miR-195-5p Suppresses Lung Cancer Cell Proliferation, Migration, and Invasion Via FOXK1

Long, Zhiqiang; Wang, Yadong

doi:10.1177/1533033820922587

Cited by 33 publications

(28 citation statements)

References 22 publications

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“…Surprisingly, even in tissues with rather strong miR-497/195 cluster expression, such as lung, muscle, and heart, a detailed histological analysis did not reveal any alterations. This appears to contradict numerous studies that suggest a tumor-suppressive role of miR-497/195 in various cancer types, among them hepatocellular carcinoma, melanoma, colorectal cancer, lung cancer, or pancreatic cancer [24][25][26][27][30][31][32]. However, one has to keep in mind that our study evaluated spontaneous tumor development, that is, we assessed whether loss of miR-497/195 on its own is sufficient to prime tissues for aberrant growth.…”

Section: Discussionmentioning

confidence: 77%

“…However, it may very well be that miR-497/195 inactivation promotes tumorigenesis only as a second or third hit, and that other driver mutations are necessary to reveal its tumor-suppressive function. To test this, we plan to investigate whether loss of the miR-497/195 cluster affects tumor onset and burden in well-established tumor models such as KrasG12D-driven lung cancer and diethylnitrosamineinduced liver carcinogenesis, two cancer entities that have been associated with miR-497/195-mediated tumor suppression in the literature [24,25,30,32].…”

Section: Discussionmentioning

confidence: 99%

“…The peripheral T-cell subsets, on the other hand, in particular central and effector memory T cells, were not affected under steady-state conditions (Fig. 4C,D nonhematopoietic cancer settings [22][23][24][25][26][27][28]. To investigate this in more detail, we crossed miR-497/195 fl/fl mice with a ubiquitous Cre deleter strain to generate miR-497/195 À/À mice lacking the cluster in all tissues.…”

Section: Immune Cell Homeostasis and Function Are Not Affected Upon Lmentioning

confidence: 99%

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Differential roles of miR‐15a/16‐1 and miR‐497/195 clusters in immune cell development and homeostasis

et al. 2020

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MicroRNAs (miRNAs) post-transcriptionally repress almost all genes in mammals and thereby form an additional layer of gene regulation. As such, miRNAs impact on nearly every physiological process and have also been associated with cancer. Prominent examples of such miRNAs can be found in the miR-15 family, composed of the bicistronic clusters miR-15a/ 16-1, miR-15b/16-2, and miR-497/195. In particular, the miR-15a/16-1 cluster is deleted in almost two thirds of all chronic B lymphocytic leukemia (CLL) cases, a phenotype that is also recapitulated by miR-15a/16-1deficient as well as miR-15b/16-2-deficient mice. Under physiological conditions, those two clusters have been implicated in T-cell function, and B-cell and natural killer (NK) cell development; however, it is unclear whether miR-497 and miR-195 confer similar roles in health and disease. Here, we have generated a conditional mouse model for tissue-specific deletion of miR-497 and miR-195. While mice lacking miR-15a/16-1 in the hematopoietic compartment developed clear signs of CLL over time, aging mice deficient for miR-497/195 did not show such a phenotype. Likewise, loss of miR-15a/16-1 impaired NK and early B-cell development, whereas miR-497/195 was dispensable for these processes. In fact, a detailed analysis of miR-497/195-deficient mice did not reveal any effect on steady-state hematopoiesis or immune cell function. Unexpectedly, even whole-body deletion of the cluster was well-tolerated and had no obvious impact on embryonic development or healthy life span. Therefore, we postulate that the miR-497/195 cluster is redundant to its paralog clusters or that its functional relevance is restricted to certain physiological and pathological conditions.

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Immune Cell Homeostasis and Function Are Not Affected Upon Lmentioning

confidence: 99%

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Differential roles of miR‐15a/16‐1 and miR‐497/195 clusters in immune cell development and homeostasis

et al. 2020

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“…Based on the ceRNA network hypothesis, we conducted bioinformatics analysis using LncBase V2.0, the results showed that OXCT1-AS1 contained a conserved target site of miR-195. Previous studies have proved that miR-195 can act as a tumor suppressor in various cancers [35][36][37]. In our study, we explored the potential targets of miR-195.…”

Section: Discussionmentioning

confidence: 99%

Novel LncRNA OXCT1-AS1 Indicates Poor Prognosis and Contributes to Tumorigenesis by Regulating miR-195/CDC25A Axis in Glioblastoma

