MicroRNA-375 inhibits oral squamous cell carcinoma cell migration and invasion by targeting platelet-derived growth factor-A

Cao, Zhenghao; Cheng, Jingliang; Zhang, Yong; Bo, Chun‐Xiao; Li, Yan‐Liang

doi:10.3892/mmr.2016.6057

Cited by 26 publications

(15 citation statements)

References 20 publications

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“…Recent studies have emphasized the utility of mir-375 as a biomarker for detection of tongue cancer ( 23 ), malignant transformation of oral lesions ( 39 ), and late stages of oral cancer ( 28 ). Mir-375 has been down-regulated in metastatic oral cancer cell lines compared with less metastatic cells, and mir-375 induced cell migration and invasion by direct targeting the platelet-derived growth factor-A ( PDGF-A ) ( 40 ). Mir-375 mediates the trichostatin-A-induced radiosensitization of tongue cancer ( 41 ), indicating a therapeutic potential of mir-375.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA meta-signature of oral cancer: evidence from a meta-analysis

Zeljić

Jovanović

et al. 2018

Upsala Journal of Medical Sciences

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AimIt was the aim of the study to identify commonly deregulated miRNAs in oral cancer patients by performing a meta-analysis of previously published miRNA expression profiles in cancer and matched normal non-cancerous tissue in such patients.Material and methodsMeta-analysis included seven independent studies analyzed by a vote-counting method followed by bioinformatic enrichment analysis.ResultsAmongst seven independent studies included in the meta-analysis, 20 miRNAs were found to be deregulated in oral cancer when compared with non-cancerous tissue. Eleven miRNAs were consistently up-regulated in three or more studies (miR-21-5p, miR-31-5p, miR-135b-5p, miR-31-3p, miR-93-5p, miR-34b-5p, miR-424-5p, miR-18a-5p, miR-455-3p, miR-450a-5p, miR-21-3p), and nine were down-regulated (miR-139-5p, miR-30a-3p, miR-376c-3p, miR-885-5p, miR-375, miR-486-5p, miR-411-5p, miR-133a-3p, miR-30a-5p). The meta-signature of identified miRNAs was functionally characterized by KEGG enrichment analysis. Twenty-four KEGG pathways were significantly enriched, and TGF-beta signaling was the most enriched signaling pathway. The highest number of meta-signature miRNAs was involved in the sphingolipid signaling pathway. Natural killer cell-mediated cytotoxicity was the pathway with most genes regulated by identified miRNAs. The rest of the enriched pathways in our miRNA list describe different malignancies and signaling.ConclusionsThe identified miRNA meta-signature might be considered as a potential battery of biomarkers when distinguishing oral cancer tissue from normal, non-cancerous tissue. Further mechanistic studies are warranted in order to confirm and fully elucidate the role of deregulated miRNAs in oral cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA meta-signature of oral cancer: evidence from a meta-analysis

Zeljić

Jovanović

et al. 2018

Upsala Journal of Medical Sciences

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“…All 14 genes contained potential HREs in their promoter regions; of them, COL18A1, RRAS2, CORO1A, F2RL1, and PTP4A1 had not previously been suggested as being regulatory targets of HIF-1α (Supplementary Table 3). Our prior work showed that VEGFA, IL6, and PDGFB are overexpressed in OSCC 21 , while other studies found that THBS1 34 , PDGFA 35 , and SPHK1 36 are upregulated and able to promote migration and invasion activities in OSCC. These six genes were previously reported as being regulated by HIF-1α in OSCC.…”

Section: Discussionmentioning

confidence: 83%

ASC modulates HIF-1α stability and induces cell mobility in OSCC

Chang

Hung

et al. 2020

Cell Death Dis

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High-level expression of ASC (Apoptosis-associated speck-like protein containing a CARD) leads to lymph node metastasis in OSCC, but the underlying mechanism remains unclear. Here, we show that HIF-1α participates in ASCinduced metastasis. We identified 195 cell-motion-associated genes that were highly activated in ASC-overexpressed SAS_ASC cells; of them, 14 representative genes were found to be overexpressed in OSCC tissues in our previously reported RNA-seq dataset, OSCC-Taiwan. Nine of the 14 genes were also upregulated in OSCC-TCGA samples. Among the nine genes, RRAS2, PDGFA, and VEGFA, were correlated with poor overall survival of patients in OSCC-TCGA dataset. We further demonstrated that the promoters of these 14 ASC-induced genes contained binding motifs for the transcription-regulating factor, HIF-1α. We observed that ASC interacted with and stabilized HIF-1α in both the cytoplasm and the nucleus under normoxia. Molecules involved in the HIF-1α pathway, such as VHL and PHD2, showed no difference in their gene and protein levels in the presence or absence of ASC, but the expression of HIF-1α-OH, and the ubiquitination of HIF-1α were both decreased in SAS_ASC cells versus SAS_con cells. The migration and invasion activities of SAS_ASC cells were reduced when cells were treated with the HIF-1α synthesis inhibitor, digoxin. Taken together, our results demonstrate that the novel ASC-HIF-1α regulatory pathway contributes to lymph node metastasis in OSCC, potentially suggesting a new treatment strategy for OSCC.

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“…Theoretically, by silencing tumor-promoting miRNAs and inducing the expression of tumor-suppressing miRNAs synchronously, it is possible to treat oral carcinoma. Specific miRNAs have multiple target genes, for example, miR-375 targets IGF1R (32), platelet-derived growth factor subunit A (131), Kruppel-like factor 5 (80) and solute carrier family 7 member 11 (81); miR-138 targets AKT serine/threonine kinase 1 (82) and yes-associated protein 1 (83); miR-203 targets B lymphoma Mo-MLV insertion region 1 homolog (84), semaphorin 6A (85) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (86); and miR-221 targets tissue inhibitor of metalloproteinase 3 (114) and phosphatase and tensin homolog (PTEN) (115). A possible treatment strategy may involve anticancer drugs that selectively regulate the expression of such miRNAs.…”

Section: Conceivable Therapeutic Value Of Mirnasmentioning

confidence: 99%

Prospective applications of microRNAs in oral cancer: A review (Review)

Fang

2019

Oncol Lett

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MicroRNAs (miRNAs) are non-coding RNA molecules that are generally encoded by endogenous genes and exert suppressive effects on post-transcriptional regulation of their target genes by translation repression or degradation of mRNA. This subsequently mediates activation or blocking of downstream signaling pathways associated with oral malignancies. Aberrant levels of certain miRNAs have been identified in cell experiments, clinical carcinomatous specimens, saliva, serum or plasma samples of patients with oral malignancies. miRNAs are associated with multiple aspects of oral cancer, including tumor growth, cellular proliferation, apoptosis, migration, invasion, metastasis, glycometabolism, radiosensitivity and chemosensitivity. miRNAs have the potential to be used in clinical applications as minimally invasive or non-invasive tools for early diagnosis and prognosis by the detection of serum, plasma and saliva levels, and may provide a new ancillary or additional reference index of traditional pathological grading and clinical staging. Furthermore, miRNAs may be used as prognostic biomarkers or targets for novel therapies for oral cancer.

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MicroRNA-375 inhibits oral squamous cell carcinoma cell migration and invasion by targeting platelet-derived growth factor-A

Cited by 26 publications

References 20 publications

MicroRNA meta-signature of oral cancer: evidence from a meta-analysis

MicroRNA meta-signature of oral cancer: evidence from a meta-analysis

ASC modulates HIF-1α stability and induces cell mobility in OSCC

Prospective applications of microRNAs in oral cancer: A review (Review)

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