MicroRNA-486-3p functions as a tumor suppressor in oral cancer by targeting DDR1

Chou, Sung Tau; Peng, Hsuan Yu; Mo, Kuan Chi; Hsu, Yuan Ming; Wu, Guan Hsun; Hsiao, Jenn Ren; Lin, Shankung; Wang, Horng-Dar; Shiah, Shine-Gwo

doi:10.1186/s13046-019-1283-z

Cited by 72 publications

(63 citation statements)

References 58 publications

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“…Therefore, it is natural to speculate that miR‐451a, miR‐194‐5p, and miR‐486‐5p, which are significantly increased in the EVs of plasma from LUAD patients, may also be involved in the occurrence and development of LUAD. However, as previously reported , the expression of miR‐451a, miR‐194‐5p, and miR‐486‐5p was significantly downregulated in LUAD tissues compared to that in normal tissue in the TCGA database (Fig. S6).…”

Section: Discussionsupporting

confidence: 78%

“…S6). Several studies have confirmed that miR‐451a, miR‐194‐5p, and miR‐486‐5p might inhibit tumor cell growth by suppressing proliferation and invasion or promote apoptosis by targeting cancer‐associated genes . Recently, some studies found that tumor suppressor gene‐induced senescent cells modulate the immune response, which promotes the establishment of the inflammatory microenvironment that contributes to metastasis .…”

Section: Discussionmentioning

confidence: 99%

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A panel of miRNAs derived from plasma extracellular vesicles as novel diagnostic biomarkers of lung adenocarcinoma

Yao

et al. 2019

FEBS Open Bio

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Lung cancer is the leading cause of cancer‐related morbidity and mortality worldwide, with lung adenocarcinoma (LUAD) being the most common histological subtype (approximately 40%). In the absence of reliable screening biomarkers for early diagnosis, most patients with LUAD are inevitably diagnosed at an advanced stage. MicroRNAs (miRNAs) encapsulated within plasma‐derived extracellular vesicles (EVs) may be suitable for use as noninvasive diagnostic biomarkers for aggressive malignancies, including LUAD. In this study, we first investigated the miRNA profiles of plasma‐derived EVs from LUAD patients and healthy donors, and then systematically evaluated the expression patterns of selected plasma‐derived EV miRNAs in a large cohort of patients with LUAD and healthy controls. Notably, we observed that miR‐451a, miR‐194‐5p, and miR‐486‐5p were significantly increased in EVs from LUAD patients, compared to healthy controls. The area under the curve values for the three miRNAs were 0.9040 (95% confidence interval [CI], 0.8633–0.9447) for miR‐451a, 0.7492 (95% CI, 0.6992–0.7992) for miR‐194‐5p, and 0.9574 (95% CI, 0.9378–0.9769) for miR‐486‐5p, while the AUC of the combination of these three miRNAs was 0.9650. Thus, these results suggest that these EV miRNAs may be promising candidates for the development of highly effective, noninvasive biomarkers for early LUAD diagnosis.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

A panel of miRNAs derived from plasma extracellular vesicles as novel diagnostic biomarkers of lung adenocarcinoma

Yao

et al. 2019

FEBS Open Bio

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“…ChIP assay was performed based on previous described [24]. For miRNA treatment, OEC-M1 cells were treated with control mimics (NC, 20 nM), or miRNA mimics (PM-30a or PM-379, 20 nM) for 48 h. For chemical treatments, DOK cells were treatment with vehicle control (DMSO, 10 nM), arecoline (50 μM) or NNK (10 μM) for 5 days.…”

