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Depletion of Jab1 inhibits proliferation of pancreatic cancer cell lines
Author(s) -
Fukumoto Akihisa,
Tomoda Kiichiro,
Yoneda-Kato Noriko,
Nakajima Yoshiyuki,
Kato Jun-ya
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.09.042
Subject(s) - gene knockdown , pancreatic cancer , cell growth , cancer research , rna interference , cell culture , apoptosis , suppressor , cancer , biology , microbiology and biotechnology , cancer cell , small interfering rna , chemistry , rna , transfection , gene , biochemistry , genetics
Jab1 overexpression is observed in many human cancers, but its physiological significance remains to be investigated. We reduced the level of Jab1 expression in pancreatic cancer cell lines, MIA PaCa‐2 and PANC‐1 by the RNA interference and found that Jab1‐knockdown resulted in impaired cell proliferation and enhanced apoptosis regardless of the genotype of the tumor suppressor p53. This growth inhibition was rescued by the introduction of siRNA‐resistant mouse Jab1 cDNA. Jab1‐knocked‐down cells expressed a higher level of c‐myc, and additional depletion of c‐myc rescued cells from Jab1‐knockdown‐mediated growth suppression. Thus, Jab1 overexpression contributes to pancreatic cancer cell proliferation and survival. Jab1 could be a novel target in cancer therapy.