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Updated: Sep 10, 2025
07:02
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
7.4K
A novel long non-coding RNA, PICSAR, promotes thyroid cancer progression through the
Maryam Hejazi1,2, Tahmineh Jafari2, AmirHossein Yari2
1Chronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Medical Oncology (Northwood, London, England)
|August 26, 2025
Summary
Overexpressed long non-coding RNA PICSAR (LINC00162) in thyroid cancer sponges microRNAs, upregulating RAPGEFL1 and promoting tumor growth. Silencing PICSAR inhibits thyroid cancer progression, suggesting it as a therapeutic target.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- Thyroid carcinoma (TC) is a prevalent endocrine cancer with significant mortality.
- Long non-coding RNAs (lncRNAs) are implicated in various cancers, including TC.
- The role of PICSAR lncRNA (LINC00162) in human cancers warrants investigation in thyroid cancer.
Purpose of the Study:
- To investigate the expression levels and functional roles of lncRNA PICSAR (LINC00162) in thyroid cancer tumorigenesis.
- To elucidate the molecular mechanisms and clinical significance of PICSAR in thyroid cancer.
- To explore the potential of PICSAR as a therapeutic target for thyroid cancer.
Main Methods:
- Utilized TCGA database for in silico analysis of LINC00162 expression and identified differentially expressed genes (DEGs).
- Employed bioinformatics tools (LncACT, miRDB) to predict lncRNA-miRNA interactions and performed functional enrichment analysis.
- Conducted qRT-PCR on 50 matched TC and normal tissue samples and performed siRNA-mediated gene silencing in a thyroid cancer cell line.
Main Results:
- LINC00162 was significantly overexpressed in thyroid cancer tissues compared to normal tissues.
- Bioinformatics analysis revealed LINC00162 acts as a molecular sponge for hsa-miR-320A and hsa-miR-485, leading to RAPGEFL1 upregulation.
- Silencing LINC00162 inhibited thyroid cancer cell growth by downregulating LINC00162 and RAPGEFL1, and upregulating hsa-miR-320A and hsa-miR-485.
Conclusions:
- LINC00162 is overexpressed in thyroid cancer and promotes tumorigenesis by sponging hsa-miR-320A/hsa-miR-485 and upregulating RAPGEFL1.
- The LINC00162-miRNA-RAPGEFL1 axis influences key carcinogenic pathways, including thiamine metabolism and cell cycle control.
- Targeting PICSAR (LINC00162) presents a potential therapeutic strategy for thyroid cancer.
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