FGF1–FGFR1 axis promotes tongue squamous cell carcinoma (TSCC) metastasis through epithelial–mesenchymal transition (EMT)

Jiao, Jiuyang; Zhao, Xiao Li; Liang, Ye‐Lin; Tang, Dongxiao; Pan, Chaobin

doi:10.1016/j.bbrc.2015.09.021

Cited by 33 publications

(42 citation statements)

References 29 publications

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“…It is well known that metastasis of TSCC is closely related to EMT (28). EMT facilitates tumor cell migration, invasion and metastasis, and may also be a major mechanism of tumor progression (29).…”

Section: Discussionmentioning

confidence: 99%

Nicotine may promote tongue squamous cell carcinoma progression by activating the Wnt/β-catenin and Wnt/PCP signaling pathways

Wang

Jin

et al. 2017

Oncology Letters

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To investigate the effects and the possible underlying mechanisms of nicotine stimulation on tongue squamous cell carcinoma (TSCC) progression, a TSCC cell line Cal27 and 34 samples of paraffin-embedded TSCC were examined. Immunofluorescence, western blot analysis, and TOP/FOP flash, CCK-8, wound healing and Transwell invasion assays were used to evaluate Cal27 in response to nicotine stimulation. We also investigated expression levels of related proteins of Wnt/β-catenin and Wnt/PCP pathways in paraffin-embedded TSCC samples with or without a history of smoking by immunohistochemistry. Nicotine stimulation can promote proliferation, migration, and invasion of TSCC cells in vitro, downregulate E-cadherin, and activate the Wnt/β-catenin and Wnt/PCP pathways, which could be antagonized by the α7 nicotine acetylcholine receptor (α7 nAChR) inhibitor α-BTX. Moreover, the expression levels of β-catenin, Wnt5a and Ror2 were higher in TSCC patients with a history of smoking than those without a history of smoking. Our results suggest nicotine may promote tongue squamous carcinoma cells progression by activating the Wnt/β-catenin and Wnt/PCP signaling pathways and may play a significant role in the progression and metastasis of smoking-related TSCC.

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Section: Discussionmentioning

confidence: 99%

Nicotine may promote tongue squamous cell carcinoma progression by activating the Wnt/β-catenin and Wnt/PCP signaling pathways

Wang

Jin

et al. 2017

Oncology Letters

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“…In this regard, UCA1 contributes to HCC tumourigenesis in part through acting as a ceRNA for miR-216b, leading to depression of fibroblast growth factor receptor 1 (FGFR1) and consequent activation of MAPK/ERK signalling [187]. As activation of FGFR1 has been documented to promote EMT in other cancers [405,406,407], it is likely that induction of FGRF1 signalling by UCA1 could promote EMT. Likewise, it has been suggested that lncRNA SLC25A25-AS1, inhibits EMT in CRC cells, possibly through inhibition of ERK and p38 signalling [252].…”

Section: Lncrnas In Signalling Pathways Governing Emtmentioning

confidence: 99%

Long Non-Coding RNAs: Key Regulators of Epithelial-Mesenchymal Transition, Tumour Drug Resistance and Cancer Stem Cells

Heery

Finn

Cuffe

et al. 2017

Cancers

156

140

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Epithelial mesenchymal transition (EMT), the adoption by epithelial cells of a mesenchymal-like phenotype, is a process co-opted by carcinoma cells in order to initiate invasion and metastasis. In addition, it is becoming clear that is instrumental to both the development of drug resistance by tumour cells and in the generation and maintenance of cancer stem cells. EMT is thus a pivotal process during tumour progression and poses a major barrier to the successful treatment of cancer. Non-coding RNAs (ncRNA) often utilize epigenetic programs to regulate both gene expression and chromatin structure. One type of ncRNA, called long non-coding RNAs (lncRNAs), has become increasingly recognized as being both highly dysregulated in cancer and to play a variety of different roles in tumourigenesis. Indeed, over the last few years, lncRNAs have rapidly emerged as key regulators of EMT in cancer. In this review, we discuss the lncRNAs that have been associated with the EMT process in cancer and the variety of molecular mechanisms and signalling pathways through which they regulate EMT, and finally discuss how these EMT-regulating lncRNAs impact on both anti-cancer drug resistance and the cancer stem cell phenotype.

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“…Bachis (24) correlated increased expression of BDNF with hippocampal neurogenesis, and decreased expression with anxiety disorder. FGF1 (Fibroblast growth factor 1) is a core member of the FGFs family which play important roles in cell proliferation, angiogenesis, morphogenesis and regeneration, and is closely related to tumor development (25). FGF1 also has a nutritive function in the regeneration of central nervous system and impaired neuronal repair (26).…”

Section: Discussionmentioning

confidence: 99%

Identifying miRNA‑mRNA regulation network of major depressive disorder in ovarian cancer patients

Zhao

Liu

et al. 2018

Oncol Lett

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Major depression disorder (MDD) has become increasingly common in patients with ovarian cancer, which complicates the treatment course. The microRNA (miRNA)-mRNA regulation network may help elucidate the potential mechanism of MDD in ovarian cancer. The differentially expressed microRNAs (DEmiRs) and mRNAs (DEmRNAs) were therefore identified from the GSE61741, GSE58105 and GSE9116 ovarian cancer datasets using GEO2R. The target genes of the DEmiRs were then obtained using the TargetScan, microRNAorg, microT-CDS, miRDB and miRTarBase prediction tools. The DAVID program was used to identify the KEGG pathways of target genes, and the core genes of major depressive disorder (MDD) were identified using the Kaplan-Meier Plotter for ovarian cancer. A total of 5 DEmiRs (miR-23b-3p, miR-33b-3p, miR-1265, miR-933 and miR-629-5p) were obtained from GSE61741 and GSE58105. The target genes of these DEmiRs were enriched in pathways that were considered high risk for developing MDD in ovarian cancer. A total of 11 risk genes were selected from these pathways as the core genes in the miRNA-mRNA network of MDD in ovarian cancer, and eventually identified the following 12 miRNA-mRNAs pairs: miR-629-5p-FGF1, miR-629-5p-AKT3, miR-629-5p-MAGI2, miR-933-BDNF, miR-933-MEF2A, miR-23b-3p-TJP1, miR-23b-3p-JMJD1, miR-23b-3p-APAF1, miR-23b-3p-CAB39, miR-1265-CDKN1B, miR-33b-3p-CDKN1B, and miR-33b-3p-F2R. These results may provide novel insights into the mechanisms of developing MDD in ovarian cancer patients.

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FGF1–FGFR1 axis promotes tongue squamous cell carcinoma (TSCC) metastasis through epithelial–mesenchymal transition (EMT)

Cited by 33 publications

References 29 publications

Nicotine may promote tongue squamous cell carcinoma progression by activating the Wnt/β-catenin and Wnt/PCP signaling pathways

Nicotine may promote tongue squamous cell carcinoma progression by activating the Wnt/β-catenin and Wnt/PCP signaling pathways

Long Non-Coding RNAs: Key Regulators of Epithelial-Mesenchymal Transition, Tumour Drug Resistance and Cancer Stem Cells

Identifying miRNA‑mRNA regulation network of major depressive disorder in ovarian cancer patients

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