Biochanin A reduces pancreatic cancer survival and progression

被引:35
作者
Bhardwaj, Vikas [1 ]
Tadinada, Satya Murthy [2 ]
Jain, Aditi [3 ]
Sehdev, Vikas [4 ]
Daniels, Christopher K. [5 ]
Lai, James C. K. [5 ]
Bhushan, Alok [6 ]
机构
[1] Vanderbilt Univ, Dept Surg, Med Ctr, Nashville, TN 37240 USA
[2] Univ Iowa, Dept Biol Sci, Iowa City, IA USA
[3] Univ Kentucky, Dept Mol & Biomed Pharmacol, Lexington, KY USA
[4] Long Isl Univ, Dept Pharmaceut Sci, Brookville, NY USA
[5] Idaho State Univ, Coll Pharm, Dept Biomed & Pharmaceut Sci, Pocatello, ID 83209 USA
[6] Thomas Jefferson Univ, Jefferson Sch Pharm, Dept Pharmaceut Sci, Philadelphia, PA 19107 USA
关键词
biochanin A; epidermal growth factor receptor; pancreatic cancer; GROWTH-FACTOR RECEPTOR; IN-VITRO; EPIDEMIOLOGY; EFFICACY; CELLS; RISK;
D O I
10.1097/CAD.0000000000000044
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:296 / 302
页数:7
相关论文
共 34 条
[1]   HEPARIN-BINDING EGF-LIKE GROWTH-FACTOR - CHARACTERIZATION OF RAT AND MOUSE CDNA CLONES, PROTEIN DOMAIN CONSERVATION ACROSS SPECIES, AND TRANSCRIPT EXPRESSION IN TISSUES [J].
ABRAHAM, JA ;
DAMM, D ;
BAJARDI, A ;
MILLER, J ;
KLAGSBRUN, M ;
EZEKOWITZ, RAB .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1993, 190 (01) :125-133
[2]  
[Anonymous], J ONCOL
[3]   A CASE-CONTROL STUDY OF DIET AND CANCER OF THE PANCREAS [J].
BAGHURST, PA ;
MCMICHAEL, AJ ;
SLAVOTINEK, AH ;
BAGHURST, KI ;
BOYLE, P ;
WALKER, AM .
AMERICAN JOURNAL OF EPIDEMIOLOGY, 1991, 134 (02) :167-179
[4]   Multi-targeted therapy of cancer by genistein [J].
Banerjee, Sanjeev ;
Li, Yiwei ;
Wang, Zhiwei ;
Sarkar, Fazlul H. .
CANCER LETTERS, 2008, 269 (02) :226-242
[5]   RETRACTED: In vitro and in vivo molecular evidence of genistein action in augmenting the efficacy of cisplatin in pancreatic cancer (Retracted article.See vol.139, pg.2145,2016) [J].
Banerjee, Sanjeev ;
Zhang, Yuxiang ;
Wang, Zhiwei ;
Che, Mingxin ;
Chiao, Paul J. ;
Abbruzzese, James L. ;
Sarkar, Fazlul H. .
INTERNATIONAL JOURNAL OF CANCER, 2007, 120 (04) :906-917
[6]  
Baselga J, 2002, ONCOLOGIST, V7, P2
[7]  
Bhardwaj V, 2010, ANTICANCER RES, V30, P743
[8]   EPIDEMIOLOGY OF PANCREAS CANCER (1988) [J].
BOYLE, P ;
HSIEH, CC ;
MAISONNEUVE, P ;
LAVECCHIA, C ;
MACFARLANE, GJ ;
WALKER, AM ;
TRICHOPOULOS, D .
INTERNATIONAL JOURNAL OF PANCREATOLOGY, 1989, 5 (04) :327-346
[9]   Recent Advances and Developments in Treatment Strategies Against Pancreatic Cancer [J].
Fryer, Rosemary A. ;
Galustian, Christine ;
Dalgelish, Angus G. .
CURRENT CLINICAL PHARMACOLOGY, 2009, 4 (02) :102-112
[10]  
Funatomi H, 1997, INT J CANCER, V72, P512, DOI 10.1002/(SICI)1097-0215(19970729)72:3<512::AID-IJC21>3.0.CO