Chen

Zhou

et al. 2020

Preprint

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BackgroundIt’s well known that long noncoding RNAs (lncRNAs) contribute to multiple biological processes of human glioblastoma (GBM). However, identifying a specific lncRNA target is still the major difficulty. In this study, bioinformatics methods and competing endogenous RNA network (ceRNA) regulatory rules was used to identify GBM related lncRNAs, and found OXCT1 antisense RNA 1 (OXCT1-AS1) may acted as a potential therapeutic target for treatment of glioma.MethodsBased on the Gene Expression Omnibus (GEO) date set, we identified differential lncRNAs, microRNAs and mRNAs and constructed a lncRNA associated ceRNA network.Novel lncRNA OXCT1-AS1 was proposed to exercise its function as a ceRNA, and its potential targeted miRNAs was predicted through the database LncBase Predicted v.2. The expression pattern of OXCT1-AS1 was measured in glioma and normal tissue samples. Effect of OXCT1-AS1 on glioma cells were checked by cell count kit 8 assay, cell clone formation assay, transwell assay and flow cytometry in vitro, respectively. The dual-luciferase activity assay was performed to investigate the potential mechanism of ceRNA network. Finally, orthotopic mouse models of glioma was created to evaluate the influence of OXCT1-AS1 on tumor growth in vivo.ResultsIn this study, it was found that the expression of lncRNA OXCT1-AS1 is upregulated in both The Cancer Genome Atlas (TCGA) GBM cases and GBM tissue samples we collected, and a high expression of OXCT1-AS1 predicts poor prognosis of gliomas. Suppressing OXCT1-AS1 expression significantly decreased the proliferation of GBM cells and inhibited cell migration and invasion. We further investigated the potential mechanism and found OXCT1-AS1 may acted as a ceRNA of miR-195 to enhance CDC25A expression and attenuate glioma cells progression. Finally, knocking down of OXCT1-AS1 notably attenuated the severity of glioma in vivo.ConclusionOXCT1-AS1 inhibited glioma progression by regulating miR-195-5p/ CDC25A axis and can be a specific tumor marker and a novel potential therapeutic target for glioma treatment.

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“…FOX could also promote bladder carcinoma progression [24]. FOXK1 was reported to be involved in miR-365-3p-mediated breast cancer [25], miR-195-5p-mediated lung cancer [26], miR-646-meidated gastric cancer [27], circMAN2B2/miR-1275-mediated lung cancer [28], and LINC01503/miR-4492-mediated colorectal cancer [29]. However, the role of FOXK1 in bladder carcinoma has not been reported.…”

Section: Introductionmentioning

confidence: 99%

LINC00460 Enhances Bladder Carcinoma Cell Proliferation and Migration by Modulating miR-612/FOXK1 Axis

Huang

Zhang

et al. 2020

Pharmacology

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Introduction: LincRNA (long intergenic noncoding RNA) has been indicated as a mediator in tumorigenesis of bladder carcinoma. This study was performed to evaluate the role of LINC00460 in bladder carcinoma progression. Methods: Expression levels of LINC00460 in bladder carcinoma tissues and cell lines were analyzed via qRT-PCR. MTT, EdU (5-ethynyl-2′-deoxyuridine) staining, and colony formation assays were utilized to evaluate cell viability and proliferation. The wound healing assay was performed to evaluate bladder cancer cell migration, and the transwell assay was used to evaluate cell invasion. The microRNA (miRNA) target of LINC00460 and the corresponding target gene were validated via the dual luciferase activity assay. The tumorigenic function of LINC00460 was determined via establishment of a xenotransplanted tumor model. Results: LINC00460 was elevated in bladder carcinoma tissues and cell lines. Elevated LINC00460 was associated with shorter overall survival of bladder carcinoma patients. Overexpression of LINC00460 promoted cell viability, proliferation, invasion, and migration, while silencing of LINC00460 indicated the opposite effect on bladder carcinoma progression. LINC00460 could directly bind to miR-612 and inhibit miR-612 expression. Moreover, LINC00460 expression was negatively correlated with miR-612 in patients with bladder carcinoma. FOXK1 (Forkhead Box K1) was identified as the target of miR-612 and upregulated in patients with bladder carcinoma. Overexpression of FOXK1 attenuated interference of LINC00460-inhibited bladder carcinoma progression. Knockdown of LINC00460 suppressed in vivo bladder carcinoma growth. Conclusions: LINC00460 promoted bladder carcinoma progression via sponging miR-162 to facilitate FOXK1 expression, suggesting that LINC00460 might have the potential of being explored as a therapeutic target for treatment of bladder carcinoma.

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miR-195-5p Suppresses Lung Cancer Cell Proliferation, Migration, and Invasion Via FOXK1

Cited by 33 publications

References 22 publications

Differential roles of miR‐15a/16‐1 and miR‐497/195 clusters in immune cell development and homeostasis

Differential roles of miR‐15a/16‐1 and miR‐497/195 clusters in immune cell development and homeostasis

Novel LncRNA OXCT1-AS1 Indicates Poor Prognosis and Contributes to Tumorigenesis by Regulating miR-195/CDC25A Axis in Glioblastoma

LINC00460 Enhances Bladder Carcinoma Cell Proliferation and Migration by Modulating miR-612/FOXK1 Axis

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