MiR-152 suppresses the proliferation and invasion of NSCLC cells by inhibiting FGF2

Cheng, Zhenshun; Ma, Ran; Tan, Wenfeng; Zhang, Li

doi:10.1038/emm.2014.51

Cited by 65 publications

(55 citation statements)

References 35 publications

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“…In these reports, overexpression of miRNAs targeting PTEN has been considered a contributing factor for tumor development (Huse et al, 2009). However, as our study indicated, miR-152 is also a potential regulator of PTEN; most previous reports have indicated that miR-152 acts as a tumor suppressor by targeting proteins other than PTEN (Cheng et al, 2014;He et al, 2015;. Therefore, although our data suggest a protective function of miR-152 during hypoxiainduced apoptosis in primary microvascular endothelial cells, the miR-152-PTEN relationship and its effects on the development and progression of cancer requires further investigation.…”

Section: Discussioncontrasting

confidence: 38%

A microRNA-152 that targets the phosphatase and tensin homolog to inhibit low oxygen induced-apoptosis in human brain microvascular endothelial cells

Cao

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Brain damage caused by perinatal asphyxia is dangerous for neonatal infants, but the mechanism by which it occurs remains elusive. In this study, microRNA-152 (miR-152) expression was induced by low oxygen levels in rat models of hypoxia brain damage, as well as in human brain microvascular endothelial cells (HBMECs) cultured in vitro. Analysis of the sequence of miR-152 revealed that the phosphatase and tensin homolog gene (PTEN) is probably the target of miR-152 both in humans and rats. When HBMECs were transfected with miR-152 mimics, PTEN expression was inhibited at both the mRNA and protein levels. Moreover, transfection with the miR-152 mimic also inhibited apoptosis induced by hypoxia. Furthermore, expression of the pro-apoptotic gene Bax was downregulated while the anti-apoptotic gene Bcl2 was upregulated after miR-152 mimic transfection. Taken together, these results indicate that miR-152 induced by hypoxia suppresses cell apoptosis and acts as a protective factor during hypoxia by repressing PTEN.

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Section: Discussioncontrasting

confidence: 38%

A microRNA-152 that targets the phosphatase and tensin homolog to inhibit low oxygen induced-apoptosis in human brain microvascular endothelial cells

Cao

et al. 2016

Genet. Mol. Res.

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“…For Trim72 (an E3 ubiquitin ligase) and Fga (the extracellular matrix protein fibrinogen involved in blood clot formation), there is little information associating them to metastasis or cancer. Studies have shown that miR-152 and miR-345 are associated with cancer and metastasis (Cheng et al, 2014; Tang et al, 2011). FGF2 and BAG3 , which promote metastasis, were predicted targets of miR-152 and miR-345 , thus loss of these microRNAs may lead to acceleration of metastases likely due to de-repression of these genes (Cheng et al, 2014; Tang et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Genome-wide CRISPR Screen in a Mouse Model of Tumor Growth and Metastasis

Chen

Sanjana

Zheng

et al. 2015

Cell

789

650

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Summary Genetic screens are powerful tools for identifying genes responsible for diverse phenotypes. Here we describe a genome-wide CRISPR-Cas9-mediated loss-of-function screen in tumor growth and metastasis. We mutagenized a non-metastatic mouse cancer cell line using a genome-scale library with 67,405 single guide RNAs (sgRNAs). The mutant cell pool rapidly generates metastases when transplanted into immunocompromised mice. Enriched sgRNAs in lung metastases and late stage primary tumors were found to target a small set of genes, suggesting specific loss-of-function mutations drive tumor growth and metastasis. Individual sgRNAs and a small pool of 624 sgRNAs targeting the top scoring genes from the primary screen dramatically accelerate metastasis. In all of these experiments, the effect of mutations on primary tumor growth positively correlates with the development of metastases. Our study demonstrates Cas9-based screening as a robust method to systematically assay gene phenotypes in cancer evolution in vivo.

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“…39 We suppresses cell proliferation and invasion of non-small-cell lung cancer by inhibiting FGF2. 61 Considering the up-regulation of miR-152 in hiPSCs-SLE, it would be interesting to investigate whether the AA-H 2 O 2 condition may suppress their proliferative potential through a similar mechanism previously described by Cheng et al…”

Section: Discussionmentioning

confidence: 88%

Establishment and characterization of induced pluripotent stem cells (iPSCs) from central nervous system lupus erythematosus

Angelis

Santamaria

Parrotta

et al. 2019

J Cellular Molecular Medi

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Involvement of the central nervous system (CNS) is an uncommon feature in systemic lupus erythematosus (SLE), making diagnosis rather difficult and challenging due to the poor specificity of neuropathic symptoms and neurological symptoms. In this work, we used human‐induced pluripotent stem cells (hiPSCs) derived from CNS‐SLE patient, with the aim to dissect the molecular insights underlying the disease by gene expression analysis and modulation of implicated pathways. CNS‐SLE‐derived hiPSCs allowed us to provide evidence of Erk and Akt pathways involvement and to identify a novel cohort of potential biomarkers, namely CHCHD2, IDO1, S100A10, EPHA4 and LEFTY1, never reported so far. We further extended the study analysing a panel of oxidative stress‐related miRNAs and demonstrated, under normal or stress conditions, a strong dysregulation of several miRNAs in CNS‐SLE‐derived compared to control hiPSCs. In conclusion, we provide evidence that iPSCs reprogrammed from CNS‐SLE patient are a powerful useful tool to investigate the molecular mechanisms underlying the disease and to eventually develop innovative therapeutic approaches.

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MiR-152 suppresses the proliferation and invasion of NSCLC cells by inhibiting FGF2

Cited by 65 publications

References 35 publications

A microRNA-152 that targets the phosphatase and tensin homolog to inhibit low oxygen induced-apoptosis in human brain microvascular endothelial cells

A microRNA-152 that targets the phosphatase and tensin homolog to inhibit low oxygen induced-apoptosis in human brain microvascular endothelial cells

Genome-wide CRISPR Screen in a Mouse Model of Tumor Growth and Metastasis

Establishment and characterization of induced pluripotent stem cells (iPSCs) from central nervous system lupus erythematosus

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