Pancreatic cancer apoptosis linked to 3,3'-diindolylmethane - AnabolicMinds.com

Pancreatic cancer apoptosis linked to 3,3'-diindolylmethane

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    Post Pancreatic cancer apoptosis linked to 3,3'-diindolylmethane


    Pancreatic cancer apoptosis linked to 3,3'-diindolylmethane

    NewsRx.com

    05-23-06

    Pancreatic cancer apoptosis could be linked to 3,3'-diindolylmethane (DIM).

    According to recent research from the United States, "DIM, ring-substituted DIMs and 1,1-bis(3'-indolyl)-1-(p-substituted phenyl)methanes (C-DIMs) inhibit growth of Panc-1 and Panc-28 pancreatic cancer cells. Although DIMs (diarylmethanes) and selected C-DIMs (triarylmethanes), such as the p-t-butyl derivative (DIM-C-pPhtBu), activate the aryl hydrocarbon receptor and peroxisome proliferator-activated receptor gamma, respectively, this study shows that both DIM and DIM-C-pPhtBu induce common receptor-independent pathways."

    "Both DIM and DIM-C-pPhtBu increased endoplasmic reticulum (ER) staining and ER calcium release in Panc-1 cells, and this was accompanied by increased expression of glucose related protein 78 and C/EBP homologous transcription factor (CHOP/GADD153) proteins. Similar results were observed after treatment with thapsigargin (Tg), a prototypical inducer of ER stress. The subsequent downstream effects of DIM/DIM-C-pPhtBu- and Tg-induced ER stress included CHOP-dependent induction of death receptor DR5 and subsequent cleavage of caspase 8, caspase 3, Bid and PARP," explained M. Abdelrahim and colleagues, Texas A & M University.

    The researchers concluded, "Activation of both receptor-dependent and receptor-independent (ER stress) pathways by DIM and DIM-C-pPhtBu in pancreatic cancer cells enhances the efficacy and potential clinical importance of these compounds for cancer chemotherapeutic applications."

    Abdelrahim and colleagues published their study in Carcinogenesis (3,3'-diindolylmethane (DIM) and its derivatives induce apoptosis in pancreatic cancer cells through endoplasmic reticulum stress-dependent upregulation of DR5. Carcinogenesis, 2006;27(4):717-728).

    For additional information, contact S. Safe, Texas A & M University, Dept. Vet. Physiol & Pharmacology, 4466 TAMU, College Station, TX 77843, USA.

    Publisher contact information for the journal Carcinogenesis is: Oxford University Press, Great Clarendon St., Oxford OX2 6DP, England.

    Keywords: College Station, Texas, United States, Apoptosis, Carcinogenesis, Gastroenterology, Oncology, Pancreas, Pancreatic Cancer, Pancreatic Carcinoma, Cancer Therapy. This article was prepared by Biotech Week editors from staff and other reports. Copyright 2006, Biotech Week via NewsRx.com.

    To see more of the NewsRx.com, or to subscribe, go to http://www.newsrx.com.

  2. Tiberius's Avatar
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    Kickass! I was wondering what causes activation of the aryl hydrocarbon receptor and peroxisome proliferator-activated receptor gamma!
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    Quote Originally Posted by yeahright View Post
    Pancreatic cancer apoptosis linked to 3,3'-diindolylmethane

    NewsRx.com

    05-23-06

    Pancreatic cancer apoptosis could be linked to 3,3'-diindolylmethane (DIM).

    According to recent research from the United States, "DIM, ring-substituted DIMs and 1,1-bis(3'-indolyl)-1-(p-substituted phenyl)methanes (C-DIMs) inhibit growth of Panc-1 and Panc-28 pancreatic cancer cells. Although DIMs (diarylmethanes) and selected C-DIMs (triarylmethanes), such as the p-t-butyl derivative (DIM-C-pPhtBu), activate the aryl hydrocarbon receptor and peroxisome proliferator-activated receptor gamma, respectively, this study shows that both DIM and DIM-C-pPhtBu induce common receptor-independent pathways."

    "Both DIM and DIM-C-pPhtBu increased endoplasmic reticulum (ER) staining and ER calcium release in Panc-1 cells, and this was accompanied by increased expression of glucose related protein 78 and C/EBP homologous transcription factor (CHOP/GADD153) proteins. Similar results were observed after treatment with thapsigargin (Tg), a prototypical inducer of ER stress. The subsequent downstream effects of DIM/DIM-C-pPhtBu- and Tg-induced ER stress included CHOP-dependent induction of death receptor DR5 and subsequent cleavage of caspase 8, caspase 3, Bid and PARP," explained M. Abdelrahim and colleagues, Texas A & M University.

    The researchers concluded, "Activation of both receptor-dependent and receptor-independent (ER stress) pathways by DIM and DIM-C-pPhtBu in pancreatic cancer cells enhances the efficacy and potential clinical importance of these compounds for cancer chemotherapeutic applications."

    Abdelrahim and colleagues published their study in Carcinogenesis (3,3'-diindolylmethane (DIM) and its derivatives induce apoptosis in pancreatic cancer cells through endoplasmic reticulum stress-dependent upregulation of DR5. Carcinogenesis, 2006;27(4):717-728).

    For additional information, contact S. Safe, Texas A & M University, Dept. Vet. Physiol & Pharmacology, 4466 TAMU, College Station, TX 77843, USA.

    Publisher contact information for the journal Carcinogenesis is: Oxford University Press, Great Clarendon St., Oxford OX2 6DP, England.

    Keywords: College Station, Texas, United States, Apoptosis, Carcinogenesis, Gastroenterology, Oncology, Pancreas, Pancreatic Cancer, Pancreatic Carcinoma, Cancer Therapy. This article was prepared by Biotech Week editors from staff and other reports. Copyright 2006, Biotech Week via NewsRx.com.

    To see more of the NewsRx.com, or to subscribe, go to http://www.newsrx.com.
    Bah... my issue here is that to many people will be closed minded and argue the importance of long term applications when they know it's not necessary. Now, honestly, considering the study, one would go as far as to assume that they will be testing this with different regions and maybe a variety of carcinogenic sites...
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