Newsgroup: it.salute
Titolo: Pubblicità - Capsaicin induced apoptosis in colon cancer cells

Capsaicin induces apoptosis by generating reactive oxygen species and 
disrupting mitochondrial transmembrane potential in human colon cancer cell 
lines.
Yang KM, Pyo JO, Kim GY, Yu R, Han IS, Ju SA, Kim WH, Kim BS.
Cell Mol Biol Lett. 2009 Apr 16
Department of Internal Medicine, Institute of Gastroenterology, Brain Korea 
21 for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Although genetic factors are a well-known cause of colorectal cancer, 
environmental factors contribute more to its development. Despite advances 
in the fields of surgery, radiotherapy and chemotherapy, the cure rates for 
colon cancer have not substantially improved over the past few decades. 
Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide), the principal pungent 
ingredient of hot chili pepper, has exhibited an anti-tumor effect in many 
cell types. However, the mechanisms responsible for the anti-tumor effect of 
capsaicin are not yet completely understood. In this study, we investigated 
whether capsaicin induces apoptosis in colon cancer cell lines. Capsaicin 
decreased cell viability in a dose-dependent manner in Colo320DM and LoVo 
cells. In addition, capsaicin produced cell morphology changes and DNA 
fragmentation, decreased the DNA contents, and induced phosphatidylserine 
translocation, which is a hallmark of apoptotic cell death. We showed that 
capsaicin-induced apoptosis is associated with an increase in ROS generation 
and a disruption of the mitochondrial transmenbrane potential. A possible 
mechanism of capsaicin-induced apoptosis is the activation of caspase 3, a 
major apoptosis-executing enzyme. Treatment with capsaicin induced a 
dramatic increase in caspase 3 activity, as assessed by the cleavage of 
Ac-DEVD-AMC, a fluorogenic substrate. In conclusion, our results clearly 
showed that capsaicin induced apoptosis in colon cancer cells. Although the 
actual mechanisms of capsaicin-induced apoptosis remain uncertain, it may be 
a beneficial agent for colon cancer treatment and chemoprevention.
PMID: 19381455 [PubMed - as supplied by publisher
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gg 

gg ha scritto:
 > Capsaicin induces apoptosis by generating reactive oxygen species
 > and disrupting mitochondrial transmembrane potential in human
 > colon cancer cell lines.
Allora vediamo chi ce l'ha più lungo...
 
http://www.ncbi.nlm.nih.gov/pubmed/18339878
  Cancer Res. 2008 Mar 15;68(6):1962-9.
  Diphenyl difluoroketone: a curcumin derivative
  with potent in vivo anticancer activity.
  Subramaniam D, May R, Sureban SM, Lee KB, George R, Kuppusamy P,
  Ramanujam RP, Hideg K, Dieckgraefe BK, Houchen CW, Anant S.
  Section of Digestive Diseases and Nutrition, Department of Medicine,
  University of Oklahoma Health Sciences Center, Oklahoma City,
  OK 73126, USA.
  Diphenyl difluoroketone (EF24), a molecule having structural similarity
  to curcumin, was reported to inhibit proliferation of a variety of
  cancer cells in vitro. However, the efficacy and in vivo mechanism
  of action of EF24 in gastrointestinal cancer cells have not been
  investigated. Here, we assessed the in vivo therapeutic effects of EF24
  on colon cancer cells. Using hexosaminidase assay, we determined that
  EF24 inhibits proliferation of HCT-116 and HT-29 colon and AGS gastric
  adenocarcinoma cells but not of mouse embryo fibroblasts. Furthermore,
  the cancer cells showed increased levels of activated caspase-3 and
  increased Bax to Bcl-2 and Bax to Bcl-xL ratios, suggesting that the
  cells were undergoing apoptosis. At the same time, cell cycle analysis
  showed that there was an increased number of cells in the G(2)-M phase.
  To determine the effects of EF24 in vivo, HCT-116 colon cancer
  xenografts were established in nude mice and EF24 was given i.p. EF24
  significantly suppressed the growth of colon cancer tumor xenografts.
  Immunostaining for CD31 showed that there was a lower number of
  microvessels in the EF24-treated animals coupled with decreased
  cyclooxygenase-2, interleukin-8, and vascular endothelial growth
  factor mRNA and protein expression. Western blot analyses also
  showed decreased AKT and extracellular signal-regulated kinase
  activation in the tumors. Taken together, these data suggest that
  the novel curcumin-related compound EF24 is a potent antitumor agent
  that induces caspase-mediated apoptosis during mitosis and has
  significant therapeutic potential for gastrointestinal cancers.
Full Text: 
http://cancerres.aacrjournals.org/cgi/reprint/68/6/1962.pdf
  "In conclusion, our studies show that EF24 treatment of intestinal
  cancer cells results in growth inhibition in vitro and in vivo.
  Our in vitro and in vivo studies in combination with the observation
  that EF24 does not affect proliferation of normal human fibroblasts
  strongly suggest that EF24 has promising potential for use
  as a therapeutic or chemopreventative agent for intestinal cancer.
  Similar to curcumin, EF24 also seems to have multiple molecular
  targets and its enhanced potency in cancer cell lines and xenograft
  tumors renders it a strong candidate for therapeutic applications
  for colon cancer as well as other cancers and inflammatory disease
  states."
Bye,
   *GB*