Acetylshikonin Inhibits Human Pancreatic PANC-1 Cancer Cell Proliferation by Suppressing the NF-kappaB Activity.
10.4062/biomolther.2015.102
- Author:
Seok Cheol CHO
1
;
Bu Young CHOI
Author Information
1. Department of Food Science & Engineering, Seowon University, Cheongju 361-742, Republic of Korea.
- Publication Type:Original Article
- Keywords:
Acetylshikonin;
Phorbol 12-myristate 13-acetate;
Tumor necrosis-alpha;
NF-kappaB;
Matrix metalloproteinase;
Pancreatic cancer
- MeSH:
Carcinogenesis;
Cell Line;
Cell Proliferation*;
Cytokines;
Humans*;
Inflammation;
NF-kappa B*;
Pancreatic Neoplasms;
Proteome
- From:Biomolecules & Therapeutics
2015;23(5):428-433
- CountryRepublic of Korea
- Language:English
-
Abstract:
Acetylshikonin, a natural naphthoquinone derivative compound, has been used for treatment of inflammation and cancer. In the present study, we have investigated whether acetylshikonin could regulate the NF-kappaB signaling pathway, thereby leading to suppression of tumorigenesis. We observed that acetylshikonin significantly reduced proliferation of several cancer cell lines, including human pancreatic PANC-1 cancer cells. In addition, acetylshikonin inhibited phorbol 12-myristate 13-acetate (PMA) or tumor necrosis-alpha (TNF-alpha)-induced NF-kappaB reporter activity. Proteome cytokine array and real-time RT-PCR results illustrated that acetylshikonin inhibition of PMA-induced production of cytokines was mediated at the transcriptional level and it was associated with suppression of NF-kappaB activity and matrix metalloprotenases. Finally, we observed that an exposure of acetylshikonin significantly inhibited the anchorage-independent growth of PANC-1 cells. Together, our results indicate that acetylshikonin could serve as a promising therapeutic agent for future treatment of pancreatic cancer.