Section: Chromatin Immunoprecipitation (Chip)mentioning

confidence: 99%

MiR-30a and miR-379 modulate retinoic acid pathway by targeting DNA methyltransferase 3B in oral cancer

et al. 2020

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Background: Epigenetic silencing of retinoic acid (RA) signaling-related genes have been linked with the pathogenesis and clinical outcome in oral squamous cell carcinoma (OSCC) carcinogenesis. However, the precise mechanisms underlying the abnormal silencing of RA signaling-related genes in OSCC have not been well investigated. Methods: Using combined analysis of genome-wide gene expression and methylation profile from 40 matched normaltumor pairs of OSCC specimens, we found a set of retinoid signaling related genes are frequently hypermethylated and downregulated in OSCC patient samples, including alcohol dehydrogenase, iron containing 1 (ADHFE1) and aldehyde dehydrogenase 1 family, member A2 (ALDH1A2), which are the important rate-limiting enzymes in synthesis of RA. The expression of ADHFE1 and ALDH1A2 in OSCC patients was determine by quantitative real-time PCR (qRT-PCR) and immunohistochemistry. The binding sites of miR-30a and miR-379 with DNA methyltransferase 3B (DNMT3B) were predicted using a series of bioinformatic tools, and validated using dual luciferase assay and Western blot analyses. The functions of miR-30a, miR-379, and DNMT3B were accessed by growth and colony formation analyses using gain-and loss-of-function approaches. Chromatin immunoprecipitation (ChIP) was performed to explore the molecular mechanisms by arecoline and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) treatment. Results: We demonstrated that deregulated miR-30a and miR-379 could represent a mechanism for the silencing of ADHFE1 and ALDH1A2 in OSCC through targeting DNMT3B. Ectopic expression of miR-30a and miR-379 could induce re-expression of methylation-silenced ADHFE1 and ALDH1A2, and lead to growth inhibition in oral cancer cells. Furthermore, the dysregulation of the miRNAs and DNMT-3B may result from exposure to tobacco smoking and betel quid chewing.

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“…Previously, we showed that DDR1 is one of the top five protein tyrosine kinases overexpressed in BQ-associated OSCC cell lines [29]; overexpression of DDR1 in OSCC tissues is statistically associated with three clinical features: angiolymphatic invasion (ALI), perineural invasion (PNI), and lymph node metastasis [30]. In the present study, we validated DDR1-associated collective cell invasion in OSCC tumor sections, and provided evidence that the small molecule inhibitor DDR1-IN-1 suppressed ALI in a mouse model with statistical significance.…”

Section: Of 18mentioning

confidence: 99%

Discoidin Domain Receptor-1 (DDR1) is Involved in Angiolymphatic Invasion in Oral Cancer

Chen

Tsai

et al. 2020

Cancers

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The discoidin domain receptor-1 (DDR1) is a non-integrin collagen receptor recently implicated in the collective cell migration of other cancer types. Previously, we identified an elevated expression of DDR1 in oral squamous cell carcinoma (OSCC) cells. Through the data mining of a microarray dataset composed of matched tumor-normal tissues from forty OSCC patients, we distilled overexpressed genes statistically associated with angiolymphatic invasion, including DDR1, COL4A5, COL4A6 and PDPN. Dual immunohistochemical staining further confirmed the spatial locations of DDR1 and PDPN in OSCC tissues indicative of collective cancer cell invasion. An elevated DDR1 expression at both the transcription and protein level was observed by treating keratinocytes with collagen of fibrillar or basement membrane types. In addition, inhibition of DDR1 kinase activity in OSCC TW2.6 cells disrupted cell cohesiveness in a 2D culture, reduced spheroid invasion in a collagen gel matrix, and suppressed angiolymphatic invasion in xenograft tissues. Taken together, these results suggest that collagen deposition in the affected tissues followed by DDR1 overexpression could be central to OSCC tumor growth and angiolymphatic invasion. Thus, DDR1 inhibitors are potential therapeutic compounds in restraining oral cancer, which has not been previously explored.

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MicroRNA-486-3p functions as a tumor suppressor in oral cancer by targeting DDR1

Cited by 72 publications

References 58 publications

A panel of miRNAs derived from plasma extracellular vesicles as novel diagnostic biomarkers of lung adenocarcinoma

A panel of miRNAs derived from plasma extracellular vesicles as novel diagnostic biomarkers of lung adenocarcinoma

MiR-30a and miR-379 modulate retinoic acid pathway by targeting DNA methyltransferase 3B in oral cancer

Discoidin Domain Receptor-1 (DDR1) is Involved in Angiolymphatic Invasion in Oral Cancer

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