<scp>CircRNA RNF10</scp> inhibits tumorigenicity by targeting <scp>miR</scp>‐942‐5p/<scp>GOLIM4</scp> axis in breast cancer

Kan, Bing-hua; Gui-ru, Yan; Shao, Yuan; Xue, Hui

doi:10.1002/em.22506

Cited by 1 publication

(3 citation statements)

References 33 publications

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“…As for the biological function of circRNF10 in BC, we discovered that circRNF10 inhibited BC proliferation and progression. These findings were consistent with previous studies, which showed that circRNF10 inhibited tumorigenicity by sponging miR-934 and miR-942-5p in BC [ 15 , 16 ]. Considering the inhibitory effect of circRNF10 on BC, it raised the possibility that circRNF10 might become an agent for BC treatment.…”

Section: Discussionsupporting

confidence: 93%

“…As for the cytoplasmic circRNAs, they mostly acted as a sponge of miRNAs [ 34 ] and decoys of proteins [ 35 ]. Previous studies have explored the role of circRNF10 as an miRNA sponge [ 15 , 16 ]. Differing from these studies, we focused on the potential of circRNF10 in binding proteins and discovered a novel role in which it could bind to DHX15 in BC by interacting with the RecA2 domain.…”

Section: Discussionmentioning

confidence: 99%

“…An increasing body of evidence suggests that circRNAs have important biological functions in BC progression [ 12 – 14 ]. Previous studies have indicated that circRNF10 could act as the sponge of miR-934 and miR-942-5p [ 15 , 16 ]. Whether it could interact with proteins is still unknown.…”

Section: Introductionmentioning

confidence: 99%

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CircRNF10-DHX15 interaction suppressed breast cancer progression by antagonizing DHX15-NF-κB p65 positive feedback loop

Zheng

Wang

et al. 2023

Cell Mol Biol Lett

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Background Breast cancer (BC) is a common threat to women. The continuous activation of nuclear factor kappa B (NF-κB) signaling pathway contributes to the development of BC. This study aimed to investigate the role of a circular RNA (circRNF10) in BC progression and regulating NF-κB signaling pathway. Methods Bioinformatics analysis, RT-qPCR, subcellular fractionation, FISH, RNase R treatment, and actinomycin D assay were used to explore the expression and characteristics of circRNF10 in BC. The biological functions of circRNF10 in BC were analyzed by MTT assay, colony formation assay, wound healing assay, and Transwell assay. RNA pulldown and RIP assay were used to identify the interaction between circRNF10 and DEAH (Asp-Glu-Ala-His) box helicase 15 (DHX15). The impact of circRNF10-DHX15 interaction on NF-κB signaling pathway was explored by western blot, IF, and co-IP. Furthermore, dual-luciferase reporter assay, ChIP, and EMSA were performed to assess the effect of NF-κB p65 on DHX15 transcription. Results CircRNF10 was downregulated in BC, and lower expression of circRNF10 was related to poor prognosis of patients with BC. CircRNF10 inhibited the proliferation and migration of BC. Mechanically, circRNF10-DHX15 interaction sequestered DHX15 from NF-κB p65, thereby inhibiting the activation of NF-κB signaling pathway. On the other hand, NF-κB p65 enhanced DHX15 transcription by binding to the promoter of DHX15. Altogether, circRNF10 impaired the DHX15-NF-κB p65 positive feedback loop and suppressed the progression of BC. Conclusion CircRNF10-DHX15 interaction suppressed the DHX15-NF-κB p65 positive feedback loop, thereby inhibiting BC progression. These findings provide new insights in the continuous activation of NF-κB signaling pathway and raised potential therapeutic approach for BC treatment.

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Section: Discussionsupporting

confidence: 93%