FAM172A protein promotes the proliferation of human papillary thyroid carcinoma cells via the p38 mitogen-activated protein kinase pathway

• Published in: Molecular medicine reports Vol. 13; no. 1; pp. 353 - 358
• Main Authors: LI, MEI-FANG, ZHANG, RONG, GUO, MING-GAO, LI, LIAN-XI, LU, HAN-KUI, LU, JUN-XI, JIA, WEI-PING
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.01.2016; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: 1-Phosphatidylinositol 3-kinase; Adenoma; Adult; Aged; Aorta; Cancer; Carcinoma; Carcinoma - enzymology; Carcinoma - pathology; Carcinoma, Papillary; Care and treatment; Cell activation; Cell growth; Cell Line, Tumor; Cell Proliferation; Development and progression; family with sequence similarity 172 member A; Female; Humans; Immunohistochemistry; Insulin; Kinases; Male; MAP kinase; MAP Kinase Signaling System; Middle Aged; p38 mitogen- activated protein kinase; p38 Mitogen-Activated Protein Kinases - metabolism; Papillary thyroid carcinoma; Physiological aspects; Protein kinase; Protein kinases; Proteins - metabolism; Risk factors; Signal transduction; Smooth muscle; Studies; Thyroid; Thyroid cancer; Thyroid Cancer, Papillary; Thyroid diseases; Thyroid Neoplasms - enzymology; Thyroid Neoplasms - pathology; Western blotting; China; United States > US
• ISSN: 1791-2997; 1791-3004
• DOI: 10.3892/mmr.2015.4548

Family with sequence similarity 172, member A (FAM172A), was cloned from human aortic tissues and confirmed in our previous study in 2009, however, its functions remain to be fully elucidated. In our previous studies, the protein expression of FAM172A in human aortic smooth muscle cells was found to be upregulated by high glucose in a concentration- and time-dependent manner. Several reports have shown that insulin resistance is associated with papillary thyroid carcinoma (PTC). Thus, in the present study, the protein expression levels of FAM172A in human papillary thyroid carcinoma were investigated, and the effect of the FAM172A protein on the proliferation of IHH-4 human papillary thyroid carcinoma cells, and its potential molecular underlying mechanisms were examined. Immunohistochemistry and western blotting demonstrated that the protein expression of FAM172A in papillary thyroid carcinoma tissues was not only significantly higher than that in noncancerous tissues adjacent to the carcinoma tissues, but it was also markedly higher than that in normal thyroid and thyroid adenoma tissues. Overexpression of the FAM172A protein activated the p38 MAPK pathway, but not the PI3K and AMPK pathways, in the IHH-4 cells. In addition, overexpression of the FAM172A protein accelerated IHH-4 cell proliferation, compared with the control group, and the pro-proliferative effect of FAM172A protein on IHH4 cells was markedly attenuated by SB202190, an inhibitor of p38 MAPK. Taken together, these results suggest that the FAM172A protein is expressed at high levels in human PTC, which may promote cell proliferation via activation of the p38 MAPK signaling pathway, and be involved in the pathogenesis of PTC.