R.B.
06-14-2007, 02:53 AM
Another one for the EPA DHA possible risk reduction list.
This would also appear to link to pregnancy.
Telomerase are bits that protect genes from change, and connect to ageing, so damage to telomerase could equate in some circumstances to genetic damage etc. http://en.wikipedia.org/wiki/Telomerase
EPA and DHA may down regulate c-Myc which has a "pivotal role" in BC.
Something else I found a while ago and have just refound, and better realised its significance. I can see the wood even if the trees are a blur.
RB
Dual mechanisms for telomerase inhibition in DLD-1 human colorectal adenocarcinoma cells by polyunsaturated fatty acids
Takahiro Eitsuka A1, Kiyotaka Nakagawa A1, Teruo Miyazawa A1
http://iospress.metapress.com/app/home/contribution.asp?referrer=parent&backto=issue,5,83;journal,16,48;linkingpublication results,1:103144,1
Abstract:
Polyunsaturated fatty acids (PUFAs) have been reported to have antitumor activity. In this study, we have tested whether telomerase might be a target for the antitumor effect of fatty acids using DLD-1 colorectal adenocarcinoma cells. In a cell-free approach, fatty acids were added directly to cell lysates, and we confirmed that increasing fatty acid unsaturation correlates with increased inhibition of telomerase activity. Using a cell culture approach, DLD-1 cells were cultured with fatty acids. In a time and dose dependent manner, EPA and DHA suppressed cellular telomerase activity and the mRNAs encoding hTERT (human telomerase reverse transcriptase) and c-myc. Based on these observations, we suggest that PUFAs inhibit telomerase activity through dual mechanisms: direct inhibition of enzymatic activity and down regulation of hTERT, one of the telomerase components.
Knockdown of c-Myc expression by RNAi inhibits MCF-7 breast tumor cells growth in vitro and in vivo
http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=15743499
Abstracts
"Breast cancer is the leading cause of cancer death in women worldwide. Elevated expression of c-Myc is a frequent genetic abnormality seen in this malignancy.............c-Myc has a pivotal function in the development of breast cancer. Our data show that decreasing the c-Myc protein level in MCF-7 cells by RNAi could significantly inhibit tumor growth both in vitro and in vivo, and imply the therapeutic potential of RNAi on the treatment of breast cancer by targeting overexpression oncogenes such as c-myc, and c-myc might be a potential therapeutic target for human breast cancer. …………
c-Myc is believed to participate in most aspects of cellular function, including replication, growth, metabolism, differentiation, and apoptosis [2]…
This would also appear to link to pregnancy.
Telomerase are bits that protect genes from change, and connect to ageing, so damage to telomerase could equate in some circumstances to genetic damage etc. http://en.wikipedia.org/wiki/Telomerase
EPA and DHA may down regulate c-Myc which has a "pivotal role" in BC.
Something else I found a while ago and have just refound, and better realised its significance. I can see the wood even if the trees are a blur.
RB
Dual mechanisms for telomerase inhibition in DLD-1 human colorectal adenocarcinoma cells by polyunsaturated fatty acids
Takahiro Eitsuka A1, Kiyotaka Nakagawa A1, Teruo Miyazawa A1
http://iospress.metapress.com/app/home/contribution.asp?referrer=parent&backto=issue,5,83;journal,16,48;linkingpublication results,1:103144,1
Abstract:
Polyunsaturated fatty acids (PUFAs) have been reported to have antitumor activity. In this study, we have tested whether telomerase might be a target for the antitumor effect of fatty acids using DLD-1 colorectal adenocarcinoma cells. In a cell-free approach, fatty acids were added directly to cell lysates, and we confirmed that increasing fatty acid unsaturation correlates with increased inhibition of telomerase activity. Using a cell culture approach, DLD-1 cells were cultured with fatty acids. In a time and dose dependent manner, EPA and DHA suppressed cellular telomerase activity and the mRNAs encoding hTERT (human telomerase reverse transcriptase) and c-myc. Based on these observations, we suggest that PUFAs inhibit telomerase activity through dual mechanisms: direct inhibition of enzymatic activity and down regulation of hTERT, one of the telomerase components.
Knockdown of c-Myc expression by RNAi inhibits MCF-7 breast tumor cells growth in vitro and in vivo
http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=15743499
Abstracts
"Breast cancer is the leading cause of cancer death in women worldwide. Elevated expression of c-Myc is a frequent genetic abnormality seen in this malignancy.............c-Myc has a pivotal function in the development of breast cancer. Our data show that decreasing the c-Myc protein level in MCF-7 cells by RNAi could significantly inhibit tumor growth both in vitro and in vivo, and imply the therapeutic potential of RNAi on the treatment of breast cancer by targeting overexpression oncogenes such as c-myc, and c-myc might be a potential therapeutic target for human breast cancer. …………
c-Myc is believed to participate in most aspects of cellular function, including replication, growth, metabolism, differentiation, and apoptosis [2]…