MicroRNA expression patterns in oral squamous cell carcinoma: hsa‐mir‐99b‐3p and hsa‐mir‐100‐5p as novel prognostic markers for oral cancer

Jakob, Mark; Mattes, L; Küffer, Stefan; Unger, Kristian; Heß, Julia; Bertlich, Mattis; Haubner, Frank; Ihler, Friedrich; Canis, Martin; Weiss, Bernhard G.; Kitz, Julia

doi:10.1002/hed.25866

Cited by 48 publications

(51 citation statements)

References 82 publications

(262 reference statements)

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“…This may be significant as over-expression of miR-155 appears to directly promote cellular proliferation in oral cancers [35][36][37]. These observations may conform with additional evidence that has demonstrated miR-155 may be an indicator of poor prognosis among oral cancers [18,37,38].…”

Section: Discussionsupporting

confidence: 57%

Differential exosome miRNA expression in oral cancer stem cells

Shoff

Booker

Leavitt

et al. 2020

ExRNA

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Background: Oral squamous cell carcinomas (OSCC) secrete exosomes into the surrounding extracellular environment to promote the horizontal transfer of bioactive molecules including microRNA (miRNA). The primary objective of this study was to explore potential differences in miRNA content between OSCC and OSCC stem cells.Methods: The OSCC cell lines SCC4, SCC15, SCC25 and CAL27 were used in these studies. The corresponding OSCC stem cells that demonstrated phenotypic adhesion independent tumor spheres (AiTS) were manually isolated. All cells were cultured in DMEM containing 10% exosome-free fetal bovine serum. Exosomes were isolated using Total Exosome Isolation reagent (Invitrogen) and RNA was purified using Total Exosome RNA isolation kit (Invitrogen). Exosome miRNA content was evaluated using miRNA Advanced Taqman Assays for miR-21, − 155, − 133, − 34, − 31, − 32, and − 365. The fold change of miRNA content was calculated using the comparative CT (ΔΔCT) method using miR-16 as an endogenous control. Results: After successful cell cultures were established, AiTS (cancer stem cells) were manually separated and confirmed using CD133 and Sox-2 biomarkers. Exosomes and extracellular vesicles were successfully isolated from all cell lines and AiTS isolates for miRNA screening. All isolates exhibited miR-16 expression (positive control), but none contained mir-31, − 32, or 133a. Differential expression of miR-21, miR-34 and miR-155 were observed with patterns observed among the cancer cell lines which were distinct from the corresponding AiTS isolates. Conclusions: Exosomes isolated from these different OSCC stem cell populations displayed nearly consistent downregulation/loss of miR-21 and miR-34 suggesting the possibility of a unique miRNA profile characteristic of oral cancer stem cells. These findings highlight the need to investigate the comprehensive functions of miR-21 and miR-34 in tumor progression and continued research to refine a miRNA profile that could aid in distinguishing tumors with poor prognosis.

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Section: Discussionsupporting

confidence: 57%

Differential exosome miRNA expression in oral cancer stem cells

Shoff

Booker

Leavitt

et al. 2020

ExRNA

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“…By binding to their complementary sequences in the 3'-untranslated regions (3'-UTRs) at the miRNA recognition elements (MREs) of target mRNAs, miRNAs effectively degrade mRNAs and/or inhibit their translation and subsequently regulate EMT functioning, invasiveness, and metastasis of epithelial cancer cells [23]. Several miRNAs (including miR-143-3p, miR-300, miR-99a-5p, miR-99b-3p, let-7c-5p, miR-100-5p, and miR-125b-5p) have been implicated in OSCC proliferation, migration, and invasion [24,25] and, in particular, low levels of miR-143-3p, miR-300 and miR-99a-5p expression are significantly associated with poor overall survival (OS) in patients with OSCC [24][25][26]. Moreover, miR-300 inhibits EMT by significantly increasing mRNA levels of E-cadherin and significantly decreasing mRNA levels of vimentin, N-cadherin, matrix metalloproteinase-2 (MMP-2), and Snail1 in OSCC cells [25].…”

Section: Introductionmentioning

confidence: 99%

WISP-1 Promotes Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma Cells via the miR-153-3p/Snail Axis

