EMERYVILLE, Calif., Dec. 15, 2010 /PRNewswire/ — Bionovo, Inc.
(Nasdaq:
BNVI) today announced the publication of a study entitled
“CC3/TIP30 regulates metabolic adaptation of tumor cells to glucose
limitation” in the journal Cell Cycle. The study describes
the critical linkage between the expression of the protein
CC3/TIP30 in cancer cells and their ability to adapt and survive in
adverse conditions such as lack of glucose and other nutrients.
Lack of CC3/TIP30 in a variety of human tumors allows them to
resist the death signals created by metabolic stress encountered
during aggressive tumor growth and metastases. Absence of CC3/TIP30
thus contributes to the development of aggressive and metastatic
cancers.
“The research described in this publication is a result of a
long standing interest in the metabolic changes accompanying the
development of aggressive cancers. Metabolism has recently become
the focus of intense interest in the basic and translational cancer
research,” said Emma Shtivelman, Ph.D., Director of Cancer Research
at Bionovo. “We found that a previously discovered metastasis
suppressor CC3/TIP30 affects tumor cell metabolism in unexpected
ways. Expression of CC3/TIP30 is low or even absent in a variety of
advanced cancers. Our work shows that absence of CC3 contributes to
survival of tumor cells under adverse conditions such as lack of
nutrients. Tumor cells, in particular metastatic cells, frequently
encounter conditions of low glucose availability due to inadequate
blood supply. Absence of CC3 allows tumor cells to modify their
metabolic preferences and relinquish their dependence on glucose
for glycolytic energy production. Cells lacking CC3 adapt to low
glucose conditions by activating mitochondrial respiration and
oxidative phosphorylation, and continue to survive and proliferate.
Cells expressing CC3/TIP30 fail to adapt to limited availability
of
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