ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
Crosstalk of AP4 and TGFβ receptor signaling in NSCLC.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
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- USP22 drives colorectal cancer invasion and metastasis via epithelial-mesenchymal transition by activating AP4.Oncotarget · 2017Article
- Different roles of myofibroblasts in the tumorigenesis of nonsmall cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Regulation of activating protein-4-associated metastases of non-small cell lung cancer cells by miR-144.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular regulation of growth of non-small cell lung cancer (NSCLC) has not been fully clarified. In NSCLC, we detected significantly higher levels of activating protein-4 (AP4), significantly lower levels of p21, and significantly lower levels of phosphorylated SMAD2 as an indicator of activated transforming growth factor β (TGFβ) receptor signaling, compared to the adjacent normal lung tissue. Moreover, a strong negative correlation was detected between AP4 and p21 levels. Since p21 is a potent cell-cycle inhibitor, we were thus promoted to examine the relationships among AP4, TGFβ receptor signaling, and cell growth in NSCLC. Using a human NSCLC cell line HepG2 cells, we found that activation of TGFβ receptor signaling increased p21 levels through phosphorylation of SMAD2. Moreover, AP4 inhibited phosphorylation of SMAD2 to contradict the effect of activated TGFβ receptor signaling on cell growth inhibition in NSCLC. Furthermore, binding of TGFβ1 to its receptor also directly increased AP4 transcription, which appeared to negatively control the levels of activated TGFβ receptor signaling. Taken together, our results suggest that AP4 may inhibit the phosphorylation of SMAD2, which is induced by receptor binding with TGFβ1, to abolish the inhibitory effect of activated TGFβ receptor signaling on cell growth in NSCLC. Our study thus highlights AP4 as a novel therapeutic target for NSCLC.
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