Solanine Induces Mitochondria-Mediated Apoptosis in Human Pancreatic Cancer Cells
Author(s) -
Hongwei Sun,
Chongqing Lv,
Longlong Yang,
Yingxiu Wang,
Qingshun Zhang,
Suhui Yu,
Hongru Kong,
Meng Wang,
Jianming Xie,
Chunwu Zhang,
Mengtao Zhou
Publication year - 2014
Publication title -
biomed research international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 126
eISSN - 2314-6141
pISSN - 2314-6133
DOI - 10.1155/2014/805926
Subject(s) - apoptosis , cytochrome c , pancreatic cancer , mitochondrion , chemistry , in vitro , cytosol , in vivo , cancer cell , mitochondrial permeability transition pore , microbiology and biotechnology , caspase 9 , caspase , cancer research , biology , programmed cell death , biochemistry , cancer , enzyme , genetics
Steroid alkaloids have been suggested as potential anticancer compounds. However, the underlying mechanisms of how steroid alkaloids inhibit the tumor growth are largely unknown. Here, we reported that solanine, a substance of steroid alkaloids, has a positive effect on the inhibition of pancreatic cancer cell growth in vitro and in vivo. In pancreatic cancer cells and nu/nu nude mice model, we found that solanine inhibited cancer cells growth through caspase-3 dependent mitochondrial apoptosis. Mechanically, solanine promotes the opening of mitochondrial membrane permeability transition pore (MPTP) by downregulating the Bcl-2/Bax ratio; thereafter, Cytochrome c and Smac are released from mitochondria into cytosol to process the caspase-3 zymogen into an activated form. Moreover, we found that the expression of tumor metastasis related proteins, MMP-2 and MMP-9, was also decreased in the cells treated with solanine. Therefore, our results suggested that solanine was an effective compound for the treatment of pancreatic cancer.
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