The STAT3 inhibitor NSC 74859 is effective in hepatocellular cancers with disrupted TGF-β signaling View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2009-01-12

AUTHORS

L Lin, R Amin, G I Gallicano, E Glasgow, W Jogunoori, J M Jessup, M Zasloff, J L Marshall, K Shetty, L Johnson, L Mishra, A R He

ABSTRACT

Hepatocellular carcinoma (HCC) is the third leading cause of cancer deaths worldwide, with few effective therapeutic options for advanced disease. At least 40% of HCCs are clonal, potentially arising from STAT3+, NANOG+ and OCT3/4+ liver progenitor/stem cell transformation, along with inactivation of transforming growth factor-beta (TGF-β) signaling. Here we report significantly greater signal transducer and activator of transcription 3 (STAT3) and tyrosine phosphorylated STAT3 in human HCC tissues (P<0.0030 and P<0.0455, respectively) than in human normal liver. Further, in HCC cells with loss of response to TGF-β, NSC 74859, a STAT3-specific inhibitor, markedly suppresses growth. In contrast, CD133+ status did not affect the response to STAT3 inhibition: both CD133+ Huh-7 cells and CD133– Huh-7 cells are equally sensitive to NSC 74859 treatment and STAT3 inhibition, with an IC50 of 100 μM. Thus, the TGF-β/beta2 spectrin (β2SP) pathway may reflect a more functional ‘stem/progenitor’ state than CD133. Furthermore, NSC 74859 treatment of Huh-7 xenografts in nude mice significantly retarded tumor growth, with an effective dose of only 5 mg/kg. Moreover, NSC 74859 inhibited tyrosine phosphorylation of STAT3 in HCC cells in vivo. We conclude that inhibiting interleukin 6 (IL6)/STAT3 in HCCs with inactivation of the TGF-β/β2SP pathway is an effective approach in management of HCCs. Thus, IL6/STAT3, a major signaling pathway in HCC stem cell renewal and proliferation, can provide a novel approach to the treatment of specific HCCs. More... »

PAGES

961-972

Journal

TITLE

Oncogene

ISSUE

7

VOLUME

28

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/onc.2008.448

    DOI

    http://dx.doi.org/10.1038/onc.2008.448

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1027217991

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/19137011


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