کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10803186 | 1055801 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Rapid inhibition of MAPK signaling and anti-proliferation effect via JAK/STAT signaling by interferon-α in hepatocellular carcinoma cell lines
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Rapid inhibition of MAPK signaling and anti-proliferation effect via JAK/STAT signaling by interferon-α in hepatocellular carcinoma cell lines Rapid inhibition of MAPK signaling and anti-proliferation effect via JAK/STAT signaling by interferon-α in hepatocellular carcinoma cell lines](/preview/png/10803186.png)
چکیده انگلیسی
The potential anti-proliferation effect of interferon-alpha (IFN-α) against hepatocellular carcinoma (HCC) and its growth inhibitory mechanisms remain unclear. We examined four human HCC cell lines and every cell line had the anti-proliferative effect of IFN-α. The PLC/PRF/5 cell line, which expressed the IFN receptor most abundantly, responded most effectively to IFN-α stimulation. Here, we delineate the anti-proliferative effect of IFN-α via the MAPK pathway in human HCC cell lines. IFN-α retarded G1/S transition with no evidence of apoptosis and inhibited cell proliferation. IFN-α diminished the phosphorylation of both extracellular signal-regulated kinase (ERK) and mitogen-activated ERK-regulating kinase (MEK), but not Raf, within 5 min. Knockdown of signal transducers of activation and transcription1 (STAT1) or Janus kinase1 (JAK1) suppressed the reduction of phosphorylation both of ERK and MEK and diminished the growth inhibition by IFN-α. These results suggest that IFN-α induces anti-proliferative signaling via the JAK/STAT pathway downstream of IFN-α receptors and may reduce the growth stimulation signaling by cross-talk with the MEK/ERK pathway without IFN-α-induced transcription.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1745, Issue 3, 30 September 2005, Pages 401-410
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1745, Issue 3, 30 September 2005, Pages 401-410
نویسندگان
Kentaro Inamura, Yasushi Matsuzaki, Naoya Uematsu, Akira Honda, Naomi Tanaka, Kazuhiko Uchida,