AA uptake by sodium dependent VCT2 trans. in placenta

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ofonorow
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AA uptake by sodium dependent VCT2 trans. in placenta

Post Number:#1  Post by ofonorow » Sat Jul 14, 2012 4:48 am

http://www.ncbi.nlm.nih.gov/pubmed/22745243
Ascorbic Acid Uptaken by Sodium-Dependent Vitamin C Transporter 2 Induces βhCG Expression through Sp1 and TFAP2A Transcription Factors in Human Choriocarcinoma Cells.

Conclusions:The present study revealed the novel effects of AA on polypeptide hormone, βhCG, production and the potential mechanisms governing AA-induced βhCG expression, suggesting the potentially indispensable roles of AA in placental endocrine and pregnant maintenance.



This study caught my eye because if the Beard/Kelly/Gonazlez theory of cancer is correct, then aggressive cancers are essentially "undifferentiated" placentas.
Owen R. Fonorow, Orthomolecular Naturopath
My statements have not been evaluated by the Food and Drug Administration. Any product mentioned is not intended to diagnose, treat, cure or prevent any disease.”

ofonorow
Ascorbate Wizard
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Re: AA uptake by sodium dependent VCT2 trans. in placenta

Post Number:#2  Post by ofonorow » Mon Jul 16, 2012 2:09 am

Another connection between SDVCT2 proteins and vitamin C's effectiveness against cancer.

http://www.ncbi.nlm.nih.gov/pubmed/22665050
SVCT-2 in breast cancer acts as an indicator for L-ascorbate treatment.

L-ascorbate (L-ascorbic acid, vitamin C) clearly has an inhibitory effect on cancer cells. However, the mechanism underlying differential sensitivity of cancer cells from same tissue to L-ascorbate is yet to be clarified. Here, we demonstrate that L-ascorbate has a selective killing effect, which is influenced by sodium-dependent vitamin C transporter 2 (SVCT-2) in human breast cancer cells. Treatment of human breast cancer cells with L-ascorbate differentially induced cell death, dependent on the SVCT-2 protein level. Moreover, knockdown of endogenous SVCT-2 via RNA interference in breast cancer cells expressing high levels of the protein induced resistance to L-ascorbate treatment, whereas transfection with SVCT-2 expression plasmids led to enhanced L-ascorbate chemosensitivity. Surprisingly, tumor regression by L-ascorbate administration in mice bearing tumor cell xenograft also corresponded to the SVCT-2 protein level. Interestingly, SVCT-2 expression was absent or weak in normal tissues, but strongly detected in tumor samples obtained from breast cancer patients.

In addition, enhanced chemosensitivity to L-ascorbate occurred as a result of caspase-independent autophagy, which was mediated by beclin-1 and LC3 II. In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. These results suggest that functional SVCT-2 sensitizes breast cancer cells to autophagic damage by increasing the L-ascorbate concentration and intracellular ROS production and furthermore, SVCT-2 in breast cancer may act as an indicator for commencing L-ascorbate treatment.Oncogene advance online publication, 4 June 2012; doi:10.1038/onc.2012.176.


If I read the abstract correctly, NAC actually worked against Vitamin C in the "chemotherapeutic effect" of L-ascorbate.

The number of authors is interesting! Perhaps this is the way to get vitamin C science published and preserve your reputation/grants?
Owen R. Fonorow, Orthomolecular Naturopath
My statements have not been evaluated by the Food and Drug Administration. Any product mentioned is not intended to diagnose, treat, cure or prevent any disease.”


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