MiR-1275 promotes cell migration, invasion and proliferation in squamous cell carcinoma of head and neck via up-regulating IGF-1R and CCR7

Liu, Minda; Wu, Hong; Wang, Song; Pang, Pai; Jin, Shan; Sun, Changfu; Liu, Fa‐Yu

doi:10.1016/j.gene.2017.12.049

Cited by 42 publications

(30 citation statements)

References 27 publications

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“…Other studies and meta-analyses show that in HNSCC patients some miRNAs are upregulated, such as miR-126 and miR-223 in OSCC (Tachibana et al 2016), miR-196b (Luo et al 2019, miR-31 (Kao et al 2019), miR-1275 in HNSCC (Liu et al 2018), miR-212 and miR-129 in OSCC (Scapoli et al 2010), and miR-130b in HNSCC (Chen et al 2012), while others are down-regulated, such as miR-145-5p in LSCC (Gao et al 2019), miR-29a in OSCC (Huang et al 2019), miR-200b in HNSCC (Kumarasamy et al 2019), miR-125a-5p in HNSCC (Vo et al 2019), miR-486-3p and miR-337-3p in OSCC (Chou et al 2019), miR-224 in OSCC (Lu et al 2019), miR-135b, miR-197, miR-378, miR224, and miR-34a in OSCC (Scapoli et al 2010), miR-100 and miR-375 in HNSCC (Chen et al 2012). lncRNAs lncRNAs are transcribed RNA molecules, which have a length of more than 200 nucleotides, do not encode proteins, and participate in positive and negative regulation of gene expression in the transcriptional, as well as the post-transcriptional level (Wang and Chang 2011;Chen 2016;Wei et al 2017).…”

Section: Tumor Suppressor Mirnasmentioning

confidence: 98%

Epigenetic Modifications in Head and Neck Cancer

et al. 2019

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Head and neck squamous cell carcinoma (HNSCC) is the sixth most common human malignancy in the world, with high mortality and poor prognosis for patients. Among the risk factors are tobacco and alcohol intake, human papilloma virus, and also genetic and epigenetic modifications. Many studies show that epigenetic events play an important role in HNSCC development and progression, including DNA methylation, chromatin remodeling, histone posttranslational covalent modifications, and effects of non-coding RNA. Epigenetic modifications may influence silencing of tumor suppressor genes by promoter hypermethylation, regulate transcription by microRNAs and changes in chromatin structure, or induce genome instability through hypomethylation. Moreover, getting to better understand aberrant patterns of methylation may provide biomarkers for early detection and diagnosis, while knowledge about target genes of microRNAs may improve the therapy of HNSCC and extend overall survival. The aim of this review is to present recent studies which demonstrate the role of epigenetic regulation in the development of HNSCC.

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Section: Tumor Suppressor Mirnasmentioning

confidence: 98%

Epigenetic Modifications in Head and Neck Cancer

et al. 2019

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“…miRNAs are known to be an integral component of cancer development [17][18][19]. Several studies have highlighted the role of miR-182-5p in the development of different cancers [13,14]. In glioblastoma, miR-182-5p targets protein phosphatase 1 regulatory inhibitor subunit 1C [20].…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andmentioning

confidence: 99%

“…By negatively regulating gene expression at the post-transcriptional level, these single-stranded RNAs can inhibit gene translation and trigger the direct degradation of target messenger RNAs (mRNAs) [11]. More than one-third of protein-coding genes are estimated to be under miRNA translational control, with a single miRNA able to regulate hundreds of protein-coding genes [12,13].…”

