Withdrawal: Down‐regulation of circRNA_0000143 regulates miR‐142‐3p/GRα axis to facilitate the progression of T‐ALL

Tong, Juan; Liu, Huilan; Wen, Yu-Chieh; Zhang, Lei; Song, Kang; Sun, Guangyu; Sun, Zimin

doi:10.1111/cas.15082

Cited by 2 publications

(4 citation statements)

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“…Transwell assays were performed to measure cell migration using Transwell chambers (Corning, Cambridge, MA, USA) [ 27 ]. Following the corresponding processing, 2 × 10 4 endothelial cells were harvested, resuspended in DMEM without serum, and placed into the apical chamber.…”

Section: Methodsmentioning

confidence: 99%

“…The wild-type and mutant sequences of circUSP36 were ligated into the luciferase reporter plasmid psiCHECK-2 (Promega, Madison, WI, USA) to synthesize circUSP36-WT and circUSP36-MUT [ 27 ]. WNT4-WT and WNT4-MUT constructs were acquired using the same method.…”

Section: Methodsmentioning

confidence: 99%

“…Protein isolation was carried out using RIPA buffer (Thermo Fisher Scientific), and a bicinchoninic acid assay kit (Thermo Fisher Scientific) was used for protein quantitation [ 27 ]. Protein samples were separated by 10% SDS-PAGE and transferred to polyvinylidene fluoride membranes (Millipore, Billerica, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

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A circular RNA, circUSP36, accelerates endothelial cell dysfunction in atherosclerosis by adsorbing miR-637 to enhance WNT4 expression

et al. 2021

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Atherosclerosis is a fatal disorder that is fundamental to various cardiovascular diseases and severely threatens people's health worldwide. Several studies have demonstrated the role of circular RNAs (circRNAs) in the pathogenesis of atherosclerosis. circUSP36 acts as a key modulator in the progression of atherosclerosis, but the molecular mechanism underlying this role is as yet unclear. This study aimed to elucidate the mechanism by which circUSP36 exerts its function in an in vitro cell model of endothelial cell dysfunction, which is one of pathological features of atherosclerosis. The circRNA traits of circUSP36 were confirmed, and we observed high expression of circUSP36 in endothelial cells exposed to oxidized low-density lipoprotein (ox-LDL). Functional assays revealed that overexpression of circUSP36 suppressed proliferation and migration of ox-LDL-treated endothelial cells. In terms of its mechanism, circUSP36 adsorbed miR-637 by acting as an miRNA sponge. Moreover, enhanced expression of miR-637 abated the impact of circUSP36 on ox-LDL-treated endothelial cell dysregulation. Subsequently, the targeting relationship between miR-637 and WNT4 was predicted using bioinformatics tools and was confirmed via luciferase reporter and RNA pull-down assays. Notably, depletion of WNT4 rescued circUSP36-mediated inhibition of endothelial cell proliferation and migration. In conclusion, circUSP36 regulated WNT4 to aggravate endothelial cell injury caused by ox-LDL by competitively binding to miR-637; this finding indicates circUSP36 to be a promising biomarker for the diagnosis and therapy of atherosclerosis.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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A circular RNA, circUSP36, accelerates endothelial cell dysfunction in atherosclerosis by adsorbing miR-637 to enhance WNT4 expression

et al. 2021

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“…Expression of circ_0000143 was also significantly reduced in T-ALL patient samples compared to healthy controls; overexpression of circ_0000143 inhibited T-ALL cell viability, migration and invasion, and induced apoptosis. Mechanistically, circ_0000143 acted as a molecular sponge to sequester miR-142-3p, thereby upregulating miR142-3p repressed glucocorticoid receptor α (GRα) expression [189]. Likewise, cir-cADD2 was downregulated in ALL patient samples and cell lines [190]; overexpression of circADD2 inhibited cell proliferation and promoted apoptosis; while, knockdown of circADD2 showed the opposite effect; mechanistically, circADD2 could directly sponge miR-149-5p, a positive regulator of AKT2, leading to reduction of AKT2 and pAKT2 level [190].…”

Section: Circrnas Acting As Tumor Suppressors In All Pathogenesismentioning

confidence: 99%

Linear and Circular Long Non-Coding RNAs in Acute Lymphoblastic Leukemia: From Pathogenesis to Classification and Treatment

Maimaitiyiming

Yang

et al. 2022

IJMS

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The coding regions account for only a small part of the human genome, and the remaining vast majority of the regions generate large amounts of non-coding RNAs. Although non-coding RNAs do not code for any protein, they are suggested to work as either tumor suppressers or oncogenes through modulating the expression of genes and functions of proteins at transcriptional, posttranscriptional and post-translational levels. Acute Lymphoblastic Leukemia (ALL) originates from malignant transformed B/T-precursor-stage lymphoid progenitors in the bone marrow (BM). The pathogenesis of ALL is closely associated with aberrant genetic alterations that block lymphoid differentiation and drive abnormal cell proliferation as well as survival. While treatment of pediatric ALL represents a major success story in chemotherapy-based elimination of a malignancy, adult ALL remains a devastating disease with relatively poor prognosis. Thus, novel aspects in the pathogenesis and progression of ALL, especially in the adult population, need to be further explored. Accumulating evidence indicated that genetic changes alone are rarely sufficient for development of ALL. Recent advances in cytogenic and sequencing technologies revealed epigenetic alterations including that of non-coding RNAs as cooperating events in ALL etiology and progression. While the role of micro RNAs in ALL has been extensively reviewed, less attention, relatively, has been paid to other non-coding RNAs. Herein, we review the involvement of linear and circular long non-coding RNAs in the etiology, maintenance, and progression of ALL, highlighting the contribution of these non-coding RNAs in ALL classification and diagnosis, risk stratification as well as treatment.

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Withdrawal: Down‐regulation of circRNA_0000143 regulates miR‐142‐3p/GRα axis to facilitate the progression of T‐ALL

Cited by 2 publications

References 0 publications

A circular RNA, circUSP36, accelerates endothelial cell dysfunction in atherosclerosis by adsorbing miR-637 to enhance WNT4 expression

A circular RNA, circUSP36, accelerates endothelial cell dysfunction in atherosclerosis by adsorbing miR-637 to enhance WNT4 expression

Linear and Circular Long Non-Coding RNAs in Acute Lymphoblastic Leukemia: From Pathogenesis to Classification and Treatment

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