Abstract：
:The transforming growth factor beta (TGFbeta) family of growth regulatory peptides plays an important role in the regulation of gastrointestinal epithelial cell homeostasis. Loss of growth inhibitory signalling by TGFbeta is common in the context of Ras-transformation and it has been hypothesized that loss of TGFbeta receptor II (TGFbetaRII) expression accounts for the emergence of TGFbeta resistance. Here we examine the functional significance of reduced TGFbetaRII expression in intestinal epithelial cells transformed by oncogenic Ras. TGFbeta-induced signalling events downstream of TGFbetaRII were examined in Ras-transformed RIE-1 cells (RIE-Ras) and compared to the parental RIE-1 line. RIE-Ras cells were resistant to growth inhibition by TGFbeta. Neither overexpression of TGFbetaRII in RIE-Ras cells nor expression of constitutively active TGFbetaRI restored sensitivity to TGFbeta. TGFbeta-mediated phosphorylation of Smad2 occurred in TGFbeta-resistant RIE-Ras cells, as well as other TGFbeta-resistant cells lines (HT-29, SW620) expressing low levels of TGFbetaRII. Nuclear translocation of Smad2 and Smad4 occurred equally in RIE-Ras and parental RIE cells. The activity of TIEG2, a TGFbeta-inducible SP1-like transcription factor, was reduced in RIE-Ras cells, implying that resistance in Ras-transformed RIE cells occurs by a transcriptional mechanism.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Jiang B,Zhang JS,Du J,Urrutia R,Barnard Jdoi
10.1016/s0898-6568(03)00010-xsubject
Has Abstractpub_date
2003-07-01 00:00:00pages
699-708issue
7eissn
0898-6568issn
1873-3913pii
S089865680300010Xjournal_volume
15pub_type
杂志文章abstract：:High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecologic cancer. Emerging evidence suggests that tumor-associated macrophages (TAMs) play an immunosuppressive role in the tumor microenvironment and promote tumor growth, angiogenesis, and metastasis in ovarian cancer. Therefore, targeting TAMs in pati...
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journal_title：Cellular signalling
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journal_title：Cellular signalling
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journal_title：Cellular signalling
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doi：10.1016/j.cellsig.2005.03.020
更新日期：2005-12-01 00:00:00
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journal_title：Cellular signalling
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journal_title：Cellular signalling
pub_type： 杂志文章
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更新日期：2016-01-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
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更新日期：2002-02-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/s0898-6568(01)00210-8
更新日期：2001-11-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2016.02.011
更新日期：2016-05-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章,评审
doi：10.1016/j.cellsig.2011.05.004
更新日期：2011-10-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2020.109692
更新日期：2020-09-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2010.10.017
更新日期：2011-02-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2014.02.003
更新日期：2014-06-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/0898-6568(95)00002-7
更新日期：1995-05-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
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更新日期：2019-01-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2014.09.017
更新日期：2014-12-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
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更新日期：2015-06-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
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更新日期：2003-01-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2005.08.020
更新日期：2006-07-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/0898-6568(95)00010-m
更新日期：1995-05-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2005.08.019
更新日期：2006-07-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2005.09.010
更新日期：2006-08-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章,评审
doi：10.1016/s0898-6568(99)00086-8
更新日期：2000-03-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2014.12.004
更新日期：2015-03-01 00:00:00
abstract：:The possible involvement of zeta isozyme of protein kinase C (PKC zeta) in phorbol ester-induced signal transduction was investigated in mouse epidermal cells. Western blot analysis of RESOURCE Q column chromatography eluates obtained from 105,000 g supernatants and particulate fractions of epidermal cells was perform...
journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/0898-6568(95)00019-l
更新日期：1995-07-01 00:00:00
