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.
Anticancer Drugs. 2014 Mar;25(3):296-302. doi: 10.1097/CAD.0000000000000044.
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.
胰腺癌在全球范围内的平均生存率非常低。只有少数几种化疗药物,包括吉西他滨,已被证明能改善胰腺癌患者的生存率。染料木黄酮,一种异黄酮,已知对多种癌症类型具有抗癌作用。在这项研究中,我们研究了染料木黄酮对胰腺癌细胞的抗癌特性。使用 MTT、流式细胞术和集落形成实验分析染料木黄酮对细胞存活、细胞凋亡和增殖的影响。使用 Western blot 分析确定染料木黄酮对胰腺癌细胞有丝分裂信号的影响。迁移实验和酶谱分析用于确定染料木黄酮对胰腺癌进展的影响。染料木黄酮对胰腺癌细胞(Panc1 和 AsPC-1)产生剂量依赖性毒性。它降低了 Panc1 细胞的集落形成能力,并诱导了剂量依赖性的细胞凋亡。Akt 和 MAPK 的激活受到抑制。此外,癌细胞的迁移和侵袭能力也降低了。结果表明,染料木黄酮通过抑制增殖和诱导细胞凋亡来有效减少胰腺癌细胞的存活。它影响参与癌症进展的有丝分裂、迁移和侵袭过程。这些发现可能为使用异黄酮与其他治疗药物联合治疗胰腺癌提供新的方法。