Section: Introductionmentioning

confidence: 99%

miR-182-5p Promotes Growth in Oral Squamous Cell Carcinoma by Inhibiting CAMK2N1

Nan

Zhong

et al. 2018

Cell Physiol Biochem

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Background/Aims: Emerging evidence suggests that the propagation of oral squamous cell carcinoma (OSCC) is influenced by the abnormal expression of microRNAs (miRNAs). This study aimed to characterize the involvement of miR-182-5p in OSCC by targeting the calcium/ calmodulin-dependent protein kinase II inhibitor CAMK2N1. Methods: miR-182-5p expression was quantified in OSCC tissues and cell lines with reverse transcription polymerase chain reaction (RT-PCR). Cell colony formation, Cell Counting Kit-8 (CCK-8), Ki-67, and nude mouse xenograft assays were used to characterize the role of miR-182-5p in the proliferation of OSCC. A miR-182-5p target gene was identified with western blotting, RT-PCR, and luciferase activity assays. OSCC patient survival based on CAMK2N1 expression was also analyzed. Results: miR-182-5p was up-regulated in in vitro cell lines and in vivo clinical OSCC samples. CCK-8, colony formation, and Ki-67 assays revealed that miR-182-5p promoted the growth and proliferation of OSCC cells. miR-182-5p directly targeted CAMK2N1, as evidenced by luciferase assays and target prediction algorithms. CAMK2N1 operated as a tumor suppressor gene in patients with OSCC. Down-regulating miR-182-5p expression in the CAL-27 cell line restored CAMK2N1-mediated OSCC cell proliferation. miR-182-5p expression inhibited the activation of AKT, ERK1/2, and NF-κB. Mice injected with CAL-27 cells transfected with miR-182-5p-inhibitor demonstrated a significant increase in tumor size and weight and increased CAMK2N1 mRNA and protein expression compared with the miR-negative control group. Conclusion: The miR-182-5p-CAMK2N1 pathway can be potentially targeted to regulate the proliferation of OSCC cells.

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“…Besides, IGF-1R was identified to be highly expressed in a variety of human cancers including squamous cell carcinoma of head and neck, endometrial carcinoma, and papillary thyroid cancer. 13 – 15 In our previous study, IGF-1R functioned as a tumor promoter in GC cell survival and development. 16 However, it is not clear whether miR-598 can regulate IGF-1R expression in GC.…”

Section: Introductionmentioning

confidence: 96%

miR-598 acts as a tumor suppressor in human gastric cancer by targeting IGF-1R

Liu¹,

Yang

Wang³

2018

OTT

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BackgroundIn recent years, the aberrant expression of miR-598 in tumorigenesis has been demonstrated, as well as the fact that the IGF-1R pathway is also involved in the development of human gastric cancer (GC). The present study aimed to investigate the molecular mechanisms underlying miR-598-regulated IGF-1R expression in human GC.Materials and methodsWe analyzed the expression of miR-598 and IGF-1R in GC samples and cells, and evaluated the clinical significance of miR-598 and IGF-1R in GC patients. Furthermore, in vitro and in vivo assays were used to investigate the molecular mechanisms of miR-598 and IGF-1R.ResultsmiR-598 expression was frequently downregulated in GC tissues and cells, and significantly correlated with poor prognosis, vascular invasion, TNM stage, and lymph node metastases as well as IGF-1R expression. The overexpression of miR-598 obviously inhibited cell proliferation, migration, invasion, and induced cell cycle arrest in the G1/S phase, and increased the apoptosis of GC cells. The overexpression of miR-598 also significantly inhibited ERK1/2 and Akt phosphorylation level. In vivo assay validated the inhibitory effect of miR-598 on tumor growth. Further studies showed that miR-598 inhibited IGF-1R protein expression by directly targeting its 3′-UTR. Besides, over-expression of IGF-1R reversed the inhibitory effects of miR-598, while suppression of IGF-1R expression showed inverse effects.ConclusionmiR-598 suppresses GC cell proliferation, migration and invasion by directly targeting IGF-1R expression. Thus, miR-598 may be a useful target for GC patients.

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MiR-1275 promotes cell migration, invasion and proliferation in squamous cell carcinoma of head and neck via up-regulating IGF-1R and CCR7

Cited by 42 publications

References 27 publications

Epigenetic Modifications in Head and Neck Cancer

Epigenetic Modifications in Head and Neck Cancer

miR-182-5p Promotes Growth in Oral Squamous Cell Carcinoma by Inhibiting CAMK2N1

miR-598 acts as a tumor suppressor in human gastric cancer by targeting IGF-1R

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