Sevoflurane inhibits malignant progression of colorectal cancer via hsa_circ_0000231-mediated miR-622

Wang, Jingpeng; Li, Shuyuan; Zhang, Gaofeng; Han, Huihua

doi:10.1186/s40709-021-00145-6

Cited by 8 publications

(8 citation statements)

References 33 publications

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“…1 B). Studies have found that hsa_circ_0000231 affects the progression of colorectal cancer by targeting miR-622 and miR-502-5p [ 23 , 24 ]. The results of this study also found that overexpression of hsa_circ_0000231 can promote the growth of CRC cells and lead to a poor prognosis (Figs.…”

Section: Discussionmentioning

confidence: 99%

hsa_circ_0000231 Promotes colorectal cancer cell growth through upregulation of CCND2 by IGF2BP3/miR-375 dual pathway

et al. 2022

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Background Circular RNAs (circRNAs) have emerged as vital regulators of the initiation and progression of diverse kinds of human cancers. In this study, we explored the role of hsa_circ_0000231 and its downstream pathway in CRC. Methods The expression profile of circRNAs in 5 pairs of CRC tissues and adjacent normal tissues were analyzed by Microarray. Quantitative real-time PCR and in situ hybridization and Base Scope Assay were used to determine the level and prognostic values of hsa_circ_0000231. Then, functional experiments in vitro and in vivo were performed to investigate the effects of hsa_circ_0000231 on cell proliferation. Mechanistically, fluorescent in situ hybridization, dual luciferase reporter assay, RNA pull-down and RNA immunoprecipitation experiments were performed to confirm the interaction between hsa_circ_0000231 and IGF2BP3 or has_miR-375. Results We acquired data through circRNA microarray profiles, showing that the expression of hsa_circ_0000231 was upregulated in CRC primary tissues compared to adjacent normal tissues, which was indicated poor prognosis of patients with CRC. Functional analysis indicated that inhibition of hsa_circ_0000231 in CRC cell lines could suppress CRC cell proliferation as well as tumorigenesis in vitro and in vivo. The mechanistic analysis showed that hsa_circ_0000231 might, on the one hand, act as a competing endogenous RNA of miR-375 to promote cyclin D2 (CCND2) and, on the other hand, bind to the IGF2BP3 protein to prevent CCND2 degradation. Conclusions The findings suggested that hsa_circ_0000231 facilitated CRC progression by sponging miR-375 or binding to IGF2BP3 to modulate CCND2, implying that hsa_circ_0000231 might be a potential new diagnostic and therapeutic biomarker of CRC.

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Section: Discussionmentioning

confidence: 99%

hsa_circ_0000231 Promotes colorectal cancer cell growth through upregulation of CCND2 by IGF2BP3/miR-375 dual pathway

et al. 2022

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“…Literature review reveals that nine circRNAs may regulate this coexpression network through miRNA‐200c and miR‐622 including circ_VMA21, circ_0057481, circ_GLG1, circ_TMX4, circ_MTUS1, circ_UBXN7, circ_0119872, circ_0000231 and circ_0000211. 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 …”

Section: Discussionmentioning

confidence: 99%

“…48 Januchowski et al 49 reported that the extracellular matrix (ECM) could affect drug resistance pro- TMX4, circ_MTUS1, circ_UBXN7, circ_0119872, circ_0000231 and circ_0000211. [55][56][57][58][59][60][61][62][63] Studies show that RSAD2 is up-regulated and associated with worse relapse-free survival in breast cancer. 64 Tang et al 65 reported that the overexpression of this immune-related gene is associated with tumour grade, stage and size in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

“…In this module, one TF (IRF1), one lncRNA (HCP5) and two miRNAs (miR‐200C and miR‐622) were significantly co‐expressed with the identified hub genes. Literature review reveals that nine circRNAs may regulate this coexpression network through miRNA‐200c and miR‐622 including circ_VMA21, circ_0057481, circ_GLG1, circ_TMX4, circ_MTUS1, circ_UBXN7, circ_0119872, circ_0000231 and circ_0000211 55–63 …”

Section: Discussionmentioning

confidence: 99%

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Construction of miRNA‐lncRNA‐mRNA co‐expression network affecting EMT‐mediated cisplatin resistance in ovarian cancer

