Identification of miRNA/mRNA-Negative Regulation Pairs in Nasopharyngeal Carcinoma

Liu, Minglei; Zhu, Kang-Ru; Qian, Xinmei; Li, Wei

doi:10.12659/msm.896047

Cited by 19 publications

(16 citation statements)

References 53 publications

(50 reference statements)

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“…Silencing of miR-632 inhibits EMT (epithelial-mesenchymal transition) and eliminates invasive ability in breast cancer cells. In addition, miR-632 is related to nasopharyngeal carcinoma, laryngeal cancer and myelodysplastic syndrome [16–18]. Tuberculosis risk may be influenced by miR-632-mediated regulation [19].…”

Section: Introductionmentioning

confidence: 99%

miR-632 promotes gastric cancer progression by accelerating angiogenesis in a TFF1-dependent manner

et al. 2019

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BackgroundGastric cancer (GC) is a common malignant disease worldwide. Aberrant miRNAs expression contributes to malignant cells behaviour, and in preclinical research, miRNA targeting has shown potential for improving GC therapy. Our present study demonstrated that miR-632 promotes GC progression in a trefoil factor 1 (TFF1)-dependent manner.MethodsWe collected GC tissues and serum samples to detect miR-632 expression using real-time PCR. A dual-luciferase reporter assay was used to identify whether miR-632 directly regulates TFF1 expression. Tube formation and endothelial cell recruitment assays were performed with or without miR-632 treatment. Western blot and in situ hybridization assays were performed to detect angiogenesis and endothelial recruitment markers that are affected by miR-632.ResultsOur results showed that miR-632 is highly expressed in GC tissue and serum and negatively associated with TFF1 in GC. miR-632 improves tube formation and endothelial cell recruitment by negatively regulating TFF1 in GC cells. Recombinant TFF1 reversed miR-632-mediated angiogenesis. TFF1 is a target gene of miR-632.ConclusionsOur study demonstrated that miR-632 promotes GC progression by accelerating angiogenesis in a TFF1-dependent manner. Targeting of miR-632 may be a potential therapeutic approach for GC patients.Electronic supplementary materialThe online version of this article (10.1186/s12885-018-5247-z) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

miR-632 promotes gastric cancer progression by accelerating angiogenesis in a TFF1-dependent manner

et al. 2019

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“…Although endometriosis is considered a nonmalignant condition, the characteristics of endometriosis such as infiltration of endometriosis tissues to surrounding organs and presence of angiogenesis resembles a tumour-like behavior to some extent [18, 28, 29]. Microarray studies including ours demonstrated that FJX1 is overexpressed in NPC relative to noncancerous tissues [13, 30, 31]. Overexpression of FJX1 in the transcriptomic level was also observed in RNA-Seq data from 43 head and neck cancers compared to matched normal samples from the TCGA database.…”

Section: Discussionmentioning

confidence: 96%

An Oncogenic Role for Four-Jointed Box 1 (FJX1) in Nasopharyngeal Carcinoma

et al. 2019

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Nasopharyngeal carcinoma (NPC) is a highly metastatic cancer prevalent in Southern China and Southeast Asia. The current knowledge on the molecular pathogenesis of NPC is still inadequate to improve disease management. Using gene expression microarrays, we have identified the four-jointed box 1 (FJX1) gene to be upregulated in primary NPC tissues relative to nonmalignant tissues. An orthologue of human FJX1, the four-jointed (fj) gene in Drosophila and Fjx1 in mouse, has reported to be associated with cancer progression pathways. However, the exact function of FJX1 in human is not well characterized. The overexpression of FJX1 mRNA was validated in primary NPC tissue samples, and the level of FJX1 protein was significantly higher in a subset of NPC tissues (42%) compared to the normal epithelium, where no expression of FJX1 was observed (p=0.01). FJX1 is also found to be overexpressed in microarray datasets and TCGA datasets of other cancers including head and neck cancer, colorectal, and ovarian cancer. Both siRNA knockdown and overexpression experiments in NPC cell lines showed that FJX1 promotes cell proliferation, anchorage-dependent growth, and cellular invasion. Cyclin D1 and E1 mRNA levels were increased following FJX1 expression indicating that FJX1 enhances proliferation by regulating key proteins governing the cell cycle. Our data suggest that the overexpression of FJX1 contributes to a more aggressive phenotype of NPC cells and further investigations into FJX1 as a potential therapeutic target for NPC are warranted. The evaluation of FJX1 as an immunotherapy target for NPC and other cancers is currently ongoing.

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“…In gastric cancer, DTX1 was reported specifically down-regulated and promoted cellular FLICE inhibitory protein (c-FLIP), as its E3 ligase substrate, to degrade through the endosome-lysosomal pathway 25 . DTX4 was significantly up-regulated through comparison of the interaction network between miRNAs and target genes in nasopharyngeal carcinoma samples 26 .…”

Section: Discussionmentioning

confidence: 99%

Deltex3 inhibits Epithelial Mesenchymal Transition in Papillary Thyroid Carcinoma via promoting ubiquitination of XRCC5 to regulate the AKT signal pathway

Wang¹,

Huang²,

Liu³

et al. 2021

J. Cancer

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Identification of miRNA/mRNA-Negative Regulation Pairs in Nasopharyngeal Carcinoma

Cited by 19 publications

References 53 publications

miR-632 promotes gastric cancer progression by accelerating angiogenesis in a TFF1-dependent manner

miR-632 promotes gastric cancer progression by accelerating angiogenesis in a TFF1-dependent manner

An Oncogenic Role for Four-Jointed Box 1 (FJX1) in Nasopharyngeal Carcinoma

Deltex3 inhibits Epithelial Mesenchymal Transition in Papillary Thyroid Carcinoma via promoting ubiquitination of XRCC5 to regulate the AKT signal pathway

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