{"title":"CircRNA circ_0013339 Regulates the Progression of Colorectal Cancer Through miR-136-5p/SOX9 Axis","authors":"Juan Jin, Min Du, Ding Ding, Ran Xuan","doi":"10.1007/s10528-023-10540-4","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Colorectal cancer (CRC) is a common gastrointestinal malignancy. Dysregulation of circular RNAs (circRNAs) is associated with the progression of CRC. However, the role of circ_0013339 (hsa_circ_0013339) in CRC is still not clear.</p><h3>Methods</h3><p>The levels of circ_0013339, miR-136-5p, and SRY-box transcription factor 9 (SOX9) in CRC were gauged by quantitative real-time polymerase chain reaction (qRT-PCR). Colony formation and 5-Ethynyl-2’-deoxyuridine (EdU) assays were used to detect cell proliferation. Cell counting kit-8 (CCK8) assay was used to measure cell viability. Western blot assay was performed to examine protein expression. The relationship between miR-136-5p and circ_0013339 or SOX9 was tested by dual-luciferase reporter assay. The effect of sh-circ_0013339 on tumor growth in vivo was examined by xenograft experiments.</p><h3>Results</h3><p>Circ_0013339 expression was elevated in CRC tissues and cells, and circ_0013339 knockdown diminished the growth of CRC cells. MiR-136-5p was regulated by circ_0013339. MiR-136-5p deficiency ameliorated the effects of circ_0013339 silencing on CRC cell malignant behaviors. Circ_0013339 modulated SOX9 expression through miR-136-5p. SOX9 addition reversed the effects of miR-136-5p overexpression on CRC cell behaviors. Moreover, silencing of circ_0013339 suppressed the growth of xenograft tumors in vivo.</p><h3>Conclusion</h3><p>Circ_0013339 regulates the progression of CRC through miR-136-5p-dependent regulation of SOX9, uncovering a novel regulatory mechanism of circ_0013339 in CRC.</p></div>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":"62 4","pages":"2362 - 2380"},"PeriodicalIF":2.1000,"publicationDate":"2023-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemical Genetics","FirstCategoryId":"99","ListUrlMain":"https://link.springer.com/article/10.1007/s10528-023-10540-4","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background
Colorectal cancer (CRC) is a common gastrointestinal malignancy. Dysregulation of circular RNAs (circRNAs) is associated with the progression of CRC. However, the role of circ_0013339 (hsa_circ_0013339) in CRC is still not clear.
Methods
The levels of circ_0013339, miR-136-5p, and SRY-box transcription factor 9 (SOX9) in CRC were gauged by quantitative real-time polymerase chain reaction (qRT-PCR). Colony formation and 5-Ethynyl-2’-deoxyuridine (EdU) assays were used to detect cell proliferation. Cell counting kit-8 (CCK8) assay was used to measure cell viability. Western blot assay was performed to examine protein expression. The relationship between miR-136-5p and circ_0013339 or SOX9 was tested by dual-luciferase reporter assay. The effect of sh-circ_0013339 on tumor growth in vivo was examined by xenograft experiments.
Results
Circ_0013339 expression was elevated in CRC tissues and cells, and circ_0013339 knockdown diminished the growth of CRC cells. MiR-136-5p was regulated by circ_0013339. MiR-136-5p deficiency ameliorated the effects of circ_0013339 silencing on CRC cell malignant behaviors. Circ_0013339 modulated SOX9 expression through miR-136-5p. SOX9 addition reversed the effects of miR-136-5p overexpression on CRC cell behaviors. Moreover, silencing of circ_0013339 suppressed the growth of xenograft tumors in vivo.
Conclusion
Circ_0013339 regulates the progression of CRC through miR-136-5p-dependent regulation of SOX9, uncovering a novel regulatory mechanism of circ_0013339 in CRC.
期刊介绍：
Biochemical Genetics welcomes original manuscripts that address and test clear scientific hypotheses, are directed to a broad scientific audience, and clearly contribute to the advancement of the field through the use of sound sampling or experimental design, reliable analytical methodologies and robust statistical analyses.
Although studies focusing on particular regions and target organisms are welcome, it is not the journal’s goal to publish essentially descriptive studies that provide results with narrow applicability, or are based on very small samples or pseudoreplication.
Rather, Biochemical Genetics welcomes review articles that go beyond summarizing previous publications and create added value through the systematic analysis and critique of the current state of knowledge or by conducting meta-analyses.
Methodological articles are also within the scope of Biological Genetics, particularly when new laboratory techniques or computational approaches are fully described and thoroughly compared with the existing benchmark methods.
Biochemical Genetics welcomes articles on the following topics: Genomics; Proteomics; Population genetics; Phylogenetics; Metagenomics; Microbial genetics; Genetics and evolution of wild and cultivated plants; Animal genetics and evolution; Human genetics and evolution; Genetic disorders; Genetic markers of diseases; Gene technology and therapy; Experimental and analytical methods; Statistical and computational methods.
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