Abstract:
:Genetic screening identifies the atypical tetraspanin TM4SF1 as a strong mediator of metastatic reactivation of breast cancer. Intriguingly, TM4SF1 couples the collagen receptor tyrosine kinase DDR1 to the cortical adaptor syntenin 2 and, hence, to PKCα. The latter kinase phosphorylates and activates JAK2, leading to the activation of STAT3. This non-canonical mechanism of signaling induces the expression of SOX2 and NANOG; sustains the manifestation of cancer stem cell traits; and drives metastatic reactivation in the lung, bone, and brain. Bioinformatic analyses and pathological studies corroborate the clinical relevance of these findings. We conclude that non-canonical DDR1 signaling enables breast cancer cells to exploit the ubiquitous interstitial matrix component collagen I to undergo metastatic reactivation in multiple target organs.
journal_name
Celljournal_title
Cellauthors
Gao H,Chakraborty G,Zhang Z,Akalay I,Gadiya M,Gao Y,Sinha S,Hu J,Jiang C,Akram M,Brogi E,Leitinger B,Giancotti FGdoi
10.1016/j.cell.2016.06.009subject
Has Abstractpub_date
2016-06-30 00:00:00pages
47-62issue
1eissn
0092-8674issn
1097-4172pii
S0092-8674(16)30738-3journal_volume
166pub_type
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