High expression of apolipoprotein C1 promotes proliferation and inhibits apoptosis of papillary thyroid carcinoma cells by activating the JAK2/STAT3 signaling pathway.
10.12122/j.issn.1673-4254.2025.02.17
- Author:
Yu BIN
1
;
Ziwen LI
1
;
Suwei ZUO
1
;
Sinuo SUN
1
;
Min LI
2
;
Jiayin SONG
2
;
Xu LIN
1
;
Gang XUE
2
;
Jingfang WU
1
Author Information
1. Laboratory of Morphology, Hebei North University, Zhangjiakou 075000, China.
2. Department of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China.
- Publication Type:Journal Article
- Keywords:
JAK2/STAT3 signaling pathway;
apolipoprotein C1;
apoptosis;
papillary thyroid carcinoma;
proliferation
- MeSH:
Humans;
Apoptosis;
Cell Proliferation;
STAT3 Transcription Factor/metabolism*;
Signal Transduction;
Janus Kinase 2/metabolism*;
Thyroid Neoplasms/pathology*;
Thyroid Cancer, Papillary;
Cell Line, Tumor;
Carcinoma, Papillary
- From:
Journal of Southern Medical University
2025;45(2):359-370
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To investigate the expression of apolipoprotein C1 (APOC1) in papillary thyroid carcinoma (PTC) and its effects on proliferation and apoptosis of PTC cells.
METHODS:The expression level of APOC1 in PTC and its impact on prognosis were analyzed using GEPIA 2 and Kaplan-Meier databases. Immunohistochemistry (IHC) and Western blotting were used to detect the expression of APOC1 in PTC and adjacent tissues and in 3 PTC cell lines and normal thyroid Nthyori 3-1 cells. In TPC-1 and BCPAP cells, the effect of Lipofectamine 2000-mediated transfection with APOC1 siRNA or an APOC1-overexpressing plasmid on cell growth and colony formation ability were examined by observing the growth curves and using colony-forming assay. The changes in cell cycle and apoptosis of the transfected cells were analyzed with flow cytometry. RT-qPCR and Western blotting were used to detect the changes in expressions of P21, P27, CDK4, cyclin D1, Bcl-2, Bax, caspase-3 and caspase-9 and the key proteins in the JAK2/STAT3 signaling pathway.
RESULTS:APOC1 expression was significantly higher in PTC tissues and the 3 PTC cell lines than in the adjacent tissues and Nthyori 3-1 cells, respectively. In TPC-1 and BCPAP cells, APOC1 knockdown obviously reduced cell proliferative activity, increased the percentage of G0/G1 phase cells, lowered the percentages of S and G2 phase cells, promoted cell apoptosis, and downregulated mRNA and protein expression levels of CDK4, cyclin D1 and Bcl-2 and the protein levels of p-JAK2 and p-STAT3. APOC1 overexpression in the cells produced the opposite effects on cell proliferation, apoptosis, cell cycle and the mRNA and protein expressions. The application of AG490, a JAK2 inhibitor, strongly attenuated APOC1 overexpression-induced activation of the JAK2/STAT3 signaling pathway in BCPAP cells.
CONCLUSIONS:APOC1 overexpression promotes proliferation and inhibits apoptosis of PTC cells possibly by activating the JAK2/STAT3 signaling pathway and accelerating cell cycle progression.
