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EVI1, a target gene for amplification at 3q26, antagonizes transforming growth factor-β-mediated growth inhibition in hepatocellular carcinoma.

Yasui K, Konishi C, Gen Y, Endo M, Dohi O, Tomie A, Kitaichi T, Yamada N, Iwai N, Nishikawa T, Yamaguchi K, Moriguchi M, Sumida Y, Mitsuyoshi H, Tanaka S, Arii S, Itoh Y - Cancer Sci. (2015)

Bottom Line: Knockdown of EVI1 resulted in increased induction of the cyclin-dependent kinase inhibitor p15(INK) (4B) by transforming growth factor (TGF)-β and decreased expression of c-Myc, cyclin D1, and phosphorylated Rb in TGF-β-treated cells.Consequently, knockdown of EVI1 led to reduced DNA synthesis and cell viability.Collectively, our results suggest that EVI1 is a probable target gene that acts as a driving force for the amplification at 3q26 in HCC and that the oncoprotein EVI1 antagonizes TGF-β-mediated growth inhibition of HCC cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kyoto, Japan.

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DNA copy number of EVI1 and mRNA levels of EVI1, MDS1–EVI1, and MDS1 in primary hepatocellular carcinoma (HCC) tumors. (a) DNA copy number of EVI1 in 66 primary HCC tumors and four normal peripheral blood lymphocytes was determined by quantitative PCR. $Primary tumors showing copy number gain. (b) Relative levels of EVI1, MDS1–EVI1, and MDS1 mRNA in paired tumor and non-tumor tissues from 36 patients with primary HCC.
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fig03: DNA copy number of EVI1 and mRNA levels of EVI1, MDS1–EVI1, and MDS1 in primary hepatocellular carcinoma (HCC) tumors. (a) DNA copy number of EVI1 in 66 primary HCC tumors and four normal peripheral blood lymphocytes was determined by quantitative PCR. $Primary tumors showing copy number gain. (b) Relative levels of EVI1, MDS1–EVI1, and MDS1 mRNA in paired tumor and non-tumor tissues from 36 patients with primary HCC.

Mentions: To determine whether the amplification of EVI1 that was observed in JHH-1 cells was relevant to primary human carcinomas, the copy number of EVI1 in primary HCC tumors was determined by quantitative PCR using a method similar to that used for the cell lines. A copy number gain of EVI1 was observed in 24 (36%) of the 66 tumors (Fig.3a).


EVI1, a target gene for amplification at 3q26, antagonizes transforming growth factor-β-mediated growth inhibition in hepatocellular carcinoma.

Yasui K, Konishi C, Gen Y, Endo M, Dohi O, Tomie A, Kitaichi T, Yamada N, Iwai N, Nishikawa T, Yamaguchi K, Moriguchi M, Sumida Y, Mitsuyoshi H, Tanaka S, Arii S, Itoh Y - Cancer Sci. (2015)

DNA copy number of EVI1 and mRNA levels of EVI1, MDS1–EVI1, and MDS1 in primary hepatocellular carcinoma (HCC) tumors. (a) DNA copy number of EVI1 in 66 primary HCC tumors and four normal peripheral blood lymphocytes was determined by quantitative PCR. $Primary tumors showing copy number gain. (b) Relative levels of EVI1, MDS1–EVI1, and MDS1 mRNA in paired tumor and non-tumor tissues from 36 patients with primary HCC.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4520646&req=5

fig03: DNA copy number of EVI1 and mRNA levels of EVI1, MDS1–EVI1, and MDS1 in primary hepatocellular carcinoma (HCC) tumors. (a) DNA copy number of EVI1 in 66 primary HCC tumors and four normal peripheral blood lymphocytes was determined by quantitative PCR. $Primary tumors showing copy number gain. (b) Relative levels of EVI1, MDS1–EVI1, and MDS1 mRNA in paired tumor and non-tumor tissues from 36 patients with primary HCC.
Mentions: To determine whether the amplification of EVI1 that was observed in JHH-1 cells was relevant to primary human carcinomas, the copy number of EVI1 in primary HCC tumors was determined by quantitative PCR using a method similar to that used for the cell lines. A copy number gain of EVI1 was observed in 24 (36%) of the 66 tumors (Fig.3a).

Bottom Line: Knockdown of EVI1 resulted in increased induction of the cyclin-dependent kinase inhibitor p15(INK) (4B) by transforming growth factor (TGF)-β and decreased expression of c-Myc, cyclin D1, and phosphorylated Rb in TGF-β-treated cells.Consequently, knockdown of EVI1 led to reduced DNA synthesis and cell viability.Collectively, our results suggest that EVI1 is a probable target gene that acts as a driving force for the amplification at 3q26 in HCC and that the oncoprotein EVI1 antagonizes TGF-β-mediated growth inhibition of HCC cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Show MeSH
Related in: MedlinePlus