Long noncoding RNA NEAT1 regulate papillary thyroid cancer progression by modulating miR-129-5p/KLK7expression

2018 ◽  
Vol 233 (10) ◽  
pp. 6638-6648 ◽  
Author(s):  
Hong Zhang ◽  
Yuechang Cai ◽  
Li Zheng ◽  
Zhanlei Zhang ◽  
Xiaofeng Lin ◽  
...  
Author(s):  
Ying Ye ◽  
Yanan Song ◽  
Juhua Zhuang ◽  
Saifei He ◽  
Jing Ni ◽  
...  

Long noncoding RNA CCAL has been reported to promote tumor progression in various human cancers, including hepatocellular carcinoma, osteosarcoma, and colorectal cancer. However, the role of CCAL in papillary thyroid cancer remains largely unknown. In the present study, we found that the expression of CCAL was upregulated in papillary thyroid tumor tissues compared to adjacent normal tissues. Moreover, the expression of CCAL was positively related with papillary thyroid cancer severity and TNM stage and predicated poor prognosis. Besides, we found that knockdown of CCAL significantly inhibited papillary thyroid cancer cell proliferation, migration, and invasion in vitro and reduced tumor growth and metastasis in vivo. We found that knockdown of CCAL dramatically decreased the expression of NOTCH1 and suppressed the activation of the NOTCH1 signaling pathway. Furthermore, overexpression of NOTCH1 rescued the proliferation, migration, and invasion in papillary thyroid cancer cells. Taken together, our data indicated that CCAL promoted papillary thyroid cancer development and progression by activation of the NOTCH1 pathway, which provided a new insight on the design of therapeutic targets.


2021 ◽  
Author(s):  
Luyao Wu ◽  
Yu Ding ◽  
Xi Zhuang ◽  
Jingsheng Cai ◽  
Houchao Tong ◽  
...  

Abstract Background: Long noncoding RNAs (lncRNAs) have emerged as crucial regulators in various cancers. However, the functional roles of most lncRNA in papillary thyroid cancer (PTC) are not detailly understood. This study aims to investigate the biological functions and the molecular mechanism of lncRNA FER1L4 in PTC.Methods: The expression of FER1L4 in PTC was determined via operating RT-PCR assays. Meanwhile, the clinical significance of FER1L4 in PTC patients was described. The biological functions of FER1L4 on PTC cells were evaluated by gain and loss of function experiments. Moreover, animal experiments were performed to reveal the effect on tumor growth. Subcellular distribution of FER1L4 was determined by fluorescence in situ hybridization and subcellular localization assays. Luciferase reporter assay and RNA immunoprecipitation assay were applied to define the relationship between FER1L4, miR-612, and CDH4. Results: Upregulated expression of FER1L4 in PTC tissues was correlated with higher lymph node metastasis rate (p=0.020), extrathyroidal extension (p=0.013), and advanced TNM stage (p=0.013). In addition, knockdown of FER1L4 suppressed PTC cell proliferation, migration and invasion, whereas ectopic expression of FER1L4 inversely promoted these processes. Mechanistically, FER1L4 could competitively bind with miR-612 to prevent the degradation of its target gene Cadherin 4 (CDH4). This condition was further confirmed in the rescue assays.Conclusions: This study firstly demonstrates FER1L4 plays an oncogenic role in PTC via FER1L4-miR-612-CDH4 axis and may provide a new therapeutic and diagnostic target for PTC.


2018 ◽  
Vol 14 (29) ◽  
pp. 3015-3022 ◽  
Author(s):  
Jia Liu ◽  
Hanhua Dong ◽  
Yingxu Yang ◽  
Yuejun Qian ◽  
Jianqiu Liu ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document