Dermatopontin inhibits papillary thyroid cancer cell proliferation through MYC repression. (15th January 2019)

• Record Type: Journal Article
• Authors: Guo, Yan; Li, Hai; Guan, Hongyu; Ke, Weijian; Liang, Weiwei; Xiao, Haipeng; Li, Yanbing
• Is Part Of: Molecular and cellular endocrinology. Volume 480(2019)
• Page Start: 122
• Page End: 132
• Publication Date: 2019-01-15
• Subjects: Dermatopontin -- Papillary thyroid cancer -- Proliferation -- MYC -- ERK; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2018.10.021
• Languages: English
• ISSNs: 0303-7207

Abstract

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. Highlights: In PTCs, DPT is down-regulated, which is associated with higher T classifications and tumor stages. DPT over-expression impedes PTCs proliferation in vivo and in vitro . DPT regulates the expression levels of CDK4, CDK6 and p21 through repressing MYC in PTC cells. DPT reduces MYC abundance via MEK-ERK-MYC signaling in PTC cells.