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Updated: May 7, 2026

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
Dicer is down-regulated in clear cell renal cell carcinoma and in vitro Dicer knockdown enhances malignant phenotype
1State Key Laboratory of Kidney Diseases, Department of Urology, Military Postgraduate Medical College, Chinese People's Liberation Army General Hospital, Beijing, People's Republic of China.
Objectives:
Although emerging evidence has shown that the deregulation of micro-ribonucleic acid (RNA) biogenesis machinery is involved in various human malignancies, this role has not been investigated in clear cell renal cell carcinoma (ccRCC). This study aims to determine whether Dicer, a key enzyme responsible for biogenesis of microRNA, is deregulated in ccRCC. The biological roles of Dicer in vitro are also determined.
Materials And Methods:
The expression of Dicer at messenger RNA and protein levels was detected by real-time quantitative polymerase chain reaction and western blot, respectively, in human kidney tubule epithelial cell line, nonmetastatic 786-O ccRCC cell line, and metastatic ACHN ccRCC cell line, as well as in 42 cases of ccRCC surgical specimens including 14 cases with distant metastasis and their corresponding adjacent normal renal tissues. Dicer expression levels in specimens were also measured by immunohistochemical staining. Knockdown of Dicer expression in 786-O and ACHN ccRCC cell lines was achieved by transfecting short interfering RNA against Dicer. The effects of Dicer on cell proliferation, migration, and invasion were detected by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt (MTS) assay, flow cytometric analyses, and Boyden chamber Transwell assay, respectively.
Results:
Compared with human kidney tubule epithelial cell line, Dicer expression levels were significantly down-regulated in 786-O and ACHN ccRCC cell lines, with the metastatic ACHN ccRCC cell line having even lower levels. Meanwhile, Dicer expression levels were significantly down-regulated in ccRCC surgical specimens compared with adjacent normal renal tissues, with the metastatic ones further reduced, and Dicer messenger RNA levels were significantly correlated with overall tumor-node-metastasis stage of ccRCC. In vitro, the knockdown of Dicer significantly promoted cell proliferation, migration, and invasion.
Conclusions:
Reduced expression of Dicer may play a role in the tumorigenesis of ccRCC and further decline may be associated with distant metastasis of ccRCC.
Insights
Reduced Dicer enzyme expression is linked to clear cell renal cell carcinoma (ccRCC) development and metastasis. Lower Dicer levels in ccRCC tissues correlate with advanced tumor stages and promote cancer cell growth and spread.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- MicroRNA (miRNA) biogenesis is crucial in cellular functions.
- Deregulation of miRNA machinery is implicated in human cancers.
- The role of Dicer in clear cell renal cell carcinoma (ccRCC) remains unexplored.
Purpose of the Study:
- To investigate Dicer enzyme deregulation in ccRCC.
- To determine the impact of Dicer on ccRCC cell behavior in vitro.
Main Methods:
- Dicer expression analyzed via RT-qPCR and Western blot in ccRCC cell lines and patient samples.
- Immunohistochemistry used to assess Dicer protein levels.
- Dicer knockdown performed using short interfering RNA (siRNA).
- Cell proliferation, migration, and invasion assays (MTS, flow cytometry, Transwell) evaluated Dicer's functional role.
Main Results:
- Dicer expression significantly down-regulated in ccRCC cell lines and tumors compared to normal kidney tissues.
- Lower Dicer levels observed in metastatic ccRCC and correlated with advanced tumor-node-metastasis stage.
- In vitro Dicer knockdown promoted ccRCC cell proliferation, migration, and invasion.
Conclusions:
- Reduced Dicer expression is associated with ccRCC tumorigenesis.
- Further decrease in Dicer levels may contribute to ccRCC distant metastasis.
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