MicroRNA-605 functions as a tumor suppressor by targeting INPP4B in melanoma

Chen, Lan; Cao, Yaxuan; Rong, Dongyun; Wang, Ye; Cao, Yu

doi:10.3892/or.2017.5740

Cited by 28 publications

(31 citation statements)

References 38 publications

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“…One group has carefully shown that miR-605-5p promotes the P53 stress response and inhibits apoptosis in colorectal carcinoma cells [ 118 ]. Another report recently showed evidence that miR-605-5p acts as a tumor suppressor in melanoma by inhibiting INPP4B [ 119 ]. Future studies will explore whether there a CNS-specific role for miR-605-5p exists.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Levels Are Altered in the Cerebrospinal Fluid of Patients with Young-Onset Alzheimer’s Disease

McKeever¹,

et al. 2018

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Clinical diagnosis of Alzheimer’s disease (AD) prior to the age of 65 years is classified as young-onset (YOAD), whereas diagnosis after the age of 65 years is considered late-onset (LOAD). Although rare autosomal mutations more commonly associate with YOAD, most YOAD and LOAD cases are sporadic. YOAD and LOAD share amyloid and tau pathology, but many YOAD patients show increased disease severity and rate of progression. The current study examined the microRNA (miRNA) expression profile from exosomes isolated from the cerebrospinal fluid (CSF) of YOAD patients with biomarker-confirmed AD. Results uncovered miR-16-5p, miR-125b-5p, miR-451a, and miR-605-5p as differentially expressed in the CSF-derived exosomes of YOAD patients when compared with healthy controls (HC). In a cohort of LOAD patients, miR-125b-5p, miR-451a, and miR-605-5p were similarly altered in expression, but miR-16-5p showed similar expression to control. Analysis of the mRNA targets of these miRNAs revealed transcripts enriched in biological processes relevant to the post-mortem posterior cingulate cortex transcriptome in YOAD from a previously published microarray study, including those related to neuron projections, synaptic signaling, metabolism, apoptosis, and the immune system. Hence, these miRNAs represent novel targets for uncovering disease mechanisms and for biomarker development in both YOAD and LOAD.Electronic supplementary materialThe online version of this article (10.1007/s12035-018-1032-x) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Levels Are Altered in the Cerebrospinal Fluid of Patients with Young-Onset Alzheimer’s Disease

McKeever¹,

et al. 2018

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“…SGK3 has been found in others cancers as a carcinogenic gene [ 42 , 52 – 55 ]. A recent report revealed that SGK3 plays a vital role in glioblastoma as the target gene of miR-212-3p [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG5 promotes the progression of osteosarcoma by sponging the miR-212-3p/SGK3 axis

et al. 2018

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BackgroundLong non-coding RNA (lncRNA) SNHG5 has been found to play an important role in tumors. Nevertheless, the function and mechanism of lncRNA SNHG5 in osteosarcoma (OS) remains unclear. The purpose of this study was to investigate whether lncRNA SNHG5 can regulate the occurrence and development of OS cells.MethodsWe performed quantitative real time PCR to detect the expression of lncRNA SNHG5 in OS cells. 143B, MG63 (knockdown) and U2OS, U2R (overexpression) cell lines were chosen for the function study of SNHG5. The effect of SNHG5, miR-212-3p, and SGK3 in OS cells was explored by MTT assays, clony formation, flow cytometry, transwell assays, wound healing assays, and cell spreading assays. Quantitative real-time PCR, Western blot analysis and luciferase assays were used to detect the interaction between lncRNA SNHG5 and miR-212-3p.ResultsIn this study, knockdown of lncRNA SNHG5 suppressed the growth and metastasis of OS cells, whereas the overexpression of SNHG5 produced an opposite result. Mechanistically, lncRNA SNHG5 functions as a sponger against miR-212-3p and suppresses the miR-212-3p/SGK3 signaling pathway. Introduction of miR-212-3p mimics or inhibitors reverses SNHG5 overexpression or silences the exerted tumor promoting or suppressing effect. In addition, our results showed that the function of SNHG5 can be rescued by miR-212-3p and can regulate the growth and metastasis of OS cells via SGK3, the downstream target of miR-212-3p.ConclusionsIn summary, our study demonstrated that lncRNA SNHG5 can regulate the proliferation and metastasis of OS cells through the miR-212-3p/SGK3 axis. This axis may provide a new target for future clinical treatment.Electronic supplementary materialThe online version of this article (10.1186/s12935-018-0641-9) contains supplementary material, which is available to authorized users.

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“…For example, miR-605 inhibits the progression of intrahepatic cholangiocarcinoma by suppressing gankyrin ( 34 ). miR-605 also functions as a tumor suppressor in melanoma by regulating the expression of inositol polyphosphate-4-phosphatase type II B ( 35 ). In addition, miR-605 was also demonstrated to affect the proliferation, migration and invasion of non-small cell lung cancer, prostate cancer, and breast cancer ( 18 , 19 , 36 ).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of microRNA‑605 indicates poor prognosis and promotes the progression of osteosarcoma

2020

Oncol Lett

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Osteosarcoma (OS) is a type of primary bone tumor, which is one of the leading causes of cancer-related death. MicroRNA (miR)-605 has been demonstrated to act as a prognostic biomarker and therapeutic target in various cancers, such as breast cancer and non-small cell lung cancer, but its function in OS remains unclear. The aim of the present study was to investigate the prognostic value of miR-605 in patients with OS by evaluating its expression levels and to explore the biological function of miR-605 in OS progression. For this purpose, tumor tissues and adjacent normal tissues were collected from OS patients, and the expression of miR-605 in the collected tissues and OS MG63, U2OS, HOS, and SAOS-2 cell lines was detected by quantitative real-time PCR. The prognostic value of miR-605 was evaluated by Kaplan-Meier survival curves and Cox regression analysis. The effects of miR-605 on OS cell proliferation, migration and invasion were analyzed by the CCK-8 and transwell assays, respectively. The results of the present study revealed that miR-605 was significantly downregulated in OS tissues compared with adjacent normal tissues, which was associated with the clinical stage and distant metastasis of patients. Additionally, the downregulation of miR-605 predicted the poor prognosis of patients with OS and served as an independent prognostic indicator. The downregulation of miR-605 enhanced cell proliferation, migration, and invasion of OS cells, which suggested that miR-605 may be involved in the progression of OS. The findings of the present study provide a new therapeutic target for the treatment of patients with OS.

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MicroRNA-605 functions as a tumor suppressor by targeting INPP4B in melanoma

Cited by 28 publications

References 38 publications

MicroRNA Expression Levels Are Altered in the Cerebrospinal Fluid of Patients with Young-Onset Alzheimer’s Disease

MicroRNA Expression Levels Are Altered in the Cerebrospinal Fluid of Patients with Young-Onset Alzheimer’s Disease

LncRNA SNHG5 promotes the progression of osteosarcoma by sponging the miR-212-3p/SGK3 axis

Downregulation of microRNA‑605 indicates poor prognosis and promotes the progression of osteosarcoma

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