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Biochanin A reduces pancreatic cancer survival and progression.

Abstract
Pancreatic cancer has dismally low mean survival rates worldwide. Only a few chemotherapeutic agents including gemcitabine have been shown to improve the survival of pancreatic cancer patients. Biochanin A, an isoflavone, is known to exert an anticancer effect on various cancer types. In this study, we examined the anticancer properties of biochanin A on pancreatic cancer cells. The effect of biochanin A on cellular survival, apoptosis, and proliferation was analyzed using MTT, flow cytometry, and colony formation assay. The effect of biochanin A on pancreatic cancer's mitogenic signaling was determined using western blot analysis. Migration assay and zymography were used to determine biochanin A's effect on pancreatic cancer progression. Biochanin A induced dose-dependent toxicity on pancreatic cancer cells (Panc1 and AsPC-1). It reduced colony formation ability of Panc1 cells and induced dose-dependent apoptosis. Activation of Akt and MAPK was inhibited. Furthermore, the migratory and invasive potential of the cancer cells was also reduced. The results suggest that biochanin A is effective in reducing pancreatic cancer cell survival by inhibiting their proliferation and inducing apoptosis. It affects mitogenic, migratory, and invasive processes involved in cancer progression. These findings may lead to novel approaches to treat pancreatic cancer using isoflavones in combination with other therapeutic drugs.
AuthorsVikas Bhardwaj, Satya Murthy Tadinada, Aditi Jain, Vikas Sehdev, Christopher K Daniels, James C K Lai, Alok Bhushan
JournalAnti-cancer drugs (Anticancer Drugs) Vol. 25 Issue 3 Pg. 296-302 (Mar 2014) ISSN: 1473-5741 [Electronic] England
PMID24201306 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References
  • Antineoplastic Agents
  • Genistein
  • biochanin A
Topics
  • Antineoplastic Agents (pharmacology)
  • Apoptosis (drug effects)
  • Cell Line, Tumor (drug effects)
  • Cell Proliferation (drug effects)
  • Cell Survival (drug effects)
  • Genistein (pharmacology)
  • Humans
  • Neoplasm Invasiveness
  • Pancreatic Neoplasms (pathology)
  • Signal Transduction

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