miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2

Chen, Xiaohe; Yang, Shouhang; Zeng, Jue; Chen, Ming

doi:10.3892/mmr.2018.9680

Cited by 25 publications

(26 citation statements)

References 31 publications

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“…We also examined the expression of FOXK2, which has previously exhibited reciprocal expression with miR-1271-5p in hepatocellular carcinoma tissue, but we were unable to replicate this in SH-SY5Y cells [37]. Similarly, while ZIC2 was previously shown to be modulated by the miRNA [38], it was not expressed in differentiated SH-SY5Y cells.…”

Section: Functional Analysis Of Genes Directly Targeted By Mir-1271-5pmentioning

confidence: 80%

Characterising the Transcriptional and Translational Impact of the Schizophrenia-Associated miR-1271-5p in Neuronal Cells

Kiltschewskij

Geaghan

Cairns

2020

Cells

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MicroRNA (miRNA) coordinate complex gene expression networks in cells that are vital to support highly specialised morphology and cytoarchitecture. Neurons express a rich array of miRNA, including many that are specific or enriched, which have important functions in this context and implications for neurological conditions. While the neurological function of a number of brain-derived miRNAs have been examined thoroughly, the mechanistic basis of many remain obscure. In this case, we investigated the transcriptome-wide impact of schizophrenia-associated miR-1271-5p in response to bidirectional modulation. Alteration of miR-1271-5p induced considerable changes to mRNA abundance and translation, which spanned a diverse range of cellular functions, including directly targeted genes strongly associated with cytoskeletal dynamics and cellular junctions. Mechanistic analyses additionally revealed that upregulation of miR-1271-5p predominantly repressed mRNAs through destabilisation, wherein 3′UTR and coding sequence binding sites exhibited similar efficacy. Knockdown, however, produced no discernible trend in target gene expression and strikingly resulted in increased expression of the highly conserved miR-96-5p, which shares an identical seed region with miR-1271-5p, suggesting the presence of feedback mechanisms that sense disruptions to miRNA levels. These findings indicate that, while bidirectional regulation of miR-1271-5p results in substantial remodeling of the neuronal transcriptome, these effects are not inverse in nature. In addition, we provide further support for the idea that destabilisation of mRNA is the predominant mechanism by which miRNAs regulate complementary mRNAs.

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Section: Functional Analysis Of Genes Directly Targeted By Mir-1271-5pmentioning

confidence: 80%

Characterising the Transcriptional and Translational Impact of the Schizophrenia-Associated miR-1271-5p in Neuronal Cells

Kiltschewskij

Geaghan

Cairns

2020

Cells

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“…miR-1271-5p has been reported as a tumor suppressor in several different types of tumors. Chen et al reported that miR-1271-5p suppressed cell proliferation and induced cell apoptosis via regulating ZIC2 in acute myeloid leukemia ( 25 ). In another study, miR-1271-5p negatively regulated FOXK2 and inhibited cell growth and hepatocellular carcinoma development ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

RP11‑619L19.2 promotes colon cancer development by regulating the miR‑1271‑5p/CD164 axis

Zhang

et al. 2020

Oncol Rep

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Colon cancer (CC) is one of the leading causes of cancer-related mortality in China and western countries. Several studies have demonstrated that long non-coding RNAs (lncRNAs) play critical roles in cancer development. However, the function of lncRNA RP11-619L19.2 in colon cancer remains unclear. The aim of the present study was to investigate the expression pattern, function and underlying mechanism of action of RP11-619L19.2 in CC development and metastasis. RP11-619L19.2 was found to be highly expressed in CC tissues and cell lines, and it was associated with advanced TNM stage and lymph node metastasis. Furthermore, knockdown of RP11-619L19.2 inhibited CC cell proliferation, migration, invasion and epithelial-to-mesenchymal transition (EMT). It was also observed that RP11-619L19.2 was reciprocally repressed by miR-1271-5p. Of note, miR-1271-5p negatively regulated CD164 expression by directly targeting the 3′-untranslated region of CD164. Overexpression of CD164 reversed the antimetastatic activity of RP11-619L19.2 knockdown in CC cells. Mechanistically, it was demonstrated that lncRNA RP11-619L19.2 played an oncogenic role and promoted CC development and metastasis by regulating the miR-1271-5p/CD164 axis and EMT. In conclusion, the findings of the present study indicated that RP11-619L19.2 regulates CD164 expression and EMT by sponging miR-1271-5p, which may provide novel targets for lncRNA-directed diagnosis and therapy for patients with CC.

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“…More importantly, miRNAs were known to play a pivotal role in human diseases by targeting 3'UTR of target mRNA [9]. ZIC2 was reported as a target gene of multiple miRNA in tumor, such as miR-1271-5p [26]. Surely, a miRNA may target many genes in diseases, which may ascribe to the complexity genome and multiplex regulation network of gene expression [27,28].…”

Section: Discussionmentioning

confidence: 99%

Upregulation of circ_0000069 stimulates cervical cancer development by enhancing proliferation, migration, invasion while inhibiting apoptosis through the miR-4429/ZIC2 axis

Yang

Zhao³

et al. 2020

Preprint

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Background Cervical cancer (CC) is a common female cancer according to global cancer statistics. The current study was used to investigate the regulatory mechanism of circ_0000069 in CC. Methods The real-time quantitative polymerase chain reaction (RT-qPCR) was used to assess circ_0000069, miR-4429, and zinc finger protein of the cerebellum 2 (ZIC2) expression in CC tissues and cells. Kaplan-Meier analysis was performed in CC patients to analyze the relationship between survival time and circ_0000069 expression. The proliferation, apoptosis, cell cycle of CC cells were detected by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT), colony formation, and flow cytometry analyses, respectively. In addition, western blot assay was employed to show expression levels of apoptosis/cell cycle-related proteins, as well as ZIC2. The migration and invasion of CC cells were assessed by transwell analysis. Possible target miRNAs of circ_0000069, along with the interaction between ZIC2 and miR-4429 were confirmed by pull-down and dual-luciferase reporter assays. Eventually, the functional role of circ_0000069 in vivo was clarified with the xenograft experiment in nude mice. Results Circ_0000069 was overexpressed in CC tissues and cells than controls. Furthermore, the silencing of circ_0000069 inhibited proliferation, migration, and invasion while included apoptosis and cell cycle arrest of CC cells, which was overturned by downregulation of miR-4429. Importantly, ZIC2 was a direct target of miR-4429 in CC cells, and we further confirmed that overexpression of miR-4429 suppressed CC progress by decreasing ZIC2 expression in CC cells. Surely, silencing of circ_0000069 inhibited tumorigenesis in vivo. Conclusion Our current results suggested that circ_0000069 exerted its tumorigenic roles by regulation of proliferation, apoptosis, cell cycle, migration, and invasion of CC cells, supporting that circ_0000069/miR-4429/ZIC2 axis may provide potential prognostic biomarkers for CC.

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miR‑1271‑5p inhibits cell proliferation and induces apoptosis in acute myeloid leukemia by targeting ZIC2

Cited by 25 publications

References 31 publications

Characterising the Transcriptional and Translational Impact of the Schizophrenia-Associated miR-1271-5p in Neuronal Cells

Characterising the Transcriptional and Translational Impact of the Schizophrenia-Associated miR-1271-5p in Neuronal Cells

RP11‑619L19.2 promotes colon cancer development by regulating the miR‑1271‑5p/CD164 axis

Upregulation of circ_0000069 stimulates cervical cancer development by enhancing proliferation, migration, invasion while inhibiting apoptosis through the miR-4429/ZIC2 axis

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