Clinicopathological significance of miR‐26, miR‐107, miR‐125b, and miR‐203 in head and neck carcinomas

González‐Arriagada, Wilfredo Alejandro; Olivero, Pablo; Rodríguez, Belén; Lozano-Burgos, Carlos; Oliveira, Carine Ervolino de; Coletta, Ricardo D.

doi:10.1111/odi.12872

Cited by 22 publications

(12 citation statements)

References 48 publications

(58 reference statements)

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“…Coordination of miR-211 upregulation and miR-125b downregulation thus may drive OSCC oncogenesis. While downregulation of miR-125b expression has been identified in HNSCC [36,43], upregulation of miR-125b expression in HNSCC has also been reported [42]. Our results demonstrate there is a concordance between low miR-125b expression and high PRXL2A expression in OSCC cell lines and various tumor tissues.…”

Section: Discussionsupporting

confidence: 69%

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miR-125b suppresses oral oncogenicity by targeting the anti-oxidative gene PRXL2A

Chen¹,

Wei²,

Yang

et al. 2019

Redox Biology

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Oral squamous cell carcinoma (OSCC) is a globally prevalent malignancy. The molecular mechanisms of this cancer are not well understood and acquire elucidation. Peroxiredoxin like 2A (PRXL2A) has been reported to be an antioxidant protein that protects cells from oxidative stress. Our previous study identified an association between PRXL2A upregulation in OSCC and a worse patient prognosis. MicroRNAs (miRNAs) are small non-coding RNAs that are involved in the modulation of biological/pathological properties. The miR-125 family of genes drive pluripotent regulation across a wide variety of cancers. In this study, we identify the oncogenic eligibility of PRXL2A and clarify miR-125b as its upstream regulator. Downregulation of miR-125b can be observed in OSCC tumors. Lower miR-125b expression in tumors results in a worse patient prognosis at the relatively early stage. Reporter assays are able to validate that PRXL2A is a direct target of miR-125b . Exogenous miR-125b expression in OSCC cells results in increased oxidative stress, increased drug sensitivity, and suppressor activity that is paralleled by the knockout of PRXL2A gene. The suppressor activity of miR-125b is able to be rescued by PRXL2A, which suggests the existence of a miR-125b -PRXL2A regulatory axis that is part of OSCC pathogenesis. Nuclear factor-erythroid 2-related factor 2 (NRF2) was found to be a downstream effector of the miR-125b -PRXL2A cascade. As a whole, this study has pinpointed novel clues demonstrating that downregulation of miR-125b suppressor underlies upregulation of PRXL2A in OSCC, and this then protects the affected tumor cells from oxidative stress.

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Section: Discussionsupporting

confidence: 69%

“…It is interesting to note in previous studies that NRF2 upregulates miR-125b expression in various types of cells by promoter activation [[38], [39], [40]]. However, the multi-dimensional regulatory mechanisms of miR-125b and the oncogenic stimuli leading to the miR-125b downregulation in OSCC are not fully understood [[41], [42], [43]].…”

Section: Introductionmentioning

confidence: 99%

miR-125b suppresses oral oncogenicity by targeting the anti-oxidative gene PRXL2A

Chen¹,

Wei²,

Yang

et al. 2019

Redox Biology

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“…Interestingly, miRNA-125b expression levels were elevated in primary HNSCC, contrary to results from the aforementioned study. MiRNA-125b was also associated with N stage, metastasis, and death in HNSCC patients [80]. These conflicting results demonstrate the variability of miRNA expression in different regions of HNSCC.…”

Section: Mirnas As Biomarkers For Hnsccmentioning

confidence: 99%

“…Compared to miRNAs involved with radioresistance, fewer miRNAs that regulate chemoresistance have been found. Previously, it was determined that miRNA-125b enhances radiosensitivity in OSCC patients, but serves as a prognostic biomarker in metastatic HNSCC [80,82]. Its behavior in HNSCC appears to be dependent on the region of the head and neck.…”

