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Updated: Jan 27, 2026
Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
Circular RNA circ-DONSON facilitates gastric cancer growth and invasion via NURF complex dependent activation of
Lixian Ding1,2, Yuying Zhao3, Shuwei Dang1,2
1Department of General Surgery, the Fourth Affiliated Hospital of Harbin Medical University, No. 37 Yiyuan Street, Nangang District, Harbin, 150001, People's Republic of China.
Background:
Circular RNAs (circRNAs) are a novel type of noncoding RNAs and play important roles in tumorigenesis, including gastric cancer (GC). However, the functions of most circRNAs remain poorly understood. In our study, we aimed to investigate the functions of a new circRNA circ-DONSON in GC progression.
Methods:
The expression of circ-DONSON in gastric cancer tissues and adjacent normal tissues was analyzed by bioinformatics method, qRT-PCR, Northern blotting and in situ hybridization (ISH). The effects of circ-DONSON on GC cell proliferation, apoptosis, migration and invasion were measured by using CCK8, colony formation, EdU, immunofluorescence (IF), FACS and Transwell assays. qRT-PCR and Western blotting were utilized to validate how circ-DONSON regulates SOX4 expression. ChIP, DNA fluorescence in situ hybridization (DNA-FISH) and DNA accessibility assays were used to investigate how circ-DONSON regulates SOX4 transcription. The interaction between circ-DONSON and NURF complex was evaluated by mass spectrum, RNA immunoprecipitation (RIP), pulldown and EMSA assays. Xenograft mouse model was used to analyze the effect of circ-DONSON on GC growth in vivo.
Results:
Elevated expression of circ-DONSON was observed in GC tissues and positively associated with advanced TNM stage and unfavorable prognosis. Silencing of circ-DONSON significantly suppressed the proliferation, migration and invasion of GC cells while promoting apoptosis. circ-DONSON was localized in the nucleus, recruited the NURF complex to SOX4 promoter and initiated its transcription. Silencing of the NURF complex subunit SNF2L, BPTF or RBBP4 similarly attenuated GC cell growth and increased apoptosis. circ-DONSON knockdown inhibited GC growth in vivo.
Conclusion:
circ-DONSON promotes GC progression through recruiting the NURF complex to initiate SOX4 expression.
Insights
Circular RNAs (circRNAs) promote gastric cancer (GC) progression by increasing SOX4 transcription. This study identifies circ-DONSON as a key regulator, highlighting its potential as a therapeutic target for GC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Circular RNAs (circRNAs) are emerging as critical regulators in tumorigenesis, including gastric cancer (GC).
- The specific roles of many circRNAs in GC progression remain largely unexplored.
- This study focuses on elucidating the function of a novel circRNA, circ-DONSON, in GC.
Purpose of the Study:
- To investigate the role and mechanism of circ-DONSON in gastric cancer progression.
- To determine the impact of circ-DONSON on GC cell proliferation, apoptosis, migration, and invasion.
- To identify the molecular targets and pathways regulated by circ-DONSON in GC.
Main Methods:
- Expression analysis of circ-DONSON in GC tissues and cells using qRT-PCR, Northern blotting, and ISH.
- Functional assays including CCK8, colony formation, EdU, FACS, and Transwell assays to assess GC cell behavior.
- Molecular mechanism studies involving ChIP, DNA-FISH, RIP, and Western blotting to elucidate circ-DONSON's interaction with the NURF complex and SOX4.
- In vivo validation using a xenograft mouse model.
Main Results:
- circ-DONSON expression is elevated in GC tissues and correlates with advanced TNM stage and poor prognosis.
- Silencing circ-DONSON inhibits GC cell proliferation, migration, and invasion, while promoting apoptosis.
- circ-DONSON acts in the nucleus, recruiting the NURF complex to the SOX4 promoter, thereby initiating SOX4 transcription.
- Knockdown of circ-DONSON or NURF complex subunits (SNF2L, BPTF, RBBP4) suppresses GC growth in vitro and in vivo.
Conclusions:
- circ-DONSON significantly promotes gastric cancer progression.
- The mechanism involves circ-DONSON recruiting the NURF complex to initiate SOX4 transcription.
- circ-DONSON represents a potential therapeutic target for gastric cancer treatment.
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