Talk:Betulinic acid

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James A. Duke, Ph.D, a phytochemical botanist thinks that the best source of Betulinic Acid is the Winged Bean. If true, that should go into both "betulinic acid" and "winged bean". His database is at www.ars-grin.gov/duke. Skipper2 —Preceding unsigned comment added by Skipper2 (talk • contribs) 07:09, 16 September 2008 (UTC)

Hey, I skimmed the article and found this sentence to be untrue: “In contrast, epithelial tumors, such as breast carcinoma, colon carcinoma, small cell lung carcinoma and renal cell carcinoma as well as T-cell leukemia cells were completely unresponsive to treatment with betulinic acid.[9]” searching pubmed with search words "betulinic acid cancer" shows that BA is effective against several forms listed above. I do not want to change the article before someone else agrees with me that the above sentence is untrue. Probios (talk) 16:32, 23 July 2011 (UTC)

I agree with you, numerous studies have shown betulinic acid inhibits Specificity Protein numbers 1, 2, &4 on the membrane of cancer cell mitochondria in human cancer cell lines both in vitro and in vivo as follows:

Dehelean et al. Chemistry Central Journal 2012, 6:137 http://journal.chemistrycentral.com/content/6/1/137

Study of the betulin enriched birch bark extracts effects on human carcinoma cells and ear inflammation Cristina A Dehelean1, Codruţa Şoica1*, Ionuţ Ledeţi1, Mihaela Aluaş2, Istvan Zupko3, Atena Gǎluşcan4, Simona Cinta-Pinzaru2 and Melania Munteanu5

Abstract Background: Pentacyclic triterpenes, mainly betulin and betulinic acid, are valuable anticancer agents found in the bark of birch tree. This study evaluates birch bark extracts for the active principles composition.

Results: New improved extraction methods were applied on the bark of Betula pendula in order to reach the maximum content in active principles. Extracts were analyzed by HPLC-MS, Raman, SERS and 13C NMR spectroscopy which revealed a very high yield of betulin (over 90%). Growth inhibiting effects were measured in vitro on four malignant human cell lines: A431 (skin epidermoid carcinoma), A2780 (ovarian carcinoma), HeLa (cervix adenocarcinoma) and MCF7 (breast adenocarcinoma), by means of MTT assay. All of the prepared bark extracts exerted a pronounced antiproliferative effect against human cancer cell lines. In vivo studies involved the anti-inflammatory effect of birch extracts on TPA-induced model of inflammation in mice.

Conclusions: The research revealed the efficacy of the extraction procedures as well as the anti-proliferative and anti-inflammatory effects of birch extracts.

Chintharlapalli et al. BMC Cancer 2011, 11:371 http://www.biomedcentral.com/1471-2407/11/371

Betulinic acid inhibits colon cancer cell and tumor growth and induces proteasomedependent and -independent downregulation of specificity proteins (Sp) transcription factors Sudhakar Chintharlapalli1,3, Sabitha Papineni1,4, Ping Lei1, Satya Pathi2 and Stephen Safe2*

Abstract Background: Betulinic acid (BA) inhibits growth of several cancer cell lines and tumors and the effects of BA have been attributed to its mitochondriotoxicity and inhibition of multiple pro-oncogenic factors. Previous studies show that BA induces proteasome-dependent degradation of specificity protein (Sp) transcription factors Sp1, Sp3 and Sp4 in prostate cancer cells and this study focused on the mechanism of action of BA in colon cancer cells. Methods: The effects of BA on colon cancer cell proliferation and apoptosis and tumor growth in vivo were determined using standardized assays. The effects of BA on Sp proteins and Sp-regulated gene products were analyzed by western blots, and real time PCR was used to determine microRNA-27a (miR-27a) and ZBTB10 mRNA expression.

Results: BA inhibited growth and induced apoptosis in RKO and SW480 colon cancer cells and inhibited tumor growth in athymic nude mice bearing RKO cells as xenograft. BA also decreased expression of Sp1, Sp3 and Sp4 transcription factors which are over expressed in colon cancer cells and decreased levels of several Sp-regulated genes including survivin, vascular endothelial growth factor, p65 sub-unit of NF�B, epidermal growth factor receptor, cyclin D1, and pituitary tumor transforming gene-1. The mechanism of action of BA was dependent on cell context, since BA induced proteasome-dependent and proteasome-independent down regulation of Sp1, Sp3 and Sp4 in SW480 and RKO cells, respectively. In RKO cells, the mechanism of BA-induced repression of Sp1, Sp3 and Sp4 was due to induction of reactive oxygen species (ROS), ROS-mediated repression of microRNA-27a, and induction of the Sp repressor gene ZBTB10.

Conclusions: These results suggest that the anticancer activity of BA in colon cancer cells is due, in part, to down regulation of Sp1, Sp3 and Sp4 transcription factors; however, the mechanism of this response is cell context dependent. — Preceding unsigned comment added by Carl Godin (talk • contribs) 16:03, 31 May 2015 (UTC)