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Downregulation of circ‐RAPGEF5 inhibits colorectal cancer progression by reducing the expression of polypeptide N‐acetylgalactosaminyltransferase 3 (GALNT3)
Circular RNA (circRNA) plays a crucial role in the pathogenesis and progression of colorectal cancer (CRC). However, the current understanding of the emerging function and mechanism of circ‐RAPGEF5 in CRC remains poorly understood. We first evaluated the expression level of circ‐RAPGEF5 in CRC tissues and cells by quantitative real‐time polymerase chain reaction (qRT‐PCR). Then, we analyzed cell proliferation (EdU and colony formation assay), migration (cell wound healing assay), invasion (transwell assay), and apoptosis (flow cytometry assay). To further elucidate the mechanism of circ‐RAPGEF5 in CRC, bioinformatics tools, Dual‐luciferase reporter assay, Ago2 RNA immunoprecipitation assay, and RNA pull‐down assay were employed. Moreover, we established a CRC transplantation tumor model to evaluate the effect of circ‐RAPGEF5 on tumor growth in vivo. circ‐RAPGEF5 was significantly upregulated in CRC tissues and CRC cells. Furthermore, the downregulation of circ‐RAPGEF5 restrained CRC cell proliferation, migration, and invasion, and promoted cell apoptosis in vitro. Mechanistically, circ‐RAPGEF5 accelerated the malignant behaviors of CRC cells by sponging miR‐545‐5p, which targeted polypeptide N‐acetylgalactosaminyltransferase 3 (GALNT3). In addition, we revealed that circ‐RAPGEF5 silence curbed tumor growth in vivo. These findings revealed that circ‐RAPGEF5 played an oncogenic role through the miR‐545‐5p/GALNT3 axis in CRC progression, providing potential therapeutic targets for the treatment of CRC.
Downregulation of circ‐RAPGEF5 inhibits colorectal cancer progression by reducing the expression of polypeptide N‐acetylgalactosaminyltransferase 3 (GALNT3)
Circular RNA (circRNA) plays a crucial role in the pathogenesis and progression of colorectal cancer (CRC). However, the current understanding of the emerging function and mechanism of circ‐RAPGEF5 in CRC remains poorly understood. We first evaluated the expression level of circ‐RAPGEF5 in CRC tissues and cells by quantitative real‐time polymerase chain reaction (qRT‐PCR). Then, we analyzed cell proliferation (EdU and colony formation assay), migration (cell wound healing assay), invasion (transwell assay), and apoptosis (flow cytometry assay). To further elucidate the mechanism of circ‐RAPGEF5 in CRC, bioinformatics tools, Dual‐luciferase reporter assay, Ago2 RNA immunoprecipitation assay, and RNA pull‐down assay were employed. Moreover, we established a CRC transplantation tumor model to evaluate the effect of circ‐RAPGEF5 on tumor growth in vivo. circ‐RAPGEF5 was significantly upregulated in CRC tissues and CRC cells. Furthermore, the downregulation of circ‐RAPGEF5 restrained CRC cell proliferation, migration, and invasion, and promoted cell apoptosis in vitro. Mechanistically, circ‐RAPGEF5 accelerated the malignant behaviors of CRC cells by sponging miR‐545‐5p, which targeted polypeptide N‐acetylgalactosaminyltransferase 3 (GALNT3). In addition, we revealed that circ‐RAPGEF5 silence curbed tumor growth in vivo. These findings revealed that circ‐RAPGEF5 played an oncogenic role through the miR‐545‐5p/GALNT3 axis in CRC progression, providing potential therapeutic targets for the treatment of CRC.
Downregulation of circ‐RAPGEF5 inhibits colorectal cancer progression by reducing the expression of polypeptide N‐acetylgalactosaminyltransferase 3 (GALNT3)
Cheng, Duo (author) / Chu, Feifei (author) / Liang, Fang (author) / Zhang, Nan (author) / Wang, Jingjing (author) / Yue, Wenli (author)
Environmental Toxicology ; 39 ; 4249-4260
2024-08-01
12 pages
Article (Journal)
Electronic Resource
English
| British Library Online Contents | 2018