microRNA-137 is downregulated in thyroid cancer and inhibits proliferation and invasion by targeting EGFR

Luo, Yingwei; Li, Xi; Dong, Jianming; Sun, Wei

doi:10.1007/s13277-015-4611-8

Cited by 17 publications

(9 citation statements)

References 37 publications

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“…Moreover, Src induced the activation of the p38-MAPK/JNK signaling pathway in CD34+ cells [ 31 ]. Thyroid cancer cells transfected with miR-137 mimics showed a reduction in p-ERK and p-AKT [ 32 ], suggesting a negative correlation between miR-137 and the MAPK signaling pathway. These results support our conclusion that miR-137 suppressed ischemic stroke progression by targeting Src gene thus blocking the MAPK signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke

Tian

et al. 2020

Aging

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Stroke is a leading cause of death and disability worldwide. The purpose of this study was to investigate the possible role of the microRNA (miRNA or miR) miR-137 in ischemic stroke. miRNAs are very stable in the blood and may serve as potential diagnostic and therapeutic markers. Wild-type, Src-/and miR-137-/mice were treated with p38 siRNA or Erk2 siRNA to identify their roles in the inflammatory response, oxidative stress, neuronal injury and cognitive impairment in brain tissues of mice following middle cerebral artery occlusion (MCAO) operation. We evaluated several factors including; inflammatory responses, oxidative stress, viability and apoptosis of astrocytes in order to identify the functions of miR-137 and Src in ischemic stroke. miR-137 alleviated the inflammatory response, oxidative stress, neuronal injury and cognitive impairment, and restricted apoptosis via targeting Src and inactivating the MAPK signaling pathway. Furthermore, up-regulation of miR-137 or inhibition of Src inhibited the secretion of inflammatory factors, suppressed oxidative stress, and reduced apoptosis of astrocytes. In conclusion, our work suggests that, in mice, miR-137 confers neuroprotective effects against ischemic stroke via attenuation of oxidative, apoptotic, and inflammatory pathways through inhibiting Src-dependent MAPK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke

Tian

et al. 2020

Aging

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“…miR-137 is downregulated in thyroid carcinoma and acts as a tumor suppressor by targeting Stromal cell-derived factor 1 and epidermal growth factor receptor (17,18). It can also improve the dexamethasone sensitivity in multiple myeloma cells via inhibition of microphthalmia-associated transcription factor as well as the Akt signaling pathway (6).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-137 acts as a tumor suppressor in osteosarcoma by targeting enhancer of zeste homolog 2

Feng

Liu

et al. 2017

Experimental and Therapeutic Medicine

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MicroRNA (miR) are short non-coding RNA that bind to the 3′-untranslational region of their target genes, inhibiting translation and causing mRNA degradation. miR deregulation has been implicated in human cancer; however, the detailed regulatory mechanism of miR-137 in osteosarcoma (OS) remains largely unknown. In the present study, miR-137 and enhancer of zeste homologue 2 (EZH2) mRNA and protein expression levels were analyzed using reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. MTT and transwell assays were performed to evaluate cell viability and invasion capacities and a luciferase reporter gene assay was used to determine the targeting relationship. The results of the current study indicated that miR-137 expression was significantly downregulated in OS tissues and cell lines (P<0.01). Moreover, it was observed that low miR-137 expression levels were significantly associated with lung metastasis and advanced TMN stage (P<0.05), but not associated with age, gender, tumor size, location, serum lactate dehydrogenase or serum alkaline phosphatase. Increasing levels of miR-137 significantly inhibited U2OS cell viability and invasion (P<0.01). By contrast, knockdown of miR-137 markedly increased U2OS cell viability and invasion. EZH2 was identified as a direct target gene of miR-137 in U2OS cells by luciferase reporter assay and EZH2 expression was found to be significantly increased in OS tissues and cell lines (P<0.01). EZH2 was significantly downregulated following miR-137 overexpression (P<0.01), and was upregulated following miR-137 knockdown in U2OS cells. Furthermore, EZH2 overexpression significantly attenuated the suppressive effects of miR-137 on U2OS cell viability and invasion (P<0.01), suggesting that miR-137 inhibits the viability and invasion of OS cells by targeting EZH2. Therefore, the results of the current study suggest that the miR-137/EZH2 axis may be a potential target for novel potential therapeutic strategies to treat OS.

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“… 13 Located on chromosome 1p22, 14 miR-137 has attracted much attention because it is frequently downregulated in cancer tissues, such as ovarian cancer, 15 gastric cancer, 16 colorectal cancer, 17 non-small-cell lung cancer, 18 and neuroblastoma. 19 It has also been reported that miR-137 can suppress invasion in thyroid cancer, 20 non-small-cell lung cancer, 18 and breast cancer. 21 Our previous studies indicated that miR-137 expression in BC tissues is almost undetectable in comparison to their adjacent non-tumorous bladder urothelium.…”

Section: Introductionmentioning

confidence: 97%

ISO, via Upregulating MiR-137 Transcription, Inhibits GSK3β-HSP70-MMP-2 Axis, Resulting in Attenuating Urothelial Cancer Invasion

Guo

Huang

Jin

et al. 2018

Molecular Therapy - Nucleic Acids

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Our most recent studies demonstrate that miR-137 is downregulated in human bladder cancer (BC) tissues, while treatment of human BC cells with isorhapontigenin (ISO) elevates miR-137 abundance. Since ISO showed a strong inhibition of invasive BC formation in the N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced invasive BC mouse model, the elucidation of a potential biological effect of miR-137 on antagonizing BC invasion and molecular mechanisms underlying ISO upregulation of miR-137 are very important. Here we discovered that ectopic expression of miR-137 led to specific inhibition of BC invasion in human high-grade BC T24T and UMUC3 cells, while miR-137 deletion promoted the invasion of both cells, indicating the inhibitory effect of miR-137 on human BC invasion. Mechanistic studies revealed that ISO treatment induced miR-137 transcription by promoting c-Jun phosphorylation and, in turn, abolishing matrix metalloproteinase-2 (MMP-2) abundance and invasion in BC cells. Moreover, miR-137 was able to directly bind to the 3′ UTR of Glycogen synthase kinase-3β (GSK3β) mRNA and inhibit GSK3β protein translation, consequently leading to a reduction of heat shock protein-70 (HSP70) translation via targeting the mTOR/S6 axis. Collectively, our studies discover an unknown function of miR-137, directly targeting the 3′ UTR of GSK3β mRNA and, thereby, inhibiting GSK3β protein translation, mTOR/S6 activation, and HSP70 protein translation and, consequently, attenuating HSP70-mediated MMP-2 expression and invasion in human BC cells. These novel discoveries provide a deep insight into understanding the biomedical significance of miR-137 downregulation in invasive human BCs and the anti-cancer effect of ISO treatment on mouse invasive BC formation.

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microRNA-137 is downregulated in thyroid cancer and inhibits proliferation and invasion by targeting EGFR

Cited by 17 publications

References 37 publications

miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke

miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke

MicroRNA-137 acts as a tumor suppressor in osteosarcoma by targeting enhancer of zeste homolog 2

ISO, via Upregulating MiR-137 Transcription, Inhibits GSK3β-HSP70-MMP-2 Axis, Resulting in Attenuating Urothelial Cancer Invasion

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