title: 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.
authors.affiliation: aDepartment of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee bDepartment of Biological Sciences, University of Iowa, Iowa City, Iowa cDepartment of Molecular and Biomedical Pharmacology, University of Kentucky, Lexington, Kentucky dDepartment of Pharmaceutical Sciences, Long Island University, Brookville, New York eDepartment of Biomedical and Pharmaceutical Sciences, College of Pharmacy, Idaho State University, Pocatello, Idaho fDepartment of Pharmaceutical Sciences, Jefferson School of Pharmacy, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
authors.forename: Vikas
authors.initials: V
authors.lastname: Bhardwaj
authors.forename: Satya Murthy
authors.initials: SM
authors.lastname: Tadinada
authors.forename: Aditi
authors.initials: A
authors.lastname: Jain
authors.forename: Vikas
authors.initials: V
authors.lastname: Sehdev
authors.forename: Christopher K
authors.initials: CK
authors.lastname: Daniels
authors.forename: James C K
authors.initials: JC
authors.lastname: Lai
authors.forename: Alok
authors.initials: A
authors.lastname: Bhushan
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D045744:Cell Line, Tumor / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects*; D019833:Genistein / Q000494:pharmacology*; D006801:Humans; D009361:Neoplasm Invasiveness; D010190:Pancreatic Neoplasms / Q000473:pathology*; D015398:Signal Transduction
chemical_list: D000970:Antineoplastic Agents; D019833:Genistein; C004541:biochanin A