miR-639 regulates transforming growth factor beta-induced epithelial–mesenchymal transition in human tongue cancer cells by targeting FOXC1

@article{Lin2014miR639RT,
  title={miR-639 regulates transforming growth factor beta-induced epithelial–mesenchymal transition in human tongue cancer cells by targeting FOXC1},
  author={Zhao-yu Lin and Li-juan Sun and Weiliang Chen and Bodu Liu and Youyuan Wang and S. Fan and Yilin Li and Jinsong Li},
  journal={Cancer Science},
  year={2014},
  volume={105},
  pages={1288 - 1298}
}
Epithelial‐to‐mesenchymal transition (EMT) is implicated in embryonic development and various pathological events. Transforming growth factor beta (TGFβ) has been reported to induce EMT in tumor cells, which is a critical step in the process of metastasis leading to cancer spreading and treatment failure. However, the involvement of microRNA during the EMT process in tongue squamous cell carcinoma (TSCC) remains to be determined. To address this question, TSCC cell lines SCC9 and CAL27 were… Expand
MicroRNA-374c-5p regulates the invasion and migration of cervical cancer by acting on the Foxc1/snail pathway.
TLDR
It is found that miR-374c-5p was most down-regulated miRNA in TGFβ1-treated cervical cancer cells compared to the expression in parental cell lines, and this finding highlights the important role in regulating cervical cancers metastasis by targeting FOXC1. Expand
MiR-940 inhibits migration and invasion of tongue squamous cell carcinoma via regulatingCXCR2/NF-κB system-mediated epithelial–mesenchymal transition
TLDR
Investigation of the role of microRNA-940/C-X-C chemokine receptor type 2 (CXCR2) system in the metastasis ability and EMT process of IL-8-treated TSCC cells found that miR-940 up-regulation inhibited IL- 8-induced migration and invasion, which could be deprived by CX CR2 silence. Expand
Long non-coding RNA CASC15 promotes tongue squamous carcinoma progression through targeting miR-33a-5p
TLDR
The results suggested that lncRNA CASC15 and miR-33a-5p might be exploited as new markers of TSCC and were potential treatment targets for TSCC patients. Expand
LINC01783 accelerated tongue squamous cell carcinoma progression via inhibiting miR‐199b‐5p
  • Ying Hu, Xiaofeng Wang, Chong Li, Liang-bo Jiao, Yi Du
  • Medicine
  • Journal of cellular and molecular medicine
  • 2021
TLDR
The data suggested that LINC01783 functioned as one oncogene and might be one treatment target for TSCC and up-regulated in TSCC specimens when compared to no-tumour specimens. Expand
MiR-639 promoted cell proliferation and cell cycle in human thyroid cancer by suppressing CDKN1A expression.
TLDR
It was found that miR-639 expression was upregulated in TC cells and clinical tissues, and CDKN1A small interfering RNA (siRNA) abrogated the role of miR -639-in on cell proliferation of TC. Expand
Long noncoding RNA GIHCG enhanced tongue squamous cell carcinoma progression through regulating miR‐429
TLDR
Elevated expression of GIHCG promoted TSCC cell cycle, proliferation, and migration through regulating miR‐429 expression, and suggested thatGIHCG increased TSCC progression through negative modulation of miR•429. Expand
MALAT1 induces tongue cancer cells' EMT and inhibits apoptosis through Wnt/&bgr;‐catenin signaling pathway
TLDR
Upregulated MALAT1 in TSCC promoted EMT and inhibited cell apoptosis by modulating Wnt/β-catenin signaling pathway and attenuated the effect of exogenous MALat1. Expand
Chemotherapy-Induced Long Non-coding RNA 1 Promotes Metastasis and Chemo-Resistance of TSCC via the Wnt/β-Catenin Signaling Pathway.
TLDR
A chemotherapy-induced lncRNA 1 (CILA1) was discovered by using microarrays and was functionally identified as a regulator of chemo-sensitivity in TSCC cells and a therapeutic target for TSCC treatment. Expand
miR-639 Expression Is Silenced by DNMT3A-Mediated Hypermethylation and Functions as a Tumor Suppressor in Liver Cancer Cells.
