Premium
Synergistic effect of Biochanin A on antiproliferative potential of Atorvastatin
Author(s) -
Tadinada Satya Murthy,
Lai James C.K.,
Bhushan Alok
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb519
Subject(s) - pancreatic cancer , medicine , cancer , biochanin a , atorvastatin , gemcitabine , population , docetaxel , cancer cell , cancer research , pharmacology , oncology , genistein , daidzein , environmental health
Pancreatic cancer, with its dismally low survival rate, is one of the most aggressive forms of cancer and is the fourth leading cause of cancer‐related deaths in the United States. Gemcitabine, the first line drug approved by the FDA has not been a huge therapeutic success because it improves the survival by just six months. Epidemiological studies implicated a role for dietary isoflavones in lower incidence of different cancers in the Asian population. Isoflavones such as genistein have been tested for their anti‐cancer potentials in different cancers. Primarily used in management of hyperlipidemia and cardiovascular diseases, statins have been documented to exert anti‐proliferative effects. We have therefore hypothesized a combination treatment with an isoflavone (i.e., biochanin A) and a statin (i.e., atorvastatin) exerts synergistic anti‐cancer effects on pancreatic cancer cells. Our ongoing studies have demonstrated that biochanin A and atorvastatin synergistically lowered survival of AsPC1 and MIAPaCa‐2 pancreatic cancer cells. Concomitant with lowering survival of these cancer cells, biochanin A and atorvastatin combination treatment also induced morphological changes (e.g., shape & cell rounding) in these cells. Our ongoing studies to elucidate signaling mechanisms underlying the combination treatment effects suggested that the PI3K/Akt pathway was unlikely to be implicated in the combination treatment‐induced death of pancreatic cancer cells. Thus, our findings may have therapeutic potential in the design of new combination therapy for pancreatic cancer. Grant support‐ INBRE Program, NIH Grant No. P20 RR016454, Mountain States Tumor and Medical Research Institute and University Research Committee, ISU grant.