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Updated: Dec 9, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
LINC00893 inhibits papillary thyroid cancer by suppressing AKT pathway via stabilizing PTEN
Shujing Li1, Yanyan Zhang1, Jian Dong1
1Department of General Surgery, First Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
Abstract:
Long non-coding RNAs (lncRNAs) are important to the occurrence and advancement of human cancers. We found through GEPIA that LINC00893 was lowly expressed in thyroid carcinoma (THCA) tissues, whereas the specific functions of LINC00893 has never been reported in PTC. In the current study, we confirmed that LINC00893 was expressed at a low level in PTC cells. Through gain-of-function assays, we determined that LINC00893 overexpression abrogated proliferation and migration abilities of PTC cells. Through signal transduction reporter array we found that LINC00893 potentially modulated the signals of phosphatase and tensin homolog (PTEN)/AKT pathway. In addition, overexpression of LINC00893 increased the expression of PTEN but reduced the levels of phosphorylated AKT in PTC. Additionally, mechanism assays unveiled that LINC00893 stabilized PTEN mRNA via recruiting Fused in sarcoma (FUS) protein. Finally, rescue assays demonstrated that LINC00893 hampered the proliferation and migration of PTC cells via PTEN/AKT pathway. Together, our study first clarified that LINC00893 functions as a tumor suppressor in PTC by blocking AKT pathway through PTEN upregulation.
Insights
Long non-coding RNA LINC00893 acts as a tumor suppressor in papillary thyroid carcinoma (PTC). Its overexpression inhibits cancer cell proliferation and migration by upregulating PTEN and blocking the AKT pathway.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) play critical roles in human cancer development.
- LINC00893 has been identified as lowly expressed in thyroid carcinoma (THCA) via GEPIA.
- The specific function of LINC00893 in papillary thyroid carcinoma (PTC) remains uncharacterized.
Purpose of the Study:
- To investigate the role and mechanism of LINC00893 in papillary thyroid carcinoma (PTC).
- To determine the effect of LINC00893 on PTC cell proliferation and migration.
- To elucidate the molecular pathway modulated by LINC00893 in PTC.
Main Methods:
- GEPIA analysis to assess LINC00893 expression in THCA.
- Gain-of-function assays to evaluate the impact of LINC00893 overexpression on PTC cells.
- Signal transduction reporter array to identify modulated pathways.
- Western blotting and mRNA stability assays to confirm molecular mechanisms.
- Rescue assays to validate the functional role of LINC00893 in PTC.
Main Results:
- LINC00893 was confirmed to be lowly expressed in PTC cells.
- Overexpression of LINC00893 significantly inhibited PTC cell proliferation and migration.
- LINC00893 was found to modulate the PTEN/AKT pathway.
- LINC00893 overexpression led to increased PTEN expression and decreased phosphorylated AKT levels.
- LINC00893 stabilizes PTEN mRNA by recruiting FUS protein.
- LINC00893 suppressed PTC progression via the PTEN/AKT pathway.
Conclusions:
- LINC00893 functions as a tumor suppressor in papillary thyroid carcinoma (PTC).
- LINC00893 inhibits PTC proliferation and migration by upregulating PTEN and consequently inhibiting the AKT pathway.
- This study provides novel insights into the regulatory role of LINC00893 in thyroid cancer.
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