RETRACTED ARTICLE:
            <i>MiR-29a</i>
            inhibits the progression of oral squamous cell carcinoma by targeting Wnt/β-catenin signalling pathway

Huang, Chao; Wang, Lili; Song, Hongguang; Wu, Cungang

doi:10.1080/21691401.2019.1576712

Cited by 11 publications

(8 citation statements)

References 25 publications

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“…Oral squamous cell carcinoma is an important type of head and neck tumour and is known for its high recurrence rate. Local recurrence and metastasis are important factors that challenge OSCC therapy 22 . We previously showed that higher T stage of OSCC corresponds to poor prognosis and shorter tumour‐free survival or tumour‐bearing survival 23 .…”

Section: Discussionmentioning

confidence: 99%

CD147 promotes proliferation and migration of oral cancer cells by inhibiting junctions between E‐cadherin and β‐catenin

Min

Xiong

Wang

et al. 2020

J Oral Pathology Medicine

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Background Although association between oral squamous cell carcinoma (OSCC) with epithelial‐mesenchymal transition (EMT) has been demonstrated, we found CD147, one transmembrane protein we previously studied in oral submucous fibrosis, was correlated with E‐cadherin, one marker of EMT. Here, we investigated CD147 expression in the different stages of OSCC and assessed its association with epithelial‐mesenchymal transition (EMT). Materials and methods CD147 and E‐cadherin expression in tissue microarrays containing 48 OSCC specimens and matched adjacent tissues was analysed using immunohistochemistry. CD147 was overexpressed or knocked down using exogenous cloning vector and RNA interference, respectively, in OSCC cell lines. Cell proliferation and migration were measured using the CCK8 assay and scratch test, respectively. The expression and localization of EMT‐associated proteins was analysed by Western blotting and immunofluorescence. Results CD147 expression in OSCC tissues was significantly higher than that in adjacent tissues and was markedly higher in cancer tissues with metastasis (P < .05). CD147 expression showed significant negative correlation with E‐cadherin expression. CD147 overexpression downregulated E‐cadherin and inhibited its complex with β‐catenin and then upregulated N‐cadherin and vimentin. Additionally, alterations in CD147 protein expression affected proliferation and migration ability in OSCC cells and were related to β‐catenin nuclear translocation. Conclusion CD147 plays an important role in tumorigenesis and metastasis by promoting EMT progression in OSCC. It may be considered as a novel potential diagnostic and therapeutic target for OSCC.

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Section: Discussionmentioning

confidence: 99%

CD147 promotes proliferation and migration of oral cancer cells by inhibiting junctions between E‐cadherin and β‐catenin

Min

Xiong

Wang

et al. 2020

J Oral Pathology Medicine

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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: 99%

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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“…It was found that arecoline leads to epigenetic silencing of these miRNAs, and the induction of their re-expression by a combined treatment with DNA methyltransferase and histone deacetylase inhibitors reduced cell proliferation and migration [62]. Also, miR-29a acts as a suppressor of canonical Wnt signaling, and it is frequently down-regulated in OSCC [80]. In contrast, miR-21 promoted the Wnt/β-catenin pathway by reducing the expression of DKK2, which acts as the antagonist of LRP6 co-receptor.…”

Section: The Role Of Epigenetic Mechanisms In Wnt/β-catenin Pathway Amentioning

confidence: 99%

“…Due to the central role of β-catenin in mediating Wnt signal transduction and transcription activation, this protein attracted much attention when it comes to assessing the anti-cancer effects of its downregulation. The induction of β-catenin transcriptional activity in HNSCC cell lines using lithium chloride, an inhibitor of GSK-3β, led to an increased cell proliferation rate, enhanced cell migration and invasion and a reduced rate of apoptosis [80]. Accordingly, the siRNA-mediated silencing of β-catenin in tongue cancer cells led to G0/G1 arrest, growth inhibition, decreased cell migration and increased apoptosis [51,107].…”

Section: Functional Significance Of Wnt/β-catenin Pathway Dysregulationmentioning

confidence: 99%

The Significance of the Dysregulation of Canonical Wnt Signaling in Head and Neck Squamous Cell Carcinomas

Paluszczak

2020

Cells

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The knowledge about the molecular alterations which are found in head and neck squamous cell carcinomas (HNSCC) has much increased in recent years. However, we are still awaiting the translation of this knowledge to new diagnostic and therapeutic options. Among the many molecular changes that are detected in head and neck cancer, the abnormalities in several signaling pathways, which regulate cell proliferation, cell death and stemness, seem to be especially promising with regard to the development of targeted therapies. Canonical Wnt signaling is a pathway engaged in the formation of head and neck tissues, however it is not active in adult somatic mucosal cells. The aim of this review paper is to bring together significant data related to the current knowledge on the mechanisms and functional significance of the dysregulation of the Wnt/β-catenin pathway in head and neck tumors. Research evidence related to the role of Wnt signaling activation in the stimulation of cell proliferation, migration and inhibition of apoptosis in HNSCC is presented. Moreover, its role in promoting stemness traits in head and neck cancer stem-like cells is described. Evidence corroborating the hypothesis that the Wnt signaling pathway is a very promising target of novel therapeutic interventions in HNSCC is also discussed.Cells 2020, 9, 723 2 of 20 blocking the interaction between PD-1 receptor and PD-L1, may be beneficial in patients with advanced, metastatic or recurrent HNSCC [7]. However, other therapeutic options are also necessary for the better clinical management of HNSCC patients. To that end, molecular alterations observed in HNSCC need to be studied in detail, in order to point to promising drug targets. Mechanisms of Wnt/β-Catenin Pathway Activation in HNSCCRecent genomic analyses have shown the prevalence of genetic driver alterations in HNSCC, which most frequently affect genes associated with receptor tyrosine kinase (e.g., EGFR, MET, KIT), PI3K, p53, Notch or Hippo signaling pathways. On the other hand, genetic alterations in genes related to canonical Wnt signaling were rarely detected in HNSCC [8,9]. In contrast to colorectal cancers, which show molecular alterations driving Wnt signaling activation in around 90% of cases [9], HNSCC were shown to lack CTNNB1 mutations and APC mutations were present infrequently [10][11][12][13][14][15][16]. The mutations of FAT1 tumor suppressor, which encodes a protocadherin protein that binds and inactivates β-catenin, were detected in some cases of HNSCC [17]. However, the activation of the Wnt/β-catenin pathway in HNSCC seems to be more prevalent than it is suggested by genetic findings, due to cross-talk with other molecular alterations, which can lead to pathway cross-activation. Indeed, it has been shown that β-catenin can be activated via enhanced EGFR or PI3K signaling, which belong to the most frequently dysregulated signaling pathways in HNSCC. In this regard, elevated EGFR expression was associated with delocalized β-catenin expression [13]. In another study, the nuclear ...

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RETRACTED ARTICLE: MiR-29a inhibits the progression of oral squamous cell carcinoma by targeting Wnt/β-catenin signalling pathway

Cited by 11 publications

References 25 publications

CD147 promotes proliferation and migration of oral cancer cells by inhibiting junctions between E‐cadherin and β‐catenin

CD147 promotes proliferation and migration of oral cancer cells by inhibiting junctions between E‐cadherin and β‐catenin

Epigenetic Modifications in Head and Neck Cancer

The Significance of the Dysregulation of Canonical Wnt Signaling in Head and Neck Squamous Cell Carcinomas

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