Circular RNA hsa_circ_0002938 (circCRIM1) promotes the progression of esophageal squamous cell carcinoma by upregulating transcription factor 12

Li, Xiaopeng; Jia, Yunlong; Duan, Yuqing; Zhao, Yan; Yin, Xiaolei; Zhen, Shuman; Zhang, Yi; Liu, Lihua

doi:10.4149/neo_2023_220823n857

Cited by 2 publications

(1 citation statement)

References 31 publications

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“…Next, we explored the specific molecular mechanism of circCRIM1 in CIR. Studies have confirmed that circCRIM1 can function as a ceRNA to bind to miRNAs in different diseases 26,27 . Thus, we studied whether circCRIM1 exert the ceRNA function in CIR.…”

Section: Resultsmentioning

confidence: 92%

CircCRIM1/microRNA‐141‐3p/thioredoxin‐binding protein axis mediates neuronal apoptosis after cerebral ischemia‐reperfusion

Fan

et al. 2023

Environmental Toxicology

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Numerous studies have indicated enrichment of circular RNA (circRNA) in the brain takes on a momentous role in cerebral ischemia‐reperfusion (CIR) injury. A recent study discovered a novel circCRIM1, was highly expressed in the middle cerebral artery occlusion‐reperfusion (MCAO/R) model. Nevertheless, its specific biological function remained unknown. The study was to explore circCRIM1 in CIR‐induced neuronal apoptosis. As measured, circCRIM1 and TXNIP were up‐regulated, while miR‐141‐3p was down‐regulated in MCAO/R mouse model and OGD/R SH‐SY5Y cells. Depleting circCRIM1 reduced the number of apoptotic neurons in MCAO/R rats, increased the number of Nissl bodies, prevented reactive oxygen species production and oxidative stress imbalance in brain tissues, repressed cleaved caspase‐3, Bax, and Cyto C protein levels and increased Bcl‐2 levels. Overexpression of circCRIM1 further repressed neuronal activity and accelerated apoptosis in OGD/R model, disrupted redox balance. Depleting circCRIM1 had the opposite effect in OGD/R model. Knocking down miR‐141‐3p or TXNIP weakened the effects of knocking down circCRIM1 or overexpressing circCRIM1, separately. Mechanistically, circCRIM1 exerted an active role in CIR injury via miR‐141‐3p to mediate TXNIP. All in all, the circCRIM1/miR‐141‐3p/TXNIP axis might be a latent therapeutic target for CIR injury.

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Section: Resultsmentioning

confidence: 92%

CircCRIM1/microRNA‐141‐3p/thioredoxin‐binding protein axis mediates neuronal apoptosis after cerebral ischemia‐reperfusion

Fan

et al. 2023

Environmental Toxicology

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TCF12-regulated GRB7 facilitates the HER2+ breast cancer progression by activating Notch1 signaling pathway

Wang,

Wu,

et al. 2024

J Transl Med

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Background Human epidermal growth factor receptor 2-positive (HER2+) breast cancer (BC), which accounts for approximately one-fifth of all BCs, are highly invasive with a high rate of recurrence and a poor prognosis. Several studies have shown that growth factor receptor-bound protein 7 (GRB7) might be a potential therapeutic target for tumor diagnosis and prognosis. Nevertheless, the role of GRB7 in HER2+ BC and its underlying mechanisms have not been fully elucidated. The aim of this study was to investigate the biological function and regulatory mechanism of GRB7 in HER2+ BC. Methods Bioinformatics analysis was performed using the TCGA, GEO and CancerSEA databases to evaluate the clinical significance of GRB7. RT quantitative PCR, western blot and immunofluorescence were conducted to assess the expression of GRB7 in BC cell lines and tissues. MTT, EdU, colony formation, wound healing, transwell, and xenograft assays were adopted to explore the biological function of GRB7 in HER2+ BC. RNA sequencing was performed to analyze the signaling pathways associated with GRB7 in SK-BR-3 cells after the cells were transfected with GRB7 siRNA. Chromatin immunoprecipitation analysis (ChIP) and luciferase reporter assay were employed to elucidate the potential molecular regulatory mechanisms of GRB7 in HER2+ BC. Results GRB7 was markedly upregulated and associated with poor prognosis in BC, especially in HER2+ BC. Overexpression of GRB7 increased the proliferation, migration, invasion, and colony formation of HER2+ BC cells, while depletion of GRB7 had the opposite effects in HER2+ BC cells and inhibited xenograft growth. ChIP-PCR and luciferase reporter assay revealed that TCF12 directly bound to the promoter of the GRB7 gene to promote its transcription. GRB7 facilitated HER2+ BC epithelial-mesenchymal transition (EMT) progression by interacting with Notch1 to activate Wnt/β-catenin pathways and other signaling (i.e., AKT, ERK). Moreover, forced GRB7 overexpression activated Wnt/β-catenin to promote EMT progression, and partially rescued the inhibition of HER2+ BC proliferation, migration and invasion induced by TCF12 silencing. Conclusions Our work elucidates the oncogenic role of GRB7 in HER2+ BC, which could serve as a prognostic indicator and promising therapeutic target. Supplementary Information The online version contains supplementary material available at 10.1186/s12967-024-05536-6.

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Circular RNA hsa_circ_0002938 (circCRIM1) promotes the progression of esophageal squamous cell carcinoma by upregulating transcription factor 12

Cited by 2 publications

References 31 publications

CircCRIM1/microRNA‐141‐3p/thioredoxin‐binding protein axis mediates neuronal apoptosis after cerebral ischemia‐reperfusion

CircCRIM1/microRNA‐141‐3p/thioredoxin‐binding protein axis mediates neuronal apoptosis after cerebral ischemia‐reperfusion

TCF12-regulated GRB7 facilitates the HER2+ breast cancer progression by activating Notch1 signaling pathway

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