Chang

Lien

Tsai

et al. 2019

Cancers

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Around half of all patients with oral squamous cell carcinoma (OSCC) present with lymphatic metastasis, a strong predictor of poor survival. Improving survival rates depends on preventing the first step in the “invasion-metastasis cascade,” epithelial-to-mesenchymal transition (EMT), and developing antilymphangiogenesis therapies that antagonize lymphatic metastasis. The extracellular matrix-related protein WISP-1 (WNT1-inducible signaling pathway protein-1) stimulates bone remodeling and tumor progression. We have previously reported that WISP-1 promotes OSCC cell migration and lymphangiogenesis induced by vascular endothelial growth factor C (VEGF-C). This investigation sought to determine the role of WISP-1 in regulating EMT in OSCC. Our analysis of oral cancer data from The Cancer Genome Atlas (TCGA) database revealed significant and positive associations between levels of WISP-1 expression and clinical disease stage, as well as regional lymph node metastasis. We also found higher levels of WISP-1 expression in serum samples obtained from patients with OSCC compared with samples from healthy controls. In a series of in vitro investigations, WISP-1 activated EMT signaling via the FAK/ILK/Akt and Snail signaling transduction pathways and downregulated miR-153-3p expression in OSCC cells. Our findings detail how WISP-1 promotes EMT via the miR-153-3p/Snail axis in OSCC cells.

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“…Blocking miR-100-5p significantly augments the anti-tumor activity of ALK tyrosine kinase inhibitors to EML4-ALK positive NSCLC [19]. High expression of mir-100-5p predicts unfavorable clinical outcome in oral squamous cell carcinoma patients [20]. In this study, we provide evidence that stable inhibition of miR-100-5p suppressed cell viability, migration, invasiveness of HK1 cells in vitro and xenograft tumor formation in vivo, indicating an oncogenic role in NPC.…”

Section: Discussionmentioning

confidence: 55%

FOXA1 Suppresses the Growth, Migration, and Invasion of Nasopharyngeal Carcinoma Cells through Repressing miR-100-5p and miR-125b-5p

Peng¹,

Zhang²,

Li³

et al. 2020

J. Cancer

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Background: Nasopharyngeal carcinoma (NPC) is a unique subtype of head and neck cancer, within highest incidence in South China and southeastern Asia but rare in other regions worldwide. FOXA1 is a pioneer factor implicated in various human malignancies. Downregulation of FOXA1 promotes NPC cells proliferation, invasiveness in vitro and tumorigenicity in vivo. However, it is remain elusive to determine whether microRNAs (miRNAs) regulated by FOXA1 contribute to NPC progression. Methods: In this study, differentially expressed miRNAs and mRNAs induced by FOXA1 expression were determined by microarray. Integrative miRNA-mRNA regulatory networks mediated by FOXA1 in NPC were established. The expressions of differentially expressed miRNAs in NPC cells were measured by quantitative reverse-transcription PCR. Cell viability was determined by CCK-8 assays. Cell migration and invasiveness were measured by Transwell assays. The correlation between miRNAs and its target mRNAs was analyzed. Results: FOXA1 suppressed the expression of miR-100-5p and miR-125b-5p in NPC cells. Silencing either miR-100-5p or miR-125b-5p inhibited the malignant behaviors of NPC cells, whereas re-expression of miR-100-5p or miR-125b-5p restored the malignancy of NPC cells repressed by FOXA1. Mechanistically, miR-100-5p or miR-125b-5p suppressed RASGRP3 or FOXN3 expression respectively via direct binding to its 3'-UTR. Furthermore, we demonstrated that FOXA1 induced RASGRP3 or FOXN3 expression via inhibiting miR-100-5p or miR-125b-5p. Upregulation of RASGRP3 or FOXN3 contributed to inhibition of NPC by FOXA1. We also demonstrated that the mRNA levels of RASGRP3 and FOXN3 are positively correlated with FOXA1. Conclusion: Our study provided evidence the first time that FOXA1 suppresses NPC cells via downregulation of miR-100-5p or miR-125b-5p.

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MicroRNA expression patterns in oral squamous cell carcinoma: hsa‐mir‐99b‐3p and hsa‐mir‐100‐5p as novel prognostic markers for oral cancer

Cited by 48 publications

References 82 publications

Differential exosome miRNA expression in oral cancer stem cells

Differential exosome miRNA expression in oral cancer stem cells

WISP-1 Promotes Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma Cells via the miR-153-3p/Snail Axis

FOXA1 Suppresses the Growth, Migration, and Invasion of Nasopharyngeal Carcinoma Cells through Repressing miR-100-5p and miR-125b-5p

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