CDR1as is overexpressed in laryngeal squamous cell carcinoma to promote the tumour’s progression via miR‐7 signals

Zhang, Jianzhong; Hu, Huayong; Zhao, Yaoxin; Zhao, Yue

doi:10.1111/cpr.12521

Cited by 71 publications

(70 citation statements)

References 22 publications

(29 reference statements)

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“…Dysregulated circRNAs may be associated with the diagnosis and therapy of cancers . Several reports have demonstrated that circCDR1as could function as an oncogenic circRNA or tumor suppressor in different cancers because of the change of tumor microenvironment . Zhang et al .…”

Section: Discussionmentioning

confidence: 99%

“…28 Several reports have demonstrated that circCDR1as could function as an oncogenic circRNA or tumor suppressor in different cancers because of the change of tumor microenvironment. [11][12][13][14][15] Zhang et al…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, emerging evidence suggests that several circRNAs might contribute to the progression of NSCLC . Accruing evidence demonstrates that circRNA antisense to cerebellar degeneration‐related protein 1 transcript (circCDR1as) could promote the development of hepatocellular carcinoma, colorectal cancer and laryngeal squamous cell carcinoma and inhibit the progression of bladder cancer and ovarian cancer . Importantly, a previous study reveals that circCDR1as acts as an oncogene to facilitate the development of NSCLC .…”

Section: Introductionmentioning

confidence: 99%

“…[8][9][10] Accruing evidence demonstrates that circRNA antisense to cerebellar degeneration-related protein 1 transcript (circCDR1as) could promote the development of hepatocellular carcinoma, colorectal cancer and laryngeal squamous cell carcinoma and inhibit the progression of bladder cancer and ovarian cancer. [11][12][13][14][15] Importantly, a previous study reveals that circCDR1as acts as an oncogene to facilitate the development of NSCLC. 16 However, the mechanism underlying the participation of circCDR1as in the progression of NSCLC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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CircRNA CDR1as knockdown inhibits progression of non‐small‐cell lung cancer by regulating miR‐219a‐5p/SOX5 axis

Zhang

Pan

et al. 2020

Thoracic Cancer

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Background Circular RNAs (circRNAs) participate in the development of human cancers by regulating multiple cell processes. CircRNA antisense to the cerebellar degeneration‐related protein 1 transcript (circCDR1as) expression is dysregulated in many cancers, including non‐small‐cell lung cancer (NSCLC). However, the mechanism by which circCDR1as mediates the development of NSCLC remains unknown. Methods A total of 30 paired cancer and normal tissues were collected from patients with NSCLC. The expression levels of circCDR1as, microRNA (miR)‐219a‐5p and Sex determining region Y‐box protein 5 (SOX5) were measured in tissues or cells by quantitative real‐time polymerase chain reaction or western blot. Cell viability, apoptosis, migration and invasion were detected by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide, colony formation, flow cytometry and transwell assays, respectively. The target relationship between miR‐219a‐5p and circCDR1as or SOX5 was validated by dual‐luciferase reporter assay. Results CircCDR1as expression was elevated in NSCLC tissues and cells in comparison to the matched controls. Interference of circCDR1as led to obvious inhibition of cell viability, migration and invasion and increase of apoptosis in NSCLC cells. MiR‐219a‐5p acted as a target of circCDR1as and miR‐219a‐5p downregulation attenuated the regulatory effect of circCDR1as silencing on NSCLC progression. Moreover, miR‐219a‐5p targeted SOX5 to repress the progression of NSCLC in vitro. Besides, circCDR1as knockdown reduced the expression of SOX5 by increasing miR‐219a‐5p level. Conclusion Knockdown of circCDR1as inhibited the progression of NSCLC by decreasing cell viability, migration and invasion and increasing apoptosis by upregulating miR‐219a‐5p and downregulating SOX5.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CircRNA CDR1as knockdown inhibits progression of non‐small‐cell lung cancer by regulating miR‐219a‐5p/SOX5 axis

Zhang

Pan

et al. 2020

Thoracic Cancer

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“…Circular RNAa (circRNAs), a new subtype of ncRNAs, have covalently closed loop structures with a back splice site between 5′-and 3′-end and exhibit higher conservativity than the corresponding linear RNAs duo to resistance to RNase R [7]. Mounting data indicated that circRNAs act critical roles in multiple molecular mechanisms including tumor biomarkers, regulating gene expression, and sponging miRNAs in cancer [8][9][10]. Circ-DONSON [8], circAGO2 [9], circAKT3 [11], circNRIP1 [12], and circDLST [13] are upregulated in GC tissues samples, and their increased expression is associated with TNM stage and poor prognosis in patients with GC [8,11,13].…”

