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Inhibition of c-Myc by 10058-F4 Induces Growth Arrest and Chemosensitivity in Pancreatic Ductal Adenocarcinoma

Inhibition of c-Myc by 10058-F4 Induces Growth Arrest and Chemosensitivity in Pancreatic Ductal Adenocarcinoma

Meng Zhang, Hai-Yan Fan, Sheng-Chao Li

Biomed Pharmacother. 2015 Jul;73:123-8.

PMID: 26211592

Abstract:

Pancreatic ductal adenocarcinoma (PDAC) is a formidable medical challenge due to its malignancies and the absence of effective treatment. c-Myc, as an important transcription factor, plays crucial roles in cell cycle progression, apoptosis and cellular transformation. The c-Myc inhibitor, 10058-F4, has been reported act as a tumor suppressor in several different tumors. In current study, the tumor-suppressive roles of 10058-F4 was observed in human pancreatic cancer cells in vitro as demonstrated by decreased cell viability, cell cycle arrest at the G1/S transition and increased caspase3/7 activity. And tumor responses to gemcitabine were also significantly enhanced by 10058-F4 in PANC-1 and SW1990 cells. In a subcutaneous xenograft model, however, 10058-F4 showed no significant influence on pancreatic tumorigenesis. When combined with gemcitabine, tumorigenesis was drastically attenuated compared with gemcitabine group or 10058-F4 group; this synergistic effect was accompanied with decreased PCNA-positive cells and reduced TUNEL-positive cells in the combined treated group. Subsequent studies revealed that decreased glycolysis may be involved in the inhibitory effect of 10058-F4 on PDAC. Taken together, this study demonstrates the roles of 10058-F4 in PDAC and provides evidence that 10058-F4 in combination with gemcitabine showed significant clinical benefit over the usage of gemcitabine alone.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP403811552-A	10058-F4		403811-55-2	Price

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