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SOX9 — WNT11
Text-mined interactions from Literome
Dong et al., J Cell Physiol 2006
(Hypertrophy) :
Wnt8c and Wnt9a strongly
inhibited mRNA levels of
Sox9 and type II collagen ( col2a1 ) ... Wnt8c further enhanced canonical bone morphogenetic proteins ( BMP-2 ) -induced expression of Runx2 and col10a1 while
Wnt8c and Wnt9a
inhibited TGF-beta induced expression of
Sox9 and col2a1
Wang et al., Cancer Res 2007
(Neoplasm Recurrence, Local...) :
SOX9 message and protein levels in prostate cancer cells were increased by treatment with glycogen synthase kinase 3beta inhibitor ( SB415286 ), and SOX9 was reduced when beta-catenin was down-regulated by small interfering RNA ( siRNA ), indicating that
SOX9 expression in prostate cancer is
regulated by
Wnt/beta-catenin signaling
Topol et al., J Biol Chem 2009
:
Sox9 inhibits
Wnt signaling by promoting beta-catenin phosphorylation in the nucleus ... Chondrocyte fate determination and maintenance requires
Sox9 , an intrinsic transcription factor, but is
inhibited by
Wnt/beta-catenin signaling activated by extrinsic Wnt ligands
Kormish et al., Dev Dyn 2010
(Neoplasms) :
In some contexts,
Wnt signaling also
regulates SOX expression resulting in feedback regulatory loops that fine-tune cellular responses to beta-catenin/TCF activity
Bernard et al., Endocrinology 2012
:
Wnt signaling in ovarian development
inhibits Sf1 activation of
Sox9 via the Tesco enhancer ... Ectopic activation of
Wnt/ß-catenin signaling in male gonads
led to a loss of Sf1 binding to the Tesco enhancer and absent
Sox9 expression that we also observed in wild-type ovaries ... Moreover, ectopic
Wnt/ß-catenin signaling induced the expression of the female somatic cell markers, Bmp2 and Rspo1, as a likely
consequence of
Sox9 loss
Wang et al., J Biol Chem 2013
(Breast Neoplasms...) :
Consistently,
SOX9 overexpression in BCa cell lines and transgenic SOX9 expression in breast epithelium
caused increased LRP6 and TCF4 expression and
Wnt/ß-catenin activation ... These results identify
SOX9 mediated
Wnt/ß-catenin activation as one of the molecular mechanisms underlying aberrant Wnt/ß-catenin activity in BCa, especially in the BL-BCa subgroup