Section: Introductionmentioning

confidence: 99%

CircDUSP16 promotes the tumorigenesis and invasion of gastric cancer by sponging miR-145-5p

et al. 2019

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Background Circular RNAs (circRNAs) as a novel subgroup of non-coding RNAs act a critical role in the pathogenesis of gastric cancer (GC). However, the underlying mechanisms by which hsa_circ_0003855 (circDUSP16) contributes to GC are still undocumented. Materials The differentially expressed circRNAs were identified by GEO database. The association of circDUSP16 or miR-145-5p expression with clinicopathological features and prognosis in GC patients was analyzed by FISH and TCGA-seq data set. Loss-and gain-of-function experiments as well as a xenograft tumor model were performed to assess the role of circDUSP16 in GC cells. circDUSP16-specific binding with miR-145-5p was confirmed by bioinformatic analysis, luciferase reporter, and RNA immunoprecipitation assays. Results The expression levels of circDUSP16 were markedly increased in GC tissue samples and acted as an independent prognostic factor of poor survival in patients with GC. Knockdown of circDUSP16 repressed the cell viability, colony formation, and invasive potential in vitro and in vivo, but ectopic expression of circDUSP16 reversed these effects. Moreover, circDUSP16 possessed a co-localization with miR-145-5p in the cytoplasm, and acted as a sponge of miR-145-5p, which attenuated circDUSP16-induced tumor-promoting effects and IVNS1ABP expression in GC cells. MiR-145-5p had a negative correlation with circDUSP16 expression and its low expression was associated with poor survival in GC patients. Conclusions CircDUSP16 facilitates the tumorigenesis and invasion of GC cells by sponging miR-145-5p, and may provide a novel therapeutic target for GC.Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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A novel intronic circular RNA, circGNG7, inhibits head and neck squamous cell carcinoma progression by blocking the phosphorylation of heat shock protein 27 at Ser78 and Ser82

Wei

et al. 2021

Cancer Communications

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Background There is increasing evidence that circular RNAs (circRNAs) play a significant role in pathological processes including tumorigenesis. In contrast to exonic circRNAs, which are the most frequently reported circRNAs in cancer so far, the studies of intronic circRNAs have been greatly lagged behind. Here, we aimed to investigate the regulatory role of intronic circRNAs in head and neck squamous cell carcinoma (HNSCC). Methods We conducted whole‐transcriptome sequencing with four pairs of primary tumor tissues and adjacent normal tissues from HNSCC patients. Then, we characterized circGNG7 expression in HNSCC tissues and cell lines and explored its association with the prognosis of HNSCC patients. We also identified interactions between circGNG7 and functional proteins, which alter downstream signaling that regulate HNSCC progression. Results In this study, we identified a new intronic circRNA, circGNG7, and validated its functional roles in HNSCC progression. CircGNG7 was predominately localized to the cytoplasm, and its expression was downregulated in both HNSCC tissues andCAL27, CAL33, SCC4, SCC9, HN6, and HN30 cells. Low expression of circGNG7 was significantly correlated with poor prognosis in HNSCC patients. Consistent with this finding, overexpression of circGNG7 strongly inhibited tumor cell proliferation, colony formation, in vitro migration, and in vivo tumor growth. Mechanistically, the expression of circGNG7 in HNSCC cells was regulated by the transcription factor SMAD family member 4 (SMAD4). Importantly, we discovered that circGNG7 could bind to serine residues 78 and 82 of the functional heat shock protein 27 (HSP27), occupying its phosphorylation sites and hindering its phosphorylation, which reduced HSP27‐JNK/P38 mitogen‐activated protein kinase (MAPK) oncogenic signaling. Downregulation of circGNG7 expression in HNSCC increased HSP27‐JNK/P38 MAPK signaling and promoted tumor progression. Conclusions Our results revealed that a new intronic circRNA, circGNG7, functions as a strong tumor suppressor and that circGNG7/HSP27‐JNK/P38 MAPK signaling is a novel mechanism by which HNSCC progression can be controlled.

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CDR1as is overexpressed in laryngeal squamous cell carcinoma to promote the tumour’s progression via miR‐7 signals

Abstract: CDR1as is an oncogene that promotes LSCC progression by regulating miR-7 signals.

Cited by 71 publications

References 22 publications

CircRNA CDR1as knockdown inhibits progression of non‐small‐cell lung cancer by regulating miR‐219a‐5p/SOX5 axis

CircRNA CDR1as knockdown inhibits progression of non‐small‐cell lung cancer by regulating miR‐219a‐5p/SOX5 axis

CircDUSP16 promotes the tumorigenesis and invasion of gastric cancer by sponging miR-145-5p

A novel intronic circular RNA, circGNG7, inhibits head and neck squamous cell carcinoma progression by blocking the phosphorylation of heat shock protein 27 at Ser78 and Ser82

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