Section: Treatmentmentioning

confidence: 99%

The Role of MicroRNAs in Recurrence and Metastasis of Head and Neck Squamous Cell Carcinoma

Yang

Sedhom

Song

et al. 2019

Cancers

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Head and neck squamous cell carcinoma (HNSCC) affects 650,000 people worldwide and has a dismal 50% 5-year survival rate. Recurrence and metastasis are believed the two most important factors causing this high mortality. Understanding the biological process and the underlying mechanisms of recurrence and metastasis is critical to develop novel and effective treatment, which is expected to improve patients’ survival of HNSCC. MicroRNAs are small, non-coding nucleotides that regulate gene expression at the transcriptional and post-transcriptional level. Oncogenic and tumor-suppressive microRNAs have shown to regulate nearly every step of recurrence and metastasis, ranging from migration and invasion, epithelial-mesenchymal transition (EMT), anoikis, to gain of cancer stem cell property. This review encompasses an overview of microRNAs involved in these processes. The recent advances of utilizing microRNA as biomarkers and targets for treatment, particularly on controlling recurrence and metastasis are also reviewed.

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“…These criteria are necessary for a quick and accurate diagnostic process. Several studies have successfully applied miRNA expression signatures to determine cancer identification, diagnostic potential and treatment prognosis [9,[13][14][15], even with higher accuracy than using mRNA expression profiles [16]. In terms of molecular structure evolution, miRNAs are endogenous small non-coding RNA molecules, containing about 18-24 nucleotides that negatively regulate gene expression by binding to the 3 -untranslated regions (3 -UTR) of target mRNAs [17,18].…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs: Their Role in Metabolism, Tumor Microenvironment, and Therapeutic Implications in Head and Neck Squamous Cell Carcinoma

Shiah

Chou

Chang

2021

Cancers

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MicroRNAs (miRNAs) are endogenous small non-coding RNA molecules that negatively regulate gene expression by binding to target mRNAs. Deregulated miRNAs can act as either oncogenic miRNAs or tumor suppressor miRNAs in controlling proliferation, differentiation, apoptosis, metastasis, epithelial–mesenchymal transition, and immune responses, which are all involved in the carcinogenesis process of HNSCC. Recent findings have shown that metabolic reprogramming is an important hallmark of cancer, which is necessary for malignant transformation and tumor development. Some reprogrammed metabolisms are believed to be required for HNSCC against an unfavorable tumor microenvironment (TME). The TME is composed of various cell types embedded in the altered extracellular matrix, among which exosomes, secreted by cancer cells, are one of the most important factors. Tumor-derived exosomes reshape the tumor microenvironment and play a crucial role in cell-to-cell communication during HNSCC development. Exosomes encapsulate many biomolecules, including miRNAs, circulate in body fluids, and can transmit intercellular regulatory messages to nearby and distant sites, which indicates that exosomal miRNAs have the potential to become non-invasive biomarkers. This review aims to clarify the functions of diverse miRNAs in HNSCC metabolic reprogramming and tumor-derived exosomes. In addition, it also emphasizes the potential role of miRNA as a biomarker in the diagnosis, prognosis, and treatment of HNSCC cancer.

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Clinicopathological significance of miR‐26, miR‐107, miR‐125b, and miR‐203 in head and neck carcinomas

Abstract: These findings suggest that miR-26 and miR-125b may be associated with the progression and metastasis of HNSCC and that miR-203 is associated with a more favorable prognosis.

Cited by 22 publications

References 48 publications

miR-125b suppresses oral oncogenicity by targeting the anti-oxidative gene PRXL2A

miR-125b suppresses oral oncogenicity by targeting the anti-oxidative gene PRXL2A

The Role of MicroRNAs in Recurrence and Metastasis of Head and Neck Squamous Cell Carcinoma

MicroRNAs: Their Role in Metabolism, Tumor Microenvironment, and Therapeutic Implications in Head and Neck Squamous Cell Carcinoma

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