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Updated: Jul 17, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Suppressing Dicer inhibits proliferation and contributes to cellular senescence, partially via a p21-associated
Chao-Wen Cheng1,2, Wen-Fang Fang3, Yea-Mey Yang1
1Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Abstract:
Dicer is known to engage in regulating micro (mi)RNA biosynthesis. However, the role in driving thyroid carcinogenesis is unknown. In this study, we explored the role of Dicer in the carcinogenesis of well-differentiated thyroid carcinoma (WDTC). Thyroid cancer complementary (c)DNA and tissue arrays were purchased to measure Dicer messenger (m)RNA and protein levels. Additionally, research into silencing Dicer1 in papillary thyroid cancer (PTC) (TPC-1), follicular thyroid cancer (FTC), and normal thyroid (Nthy-ori 3-1) cell lines was also applied to evaluate its effects on tumour behaviors. Dicer1 mRNA was upregulated in PTC, while the Dicer protein was overexpressed in PTC and FTC tissues. Suppressing Dicer led to inhibition of cell proliferation in all cell lines, and repression of cell-cycle progression signatures in TPC-1 cells. Furthermore, p21 expression consistently increased in response to compromising Dicer in all four cell lines. Finally, Dicer1-knockdown TPC-1 and Nthy-ori 3-1 cells demonstrated nuclear phospho-H2AX staining, reduced bromodeoxyuridine incorporation ability, and G1 phase arrest of the cell cycle. Collectively, Dicer expression is increased in WDTC clinical samples, and Dicer regulates the proliferative ability of normal and WDTC cells, at least in part, through p21-dependent modulation of a cell-senescence mechanism linked to genomic instability.
Insights
Dicer enzyme is upregulated in well-differentiated thyroid carcinoma (WDTC). Suppressing Dicer inhibits cancer cell proliferation and progression, partly via p21-dependent cell senescence and genomic instability.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Dicer is recognized for its role in micro (mi)RNA biosynthesis.
- Its specific involvement in thyroid carcinogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the role of Dicer in the development of well-differentiated thyroid carcinoma (WDTC).
- To evaluate the impact of Dicer inhibition on thyroid cancer cell behavior.
Main Methods:
- Analysis of Dicer messenger RNA (mRNA) and protein levels in thyroid cancer tissues and cell lines.
- Experimental silencing of Dicer1 in papillary thyroid cancer (PTC), follicular thyroid cancer (FTC), and normal thyroid cell lines.
- Assessment of cell proliferation, cell-cycle progression, p21 expression, and markers of genomic instability (phospho-H2AX, BrdU incorporation).
Main Results:
- Dicer1 mRNA was elevated in PTC, and Dicer protein was overexpressed in both PTC and FTC tissues.
- Dicer suppression inhibited cell proliferation and repressed cell-cycle progression in thyroid cancer cell lines.
- p21 expression increased, and genomic instability markers were observed upon Dicer knockdown.
Conclusions:
- Dicer expression is elevated in WDTC.
- Dicer plays a significant role in regulating the proliferative capacity of normal and WDTC cells.
- Dicer influences cell senescence and genomic stability, at least partially through p21-dependent pathways.
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