The targeting of MTDH by miR‑145‑5p or miR‑145‑3p is associated with prognosis and regulates the growth and metastasis of prostate cancer cells

Pan, Dong; Jia, Zhang; Li, Wensheng; Dou, Zhongling

doi:10.3892/ijo.2019.4782

Cited by 12 publications

(13 citation statements)

References 54 publications

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“…Pan et al reported that MTDH functions as an oncogene in PCa and the inhibition of MTDH by miR-145-5p or miR-145-3p suppressed the growth and metastasis of PCa cells [39]. Mataki et al reported that both strands of miR-145, miR-145-5p andmiR-145-3p are functional and play pivotal roles as antitumor miRNAs in lung SCC by targeting MTDH [40].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Zhao

Zhou

et al. 2020

Bioengineered

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Neuroblastoma (NB) is responsible for 15% of all childhood cancer deaths. Despite advances in treatment and disease management, the overall 5-year survival rates remain poor in high-risk disease (25-40%). It is well known that miR-145 functions as a tumor suppressor in several types of cancer. However, the impact of miR-145 on NB is still ambiguous. Our aim was to investigate the potential tumor suppressive role and mechanisms of miR-145 in high-risk neuroblastoma. Expression levels of miR-145 in tissues and cells were determined using RT-qPCR. The effect of miR-145 on cell viability was evaluated using MTT assays, apoptosis levels were determined using TUNEL staining, and the MTDH protein expression was determined using western blot and RT-PCR. Luciferase reporter plasmids were constructed to confirm direct targeting for MTDH. The results showed that miR-145 expression was significantly lower in high-risk MYCN amplified (MNA) tumors and low miR-145 expression was associated with worse EFS and OS in our cohort. Over-expression of miR-145 reduced cell viability and increased apoptosis in SH-SY-5Y cells. We identified MTDH as a direct target for miR-145 in SH-SY-5Y cells. Targeting MTDH has the similar results as miR-145 overexpression. Our findings suggest that low miR-145 expression was associated with poor prognosis in patients with NB, and the overexpression of miR-145 inhibited NB cells growth by down-regulating MTDH, thus providing a potential target for the development of microRNA-based approach for NB therapy.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Zhao

Zhou

et al. 2020

Bioengineered

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“…3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) (KyeGEN BioTECH, Nanjing, China) was used to detect cell proliferation as described previously [19]. Cells were inoculated with the density of 1 × 10 5 cells/well in 96-well plate (Costar, Corning, NY, USA).…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

et al. 2020

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Background: Accumulating evidence indicates that the long noncoding RNA taurine upregulated gene 1(TUG1) plays a critical role in cancer progression and metastasis. However, the overall biological role and clinical significance of TUG1 in hepatocellular carcinoma (HCC) remain largely unknown. Methods:The expressions of TUG1, microRNA-216b-5p and distal-less homeobox 2 (DLX2) were detected by Quantitative real-time polymerase chain reaction (qRT-PCR). The target relationships were predicted by StarBase v.2.0 or TargetScan and confirmed by dual-luciferase reporter assay. The cell growth, apoptosis, migration and invasion were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Flow cytometry and Transwell assays, respectively. All protein expression levels were detected by western blot. Tumor xenografts were implemented to explore the role of TUG1 in vivo. Results:We found that there was a marked rise in TUG1 expression in HCC tissues and cells, and knockdown of TUG1 repressed the growth and metastasis and promoted apoptosis of HCC cells. In particular, TUG1 could act as a ceRNA, effectively becoming a sink for miR-216b-5p to fortify the expression of DLX2. Additionally, repression of TUG1 impared the progression of HCC cells by inhibiting DLX2 expression via sponging miR-216b-5p in vitro. More importantly, TUG1 knockdown inhibited HCC tumor growth in vivo through upregulating miR-216b-5p via inactivation of the DLX2.Conclusion: TUG1 interacting with miR-216b-5p contributed to proliferation, metastasis, tumorigenesis and retarded apoptosis by activation of DLX2 in HCC.

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“…Usually, localized PCa spread to lymph nodes at first and then to the bones, liver or lungs (Wang et al, 2018). Mechanisms on how PCa develop and metastasize have been extensively investigated, which mainly include the process of PCa metastasis (Weidle et al, 2019), the biomolecules such as miRNAs and enzymes involved in metastasis (Pan et al, 2019; Wu et al, 2018) or aberrant glucose metabolism of metastaic PCa (Pichla et al, 2019). However, the mechanisms still remains incomplete for limitation by the failure to holistically reproduce each individual element of the metastatic cascade in PCa metastasis (Berish et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Identification of key genes and multiple molecular pathways of metastatic process in prostate cancer

Guo

Lin

Cheng

et al. 2019

PeerJ

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Background Cancer metastasis is well known as the most adverse outcome and the major cause of mortality in cancer patients, including prostate cancer (PCa). There are no credible predictors, to this day, that can reflect the metastatic ability of localized PCa. In the present study, we firstly identified the differentially expressed genes (DEGs) and molecular pathways involved in the metastaic process of PCa by comparing gene expressions of metastaic PCa with localized PCa directly, with the purpose of identifying potential markers or therapeutic targets. Methods The gene expression profiles (GSE6919 and GSE32269) were downloaded from the Gene Expression Omnibus database, which contained 141 tissue samples, including 87 primary localized PCa samples and 54 metastaic PCa samples. After data processing, DEGs were identified by R language using the Student’s t-test adjusted via the Beniamini–Hochberg method. Subsequently, the gene ontology functional and pathway enrichment analyses of DEGs were performed and the protein–protein interaction network was constructed. Hub genes were identified using the plug-in cytoHubba in Cytoscape software by MCC and degree. Furthermore, validation and prognostic significance analysis of the hub genes were performed by UALCAN and gene expression profiling interactive analysis (GEPIA). Results A total of 90 DEGs were identified between localized and metastaic PCa, which consisted of 47 upregulated and 43 downregulated genes. The enriched functions and pathways of the DEGs include catabolic process, cell cycle, response to steroid hormone, extracellular matrix (ECM)-receptor interaction and vascular smooth muscle contraction. A total of 10 genes were identified as hub genes and biological process analysis of hub genes showed that cell cycle phase, cell division, and mitotic cell cycle process were mainly enriched. The expression of hub genes were confirmed in metastaic PCa when compared with localized PCa tissues by The Cancer Genome Atlas database. Moreover, the disease-free survival analysis of hub genes revealed that these genes may play an important role in invasion, progression or recurrence. Therefore, these hub genes might be the key genes contributed to tumor progression or metastasis in PCa and provide candidate therapeutic targets for PCa. Conclusions The present study identified some DEGs between localized and metastaic PCa tissue samples. These key genes might be potential therapeutic targets and biomarkers for the metastaic process of PCa.

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The targeting of MTDH by miR‑145‑5p or miR‑145‑3p is associated with prognosis and regulates the growth and metastasis of prostate cancer cells

Cited by 12 publications

References 54 publications

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

Identification of key genes and multiple molecular pathways of metastatic process in prostate cancer

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