTITUTE FOR BIOLOGICAL STUDIES
- **SAM.gov UEI:** NNJ6BMBTFGN5
- **Principal Investigator:** SUZANNE BOURGEOIS-COHN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $331,010
- **Award type:** 5
- **Project period:** 1978-12-01 → 1988-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3173654

## Citation

> US National Institutes of Health, RePORTER application 3173654, STUDIES OF REGULATION IN E.COLI EXTENDED TO LYMPHOMAS (5R01CA036146-15). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3173654. Licensed CC0.

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