  • J. Xiao, Yankun Liu, +7 authors Hua Tang
  • Medicine, Biology
  • Molecular therapy : the journal of the American Society of Gene Therapy
  • 2019
TLDR
It is revealed that microRNA-639 (miR- 639) expression is downregulated in liver cancer tissues and cells and DNMT3A-mediated hypermethylation suppressed miR-6 39 expression, derepressing the expression of MSYT2 and ZEB1, which promoted tumorigenesis of liver cancer. Expand
Tumor necrosis factor α induces myofibroblast differentiation in human tongue cancer and promotes invasiveness and angiogenesis via secretion of stromal cell-derived factor-1.
TLDR
The results suggest that TNFα may not only directly but also indirectly enhance cancer metastasis, EMT and angiogenesis formation in tongue cancer through myofibroblast differentiation via SDF1 secretion. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 50 REFERENCES
MiR-200b and miR-15b regulate chemotherapy-induced epithelial-mesenchymal transition in human tongue cancer cells by targeting BMI1
TLDR
Stable chemotherapy-resistant tongue squamous cell carcinoma cell lines are established by exposing the parental CAL27 and SCC25 lines to escalating concentrations of cisplatin for 6 months and it is suggested that reduced expression of miR-200b and miB-15b underscores the mechanisms of chemotherapy-induced EMT in TSCC, and may serve as therapeutic targets to reverse chemotherapy resistance in tongue cancers. Expand
Vimentin regulates EMT induction by Slug and oncogenic H-Ras and migration by governing Axl expression in breast cancer
TLDR
It is shown that vimentin functionally contributes to EMT and is required for induction of Axl expression, and regulation of breast cancer cell migration in two- and three-dimensional matrices by vimentsin is Axl- dependent and that Axl functional contributes to lung extravasation of breast cancers cells in mice. Expand
FOXC1 Contributes To Microvascular Invasion In Primary Hepatocellular Carcinoma Via Regulating Epithelial-Mesenchymal Transition
TLDR
It is demonstrated that FoxC1 is one of candidate predictive markers of MVI, and that inhibition of FOXC1 expression can partially reverse EMT program, offering a potential molecular therapeutic target for reducing tumor metastasis in HCC patients. Expand
The EMT-activator ZEB1 promotes tumorigenicity by repressing stemness-inhibiting microRNAs
TLDR
It is proposed that ZEB1 links EMT-activation and stemness-maintenance by suppressingstemness-inhibiting microRNAs (miRNAs) and thereby is a promoter of mobile, migrating cancer stem cells. Expand
NF-κB is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression
TLDR
Evidence of an essential role for NF-κB during distinct steps of breast cancer progression is provided and the cooperation of Ras- and TGF-β–dependent signaling pathways in late-stage tumorigenesis depends critically on NF-σB activity is suggested. Expand
FGFR4 promotes stroma-induced epithelial-to-mesenchymal transition in colorectal cancer.
TLDR
Proteomic analyses reveal that coculture with tumor-associated fibroblasts (TAF) induces significant overexpression of FGFR4, but not other FGFRs, in colorectal cancer cell lines, and suggests novel therapeutic opportunities for the treatment of coloreCTal cancer. Expand
Transforming Growth Factor-β (TGFβ)-mediated Phosphorylation of hnRNP E1 Induces EMT via Transcript Selective Translational Induction of Dab2 and ILEI
TLDR
The results suggest the existence of a TGF-β-inducible post-transcriptional regulon that controls EMT during the development and metastatic progression of tumours. Expand
E2F1-regulated microRNAs impair TGFbeta-dependent cell-cycle arrest and apoptosis in gastric cancer.
TLDR
Evidence is provided that the miR-106b-25 cluster, upregulated in a subset of human gastric tumors, is involved in E2F1 posttranscriptional regulation and may play a key role in the development of TGFbeta resistance in gastric cancer. Expand
TGF-β Induces Growth Arrest in Burkitt Lymphoma Cells via Transcriptional Repression of E2F-1*
TLDR
Data indicate that deregulation of c-MYC in lymphoma cells does not overcome the tumor suppressor function of TGF-β and that repression of E2F-1 transcription is sufficient for the efficient induction of cytostasis. Expand
MCF-7 Cells Expressing Nuclear Associated Lysyl Oxidase-like 2 (LOXL2) Exhibit an Epithelial-to-Mesenchymal Transition (EMT) Phenotype and Are Highly Invasive in Vitro*
TLDR
The results indicate that nuclear associated catalytically competent LOXL2 contributes to the stabilization of Snail1 transcription factor at the protein level to induce EMT and promote invasion in vitro, through repression of E-cadherin, occludin, and estrogen receptor-α, and up-regulation of vimentin, fibronectin and MT1-MMP. Expand
...
1
2
3
4
5
...