Naghsh-Nilchi

Ghahnavieh

Dehghanian

2022

J Cellular Molecular Medi

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Platinum resistance is one of the major concerns in ovarian cancer treatment. Recent evidence shows the critical role of epithelial–mesenchymal transition (EMT) in this resistance. Epithelial‐like ovarian cancer cells show decreased sensitivity to cisplatin after cisplatin treatment. Our study prospected the association between epithelial phenotype and response to cisplatin in ovarian cancer. Microarray dataset GSE47856 was acquired from the GEO database. After identifying differentially expressed genes (DEGs) between epithelial‐like and mesenchymal‐like cells, the module identification analysis was performed using weighted gene co‐expression network analysis (WGCNA). The gene ontology (GO) and pathway analyses of the most considerable modules were performed. The protein–protein interaction network was also constructed. The hub genes were specified using Cytoscape plugins MCODE and cytoHubba, followed by the survival analysis and data validation. Finally, the co‐expression of miRNA‐lncRNA‐TF with the hub genes was reconstructed. The co‐expression network analysis suggests 20 modules relating to the Epithelial phenotype. The antiquewhite4, brown and darkmagenta modules are the most significant non‐preserved modules in the Epithelial phenotype and contain the most differentially expressed genes. GO, and KEGG pathway enrichment analyses on these modules divulge that these genes were primarily enriched in the focal adhesion, DNA replication pathways and stress response processes. ROC curve and overall survival rate analysis show that the co‐expression pattern of the brown module's hub genes could be a potential prognostic biomarker for ovarian cancer cisplatin resistance.

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“…Furthermore, circCELSR1 acts as a molecular sponge and promotes paclitaxel resistance by competition with miR-1252 for binding FOXR2 [9]. For circ_0000231, it was reported [10] that circ_0000231 attenuated Sevo urane aroused repression impacts on CRC development by sponging miR-622. However, the role of circ_0000231 in OC PTX-resistance remains to be investigated.…”

Section: Introductionmentioning

confidence: 99%

Circ_0000231 Promotes Paclitaxel Resistance in Ovarian Cancer by Regulating miR-140/RAP1B

Liu

Wang

Xiao

et al. 2022

Preprint

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Purpose: Circular RNAs (circRNAs) are identified as vital regulators in a variety of cancers. However, the involvement of circ_0000231 in paclitaxel (PTX) resistant ovarian cancer (OC) remains unclear.Methods: The levels of circ_0000231, microRNA-140 (miR-140) and RAP1B were determined by quantitative real-time PCR (qRT-PCR) or Western blot assay. Cell proliferation, PTX- resistance, apoptosis, migration and invasion were assessed by Cell Counting Kit-8 (CCK-8), flow cytometry and transwell assay. The levels of resistant-related and epithelial–mesenchymal transition (EMT)-related proteins were measured by Western blot assay. Target association between miR-140 and circ_0000231 or RAP1B was demonstrated by dual[1]luciferase reporter assay or RNA Binding Protein Immunoprecipitation (RIP). Biological implications of circ_0000231 in ovarian cancer were implemented in tumor xenograft models.Results: Circ_0000231 and RAP1B levels were increased, while miR-140 level was decreased in PTX-resistant OC tissues and cells. Depletion of circ_0000231 could inhibit resistance, proliferation, invasion, migration and EMT and promoted apoptosis in PTX-resistant OC cells, which was opposited by overexpression of circ_0000231. Circ_0000231 acted as a sponge for miR- 140, and RAP1B was revealed to be target gene of miR-140. Circ_0000231 was a key molecule required for growth, migration, and PTX-resistance and was involved in EMT. Circ_0000231 knockdown increased PTX sensitivity of OC in vivo.Conclusion: Knockdown of circ_000231 suppressed PTX-resistant OC progression via regulating miR-140/RAP1B signaling pathway. Circ_0000231 might play vital roles in the tumorigenesis and chemoresistance of OC.

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Sevoflurane inhibits malignant progression of colorectal cancer via hsa_circ_0000231-mediated miR-622

Cited by 8 publications

References 33 publications

hsa_circ_0000231 Promotes colorectal cancer cell growth through upregulation of CCND2 by IGF2BP3/miR-375 dual pathway

hsa_circ_0000231 Promotes colorectal cancer cell growth through upregulation of CCND2 by IGF2BP3/miR-375 dual pathway

Construction of miRNA‐lncRNA‐mRNA co‐expression network affecting EMT‐mediated cisplatin resistance in ovarian cancer

Circ_0000231 Promotes Paclitaxel Resistance in Ovarian Cancer by Regulating miR-140/RAP1B

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