scholarly journals miRNA-148a inhibits cell growth of papillary thyroid cancer through STAT3 and PI3K/AKT signaling pathways

2017 ◽  
Vol 38 (5) ◽  
pp. 3085-3093 ◽  
Author(s):  
Yuan Xu ◽  
Yi-Fan Han ◽  
Shao-Jun Zhu ◽  
Jian-Da Dong ◽  
Bing Ye
Keyword(s):  
Thyroid Cancer ◽  
Cell Growth ◽  
Signaling Pathways ◽  
Papillary Thyroid Cancer ◽  
Akt Signaling ◽  
Papillary Thyroid

Abstract 4097: Targeting of mTOR mediated signaling pathways in papillary thyroid cancer cell.

2013 ◽  
Author(s):  
Maqbool Ahmed ◽  
Azhar R. Hussain ◽  
Fouad Al Dayel ◽  
Shahab Uddin ◽  
Khawla S. Al-Kuraya
Keyword(s):  
Thyroid Cancer ◽  
Signaling Pathways ◽  
Papillary Thyroid Cancer ◽  
Cancer Cell ◽  
Thyroid Cancer Cell ◽  
Papillary Thyroid

scholarly journals Effects of let-7 microRNA on Cell Growth and Differentiation of Papillary Thyroid Cancer

2009 ◽  
Vol 2 (4) ◽  
pp. 236-241 ◽  
Author(s):  
Jølio Cezar Marques ◽  
Ricarte-Filho ◽  
Cesar Seigi Fuziwara ◽  
Alex Shimura Yamashita ◽  
Eloiza Rezende ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cell Growth ◽  
Papillary Thyroid Cancer ◽  
Papillary Thyroid ◽  
Cell Growth And Differentiation

scholarly journals SQSTM1/p62 Promotes Cell Growth and Triggers Autophagy in Papillary Thyroid Cancer by Regulating the AKT/AMPK/mTOR Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Fangqin Yu ◽  
Runsheng Ma ◽  
Chenguang Liu ◽  
Lele Zhang ◽  
Kaixiang Feng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Thyroid Cancer ◽  
Cell Growth ◽  
Cell Line ◽  
Papillary Thyroid Cancer ◽  
Cell Lines ◽  
Papillary Thyroid ◽  
Mtor Signaling Pathway ◽  
Normal Thyroid

BackgroundThyroid cancer is one of the most common endocrine malignancies worldwide, and papillary thyroid cancer (PTC) is the most common pathologic type of thyroid cancer. SQSTM1/p62 activity mediates different biological functions. This study aimed to investigate the effect of SQSTM1/p62, a multifunctional receptor, on biological function and autophagy characteristics in the human PTC cell line TPC-1.MethodsA total of 105 primary PTC samples and matched adjacent normal thyroid tissue samples were obtained to evaluate the expression of p62 in clinical patients. A similar p62 expression pattern was found in PTC cell lines and normal human thyroid follicular epithelial cells. To evaluate the effect of SQSTM1/p62 on TPC-1 cells, we constructed the p62 knockout cell line p62-KO-TPC-1. Cell proliferation, cell cycle, and cell apoptosis were analyzed by colony formation tests, Cell Counting Kit-8 (CCK-8) assays and flow cytometry in vitro. TPC-1 and p62-KO-TPC-1 human PTC cell lines in the logarithmic growth phase were subcutaneously implanted into BALB/c nude mice to verify their proliferation effect in vivo. Furthermore, western blotting and immunohistochemistry (IHC) were used to detect the expression of AKT/AMPK/mTOR signaling pathway-related proteins.ResultsOverall, p62 expression was higher in tumor tissues than in normal tissues in 73 of 105 PTC patients (69.5%). The expression level of p62 in the PTC cell line was higher than that in the normal thyroid cell line. Our data indicated that in vitro, p62 deficiency could decrease the number of colonies, inhibit cell growth and the cell cycle, and induce apoptosis. Tumor xenograft experiments in BALB/c nude mice corroborated these findings. Moreover, the molecular mechanism was explored by western blotting, and we found that the AMPK/AKT/mTOR pathway was involved.ConclusionsThe results indicate that p62 might mediate cell autophagy and apoptosis in TPC-1 cells via the AMPK/AKT/mTOR pathway and could be used as a potential therapeutic approach for PTC.

Sign in / Sign up

Export Citation Format

Share Document