AA uptake by sodium dependent VCT2 trans. in placenta

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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, Follow #OWENRFONOROW at twitter

ofonorow
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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, Follow #OWENRFONOROW at twitter


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