Title:LINC00891 Promotes Tumorigenesis and Metastasis of Thyroid
Cancer by Regulating SMAD2/3 via EZH2
Volume: 31
Issue: 24
Author(s): Yuhao Si, Jialiang Wen, Chunlei Hu, Hao Chen, Lizhi Lin, Yiying Xu, Disuo Ren, Xinyu Meng, Yinghao Wang, Erjie Xia, Adheesh Bhandari*Ouchen Wang*
Affiliation:
- Department of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR, China
- Department of Surgery, Breast and Thyroid Unit, Primera Hospital,
Kathmandu, Nepal
- Department of Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR, China
Keywords:
LINC00891, EZH2, SMAD2/3, epithelial-to-mesenchymal transition, thyroid cancer, gene expression omnibus.
Abstract:
Background: Thyroid cancer (TC), the most common endocrine malignant tumor,
is increasingly causing a huge threat to our health nowadays.
Methods: To explore the tumorigenesis mechanism of thyroid cancer, we identified that
long intergenic non-coding RNA-00891 (LINC00891) was upregulated in TC using the
Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and local databases.
LINC00891 expression was correlated with histological type and lymph node metastasis
(LNM). The high expression of LINC00891 could serve as a diagnostic marker for TC
and its LNM. In vitro experiments demonstrated that LINC00891 knockdown could inhibit
cell proliferation, migration, invasion and prompt apoptosis and G1 arrest of TC
cells. We also investigated the related mechanisms of LINC00891 promoting TC progression
using RNA sequencing, Gene Set Enrichment Analysis, and Western blotting.
Results: Our experiments demonstrated that LINC00891 promoted TC progression via
the EZH2-SMAD2/3 signaling axis. In addition, overexpression of EZH2 could reverse
the suppressive epithelial-to-mesenchymal transition (EMT) caused by LINC00891
knockdown.
Conclusion: In conclusion, the LINC00891/EZH2/SMAD2/3 regulatory axis participated
in tumorigenesis and metastasis of thyroid cancer, which may provide a novel target
for treatment.