Related Experiment Video
Updated: Aug 15, 2025

CRISPR Gene Editing Tool for MicroRNA Cluster Network Analysis
Published on: April 25, 2022
Circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through miR-384/FN1 pathway
1Blood Purification, The Sixth Hospital of Wuhan, Affiliated Hospital of Jianghan University, No. 168, Hongkong Road, Jiang'an District, Wuhan, Hubei 430015, China.
Purpose:
Circular RNA_0101692 (circ_0101692) is overexpressed in clear cell renal cell carcinoma (ccRCC) by microarray analyses. However, its function and action mechanism in ccRCC tumorigenesis is still elusive.
Methods:
Western blotting and qRT-PCR were executed to assess the circ_0101692, miR-384 and FN1 expression in ccRCC cells and tissues. Target relationships among them were determined via dual luciferase reporter and/or RNA immunoprecipitation assays. Cell proliferation was evaluated by CCK-8 assay. Caspase-3 activity assay was utilized to analyze cell apoptosis. To find out whether ccRCC cells might migrate, a transwell assay was performed. To assess the effects of circ_0101692 on tumor development in vivo, a mouse xenograft model was used.
Results:
High expression of circ_0101692 and FN1, and decreased miR-384 were determined in ccRCC. Cell growth, migration and viability were decreased whereas cell apoptosis was stimulated when circ_0101692 was knockdown. miR-384 inhibitor transfection attenuated the inhibiting impacts of circ_0101692 silencing on ccRCC cell progression. FN1 deletion further inverted the cancer-promoting effect of miR-384 downregulation on cell viability and migration. In addition, circ_0101692 could sponge miR-384 to relieve the inhibition of miR-384 on FN1 in ccRCC.
Conclusions:
Circ_0101692 targeted miR-384/FN1 axis to facilitate cell proliferation, migration and repress apoptosis, thereby accelerating the development of ccRCC. This points out that circ_0101692/miR-384/FN1 axis might be a prospective target implemented for the future treatment of ccRCC.
Insights
Circular RNA_0101692 (circ_0101692) promotes clear cell renal cell carcinoma (ccRCC) by targeting miR-384 and FN1. Inhibiting circ_0101692 may offer a new treatment strategy for ccRCC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Circular RNA_0101692 (circ_0101692) is overexpressed in clear cell renal cell carcinoma (ccRCC).
- The precise function and mechanism of circ_0101692 in ccRCC tumorigenesis remain unclear.
Purpose of the Study:
- To investigate the role and mechanism of circ_0101692 in ccRCC progression.
- To explore the potential of the circ_0101692/miR-384/FN1 axis as a therapeutic target for ccRCC.
Main Methods:
- Assessed expression of circ_0101692, miR-384, and FN1 in ccRCC tissues and cells using Western blotting and qRT-PCR.
- Utilized dual luciferase reporter and RNA immunoprecipitation assays to confirm target interactions.
- Evaluated cell proliferation, apoptosis, and migration using CCK-8, caspase-3 activity, and transwell assays, respectively.
- Investigated the in vivo effects of circ_0101692 using a mouse xenograft model.
Main Results:
- circ_0101692 and FN1 were highly expressed, while miR-384 was decreased in ccRCC.
- Knockdown of circ_0101692 inhibited ccRCC cell proliferation, migration, and viability, and promoted apoptosis.
- circ_0101692 sponges miR-384, relieving miR-384's inhibition on FN1, thereby promoting ccRCC development.
Conclusions:
- The circ_0101692/miR-384/FN1 axis promotes ccRCC cell proliferation and migration while inhibiting apoptosis.
- This axis represents a potential therapeutic target for ccRCC treatment.
Related Concept Videos
MicroRNAs
The Retinoblastoma Gene
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...

