# C-MYC EXPRESSION AND APOPTOSIS IN A B CELL LINE

> **NIH NIH R01** · BOSTON UNIVERSITY MEDICAL CAMPUS · 1993 · $195,661

## Abstract

Apoptosis or programmed cell death (PCD) is a general mechanism of cell
suicide that has been implicated in tolerization of B lymphocytes.  For
example, treatment of the murine early B lymphoma WEHI 231 line, a model
for study of B cell tolerance, with an antiserum against its expressed
surface IgM, such as goat anti-mouse Ig (GaMIg) or anti-mu antisera,
inhibits its proliferation via apoptosis.  Oligosomal degradation of DNA
is detectable by 12 hours post-GaMIg treatment.  Recent evidence has
demonstrated that the expression of the nuclear proto-oncogene c-myc is
necessary for PCD, promoting apoptosis in a dose-dependent fashion.  Here
the role of c-myc in apoptosis will be explored using the WEHI 231 line
as model system.  The expression of c-myc in WEHI 231 cells and the
effects of apoptosis have been extensively characterized by ongoing work
from the PI's and other laboratories.  Treatment of WEHI 231 cells with
GaMIg results in an initial increase in expression of c-myc RNA of 5- to
10-fold by 1-2 hours, which is followed by a dramatic decline by 4-6
hours post-treatment.  The synthesis of c-myc protein parallels the early
changes in RNA levels; furthermore, the protein is transiently
hyperphosphorylated at 1 hour.  By 24 hours, mRNA and protein levels are
well below those observed in control cells.  A major site of control of
these changes in c-myc RNA expression is mediated at the transcription
level.  The increase in c-myc expression appears to be critical for
apoptosis.  For example, the PI's laboratory has recently shown that
treatment with an anti-delta antiserum of a WEHI 231 line stably
transfected with a delta heavy chain (WEHI 231-delta), which fails to
induce apoptosis, failed to induce c-myc protein levels, in contrast to
treatment with anti-mu serum.  Thus the aims of this proposal are to 1)
measure the effects of anti-Ig treatment on c-myc protein expression, and
2) characterize the transcription factors mediating the changes in c-myc
RNA levels; particular emphasis, will be placed on the nuclear factor
NF-KB, which the PI's laboratory has demonstrated plays a major role in
regulation of c-myc transcription.  Specifically, post-translational
modifications and association of c-myc with other cellular proteins will
be examined.  The biochemical nature and functional effects of changes in
expression of NF-KB, noted during apoptosis, will be measured.  Results
will be correlated with apoptosis through use of the WEHI 231-delta line.
These studies should provide important insights into the control of
apoptosis in lymphocytes, the development of B cell tolerance and the
role of the c-myc oncogene in these processes.

## Key facts

- **NIH application ID:** 3173903
- **Project number:** 2R01CA036355-09A2
- **Recipient organization:** BOSTON UNIVERSITY MEDICAL CAMPUS
- **SAM.gov UEI:** FBYMGMHW4X95
- **Principal Investigator:** GAIL E. SONENSHEIN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1993
- **Award amount:** $195,661
- **Award type:** 2
- **Project period:** 1984-01-01 → 1997-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3173903

## Citation

> US National Institutes of Health, RePORTER application 3173903, C-MYC EXPRESSION AND APOPTOSIS IN A B CELL LINE (2R01CA036355-09A2). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3173903. Licensed CC0.

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