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Penelitian baru menyoroti regulasi sel induk kanker
Para peneliti mengidentifikasi molekul sinyal dalam sel induk usus yang dapat menyebabkan tumor jika dibiarkan tidak diatur . Temuan menunjukkan pendekatan baru untuk menargetkan kanker usus .....read more
New study sheds
light on cancer stem cell regulation
Date:
February 6, 2015
Source:
Sanford-Burnham
Medical Research Institute
Summary:
Researchers identify
signaling molecules in intestinal stem cells that can lead to tumors if left
unregulated. The findings suggest a new approach to targeting intestinal
cancers.
............................
researchers at
Sanford-Burnham Medical Research Institute (Sanford-Burnham) have discovered a
precise stem cell signaling process that can lead to intestinal tumors if
disrupted. The findings add to our understanding of how stem cells give rise to
tumors and identify specific stem cell molecules that may be targeted to
prevent the onset, progression, and recurrence of intestinal cancers. The
results of the study appear online inCell
Reports today.
"Accumulating evidence suggests that cancer stem cells are responsible
for cancer initiation, progression, metastasis, recurrence, and drug
resistance," said Jorge Moscat, Ph.D., program director of the Cell Death
and Survival Networks Program at Sanford-Burnham. "Our new research
provides a better understanding of the signaling cascades that regulate stem
cells and is essential for the design of new and more-efficacious therapies for
cancer."
"We have shown that protein kinase C-zeta (PKC-zeta) normally inhibits
stem cell activity through downregulation of two signaling pathways:
beta-catenin and Yap," said Maria Diaz-Meco, Ph.D., senior co-author of
the paper and professor in the Program. "Previously, our lab showed that
PKC-zeta acts as a tumor suppressor that maintains homeostasis of intestinal
stem cells. The current study reveals the mechanism by which this occurs."
The intestine is covered by a single layer of epithelial cells that are
renewed every 3 to 5 days. The pool of cells that replace these epithelial
cells--intestinal stem cells--needs to be regulated to maintain homeostasis.
"Disturbing the homeostasis of the stem cell pool can go two ways--it
can either reduce intestinal epithelial cell regeneration or increase the
proliferation of stem cells," said Diaz-Meco. "Cancer is produced by
the accumulation of mutations in critical genes that control central mechanisms
of cell growth. Stem cells are a 'permanent' population in the intestine and a
reservoir for those mutations. Therefore, if stem cell activity is increased,
as in the case of intestines deficient in PKC-zeta, then the likelihood of
developing tumors is much higher, and when the tumor is initiated it becomes
more aggressive."
Using a genetically engineered mouse model for intestinal cancer, the
research team found that this process is kept under control by direct
phosphorylation by PKC-zeta of two essential tumor promoters: beta-catenin and
Yap.
"Importantly, we confirmed the tumorigenic profiles of PKC-zeta,
beta-catenin, and Yap in human colon adenocarcinoma samples. The correlation of
human results with our in-vivo mouse studies strongly suggests that Yap and
beta-catenin are potential targets of PKC-zeta function and potential targets
for new anti-cancer therapies.
"Our results offer new possibilities for the prevention and treatment
of intestinal cancers by blocking the pathways that lead to tumors," said
Moscat. "They also highlight a new strategy to promote intestinal
regeneration after acute or chronic damage, such as that triggered by
chemotherapy and radiation."
Story Source:
The above story is based on materials provided by Sanford-Burnham
Medical Research Institute. Note: Materials may be edited for content and length.
Journal Reference:
1. Victoria Llado, Yuki Nakanishi, Angeles
Duran, Miguel Reina-Campos, Phillip M. Shelton, Juan F. Linares,
Tomoko Yajima, Alex Campos, Pedro Aza-Blanc, Michael Leitges, Maria T. Diaz-Meco,
Jorge Moscat. Repression of Intestinal Stem Cell Function and
Tumorigenesis through Direct Phosphorylation of β-Catenin and Yap by PKCζ. Cell
Reports, 2015; DOI: 10.1016/j.celrep.2015.01.007
