scholarly journals Long non-coding RNA PITPNA-AS1 regulates UNC5B expression in papillary thyroid cancer via sponging miR-129-5p

2021 ◽  
pp. 172460082098552
Author(s):  
Shijuan Mei ◽  
Huafeng Zong ◽  
Haicheng Zhou

Background: Long non-coding RNA (lncRNA) PITPNA antisense RNA 1 (PITPNA-AS1) expression characteristics, function, and mechanism in papillary thyroid cancer are unclear. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was applied for detecting PITPNA-AS1, UNC-5 netrin receptor B (UNC5B) mRNA, and miR-129-5p expressions in papillary thyroid cancer tissues and cell lines. EdU assay, cell counting kit-8 (CCK-8) assay, wound healing assay, and flow cytometry analysis were performed to investigate the biological functions of PITPNA-AS1 in papillary thyroid cancer. Dual-luciferase reporter assay was utilized for determining whether PITPNA-AS1 and miR-129-5p, as well as UNC5B and miR-129-5p could directly bind to each other. Western blot assay was employed for measuring UNC5B protein expression level in papillary thyroid cancer cell lines. Results: PITPNA-AS1 and UNC5B expressions were markedly increased in papillary thyroid cancer tissues and cell lines while miR-129-5p expression was down-regulated. Knockdown of PITPNA-AS1 could significantly inhibit papillary thyroid cancer cell growth and migration and promote cell apoptosis while UNC5B overexpression plasmids or miR-129-5p inhibitors counteracted the knockdown effect of PITPNA-AS1 on papillary thyroid cancer cells. PITPNA-AS1 targeted miR-129-5p to repress its expression and miR-129-5p targeted UNC5B to repress its expression. Silencing PITPNA-AS1 reduced the expression of UNC5B via regulating miR-129-5p expression. Conclusions: PITPNA-AS1 facilitated papillary thyroid cancer cell proliferation and migration, and suppressed apoptosis through miR-129-5p/UNC5B axis.

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Zhongqin Gong ◽  
Lingbin Xue ◽  
Minghui Wei ◽  
Zhimin Liu ◽  
Alexander C. Vlantis ◽  
...  

Papillary thyroid cancer can dedifferentiate into a much more aggressive form of thyroid cancer, namely into anaplastic thyroid cancer. Nrf2 is commonly activated in papillary thyroid cancer, whereas its role in anaplastic thyroid cancer has not been fully explored. In this study, we used two cell lines and an animal model to examine the function of Nrf2 in anaplastic thyroid cancer. The role of Nrf2 in anaplastic thyroid cancer was investigated by a series of functional studies in two anaplastic thyroid cancer cell lines, FRO and KAT-18, and further confirmed with an in vivo study. The impact of Nrf2 on the sensitivity of anaplastic thyroid cancer cells to lenvatinib was also investigated to evaluate its potential clinical implication. We found that the expression of Nrf2 was significantly higher in anaplastic thyroid cancer cell line cells than in papillary thyroid cancer cells or normal control cells. Knockdown of Nrf2 in anaplastic thyroid cancer cells inhibited their viability and clonogenicity, reduced their migration and invasion ability in vitro, and suppressed their tumorigenicity in vivo. Mechanistically, knockdown of Nrf2 decreased the expression of Notch1. Lastly, knockdown of Nrf2 increased the sensitivity of anaplastic thyroid cancer cells to lenvatinib. As knockdown of Nrf2 reduced the metastatic and invasive ability of anaplastic thyroid cancer cells by inhibiting the Notch 1 signaling pathway and increased the cancer cell sensitivity to lenvatinib, Nrf2 could be a promising therapeutic target for patients with anaplastic thyroid cancer.


Human Cell ◽  
2019 ◽  
Vol 32 (3) ◽  
pp. 334-342 ◽  
Author(s):  
Yinghao Wang ◽  
Adheesh Bhandari ◽  
Jizhao Niu ◽  
Fan Yang ◽  
Erjie Xia ◽  
...  

2019 ◽  
Vol 21 (5) ◽  
pp. e3083 ◽  
Author(s):  
Zhenghui Cui ◽  
Zhiyan Luo ◽  
Zimei Lin ◽  
Liuhong Shi ◽  
Yurong Hong ◽  
...  

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