| Literature DB >> 30391671 |
Yan Guo1, Hai Li2, Hongyu Guan3, Weijian Ke4, Weiwei Liang5, Haipeng Xiao6, Yanbing Li7.
Abstract
Dermatopontin (DPT), a noncollagenous extracellular matrix component, has been illustrated to regulate cellular proliferation and invasiveness in several types of neoplasms. Nevertheless, the biological functions of DPT in cell proliferation, especially papillary thyroid cancer (PTC) cell proliferation, remain unknown, as do the mechanisms underlying its effects. In this study, we detected low DPT expression in PTC, which was related to higher T classifications. Ectopic DPT expression impeded cell proliferation both in vitro and in vivo. Furthermore, we illustrated that DPT down-regulated MYC, which in turn targeted CDK4, CDK6 and p21, through the ERK pathway. These results suggest that DPT regulates CDK4, CDK6 and p21, through MEK-ERK-MYC signaling to repress PTC proliferation.Entities:
Keywords: Dermatopontin; ERK; MYC; Papillary thyroid cancer; Proliferation
Mesh:
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Year: 2018 PMID: 30391671 DOI: 10.1016/j.mce.2018.10.021
Source DB: PubMed Journal: Mol Cell Endocrinol ISSN: 0303-7207 Impact factor: 4.102