FOXK1 plays an oncogenic role in the development of esophageal cancer

Chen, Di; Wang, Kai; Li, Xiaowei; Jiang, Mingzuo; Ni, L.; Xu, Bing; Chu, Yi; Wang, Weijie; Wang, Hua; Kang, Huijie; Wu, Kaichun; Liang, Jie; Ren, Gui

doi:10.1016/j.bbrc.2017.10.080

Cited by 38 publications

(31 citation statements)

References 22 publications

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“…Moreover, FOXK1 has also been determined to process an core role in occurrence, progression, invasion and metastasis of various tumors such as esophageal cancer [14], glioma [15], colon cancer [16] and gastric cancer [17].…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: The LncRNA XIST Promotes Colorectal Cancer Cell Growth Through Regulating miR-497-5p/FOXK1 Axis

Wang

Jia

et al. 2020

Preprint

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Background: Recently, accumulated numbers of studies have reported that long noncoding RNAs (lncRNAs) process an important role in tumorigenesis. As a new member found in lncRNAs, the role of lncRNA XIST (XIST) in colorectal cancer (CRC) was still elusive. The objective of this study was conducted to characterize a novel regulatory network involving XIST in CRC cells. Methods: The mRNAs of XIST, miR-497-5p, and forkhead box k1 (FOXK1) in CRC cells and tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). And the proliferation and apoptosis of CRC cells were determined using cell counting kit-8 assay and flow cytometry. Moreover, we also detected the cell migration and invasion using Transwell assays. The relationships between XIST, miR-497-5p, and FOXK1 were predicted and then the dual-luciferase reporter assay was used to their relationships. The protein level of FOXK1 was quantitated using western blot. Results: In CRC tissues and cell lines, XIST expression was up-regulated, in which also existed miR-497-5p down-regulation and FOXK1 up-regulation. XIST knockdown suppressed CRC cell proliferation and migration as well as its invasion. Moreover, blocking the XIST expression could inhibit CRC tumor growth in vivo and the effects were antagonized by loss of miR-497-5p. miR-497-5p was identified as a sponge of XIST and also targeted FOXK1 in CRC cells. Besides, XIST silencing-mediated inhibitory activity against CRC progression reversed miR-497-5p down-regulation or FOXK1 up-regulation. Conclusion: In conclusion, XIST promotes the malignancy of colon cancer cells partly by competitively binding to miR-497-5p, which then led to increased FOXK1 expression. We conclude that targeting XIST may be a possible treatment for colon cancer.

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Section: Introductionmentioning

confidence: 99%

WITHDRAWN: The LncRNA XIST Promotes Colorectal Cancer Cell Growth Through Regulating miR-497-5p/FOXK1 Axis

Wang

Jia

et al. 2020

Preprint

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“…Multiple genes, including retinoic acid–related orphan receptor-A,19 lethal(2) giant larvae 1,20 and zinc finger E-box binding homeobox 1,21 have been recognized as the direct downstream targets of miR-652. FOXK1, a forkhead family transcription factor31 shown to be a novel direct target of miR-652 in GBM, has been implicated in development and metabolism and is overexpressed in colorectal,32 liver,24 gastric,33 and esophageal cancers 34. FOXK1 is also expressed at high levels in GBM tissues and cell lines 23.…”

Section: Discussionmentioning

confidence: 99%

<p>MicroRNA-652 suppresses malignant phenotypes in glioblastoma multiforme via FOXK1-mediated AKT/mTOR signaling pathway</p>

Yang

Song

et al. 2019

OTT

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Purpose An increasing number of studies have documented that dysregulation of microRNAs (miRNAs) is common in glioblastoma multiforme (GBM). miR-652 is aberrantly expressed in various human cancers and plays important roles in numerous cancer-related processes. However, the expression profiles and potential roles of miR-652 in GBM remain largely unknown. Patients and methods Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine miR-652 expression in GBM tissues and cell lines. The effects of miR-652 upregulation on GBM cell proliferation, clone formation, apoptosis, migration and invasion were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, clone formation, flow cytometry and Transwell ® migration and invasion assays, respectively. In vivo xenotransplantation was utilized to determine the effect of miR-652 on GBM tumor growth in vivo. Of note, the molecular mechanisms underlying the tumor-suppressing activity of miR-652 upregulation in GBM cells were also investigated using a series of experiments, including bioinformatics analysis, luciferase reporter assay, RT-qPCR and Western blot analysis. Results miR-652 expression was considerably downregulated in GBM tissues and cell lines. Low miR-652 expression was strongly correlated with Karnofsky performance score and tumor size. Overall survival duration was shorter in GBM patients with low miR-652 expression than in those with high miR-652 expression. miR-652 resumption considerably suppressed the proliferation, clone formation, migration, and invasion and promoted the apoptosis of GBM cells in vitro. In addition, forkhead-box k1 (FOXK1) was demonstrated as the direct target gene of miR-652 in GBM cells. FOXK1 downregulation led to a tumor-suppressing activity similar to that of miR-652 upregulation. Restoration of FOXK1 expression partially neutralized the influence of miR-652 overexpression on GBM cells. Furthermore, ectopic miR-652 expression deactivated the AKT/mTOR pathway in GBM cells via FOXK1 regulation. Moreover, miR-652 impaired GBM tumor growth in vivo, probably caused by miR-652-mediated suppression of FOXK1/AKT/mTOR signaling. Conclusion miR-652 inhibits FOXK1 and deactivates the AKT/mTOR pathway, thereby resulting in the suppression of malignant phenotypes of GBM cells in vitro and in vivo.

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“…Forkhead box (FOX) K1 is a member of the FOX transcription factor superfamily, and overexpression of FOXK1 is found in a serious of cancerous human tissue types, including in GC [15,16]. Overexpression of FOXK1 usually promotes cancer cell proliferation and migration and plays an oncogenic role in cancer pathogenesis [17].…”

Section: Introductionmentioning

confidence: 99%

LINC02163 regulates growth and epithelial-to-mesenchymal transition phenotype via miR-593-3p/FOXK1 axis in gastric cancer cells

Dong

Hong

Chen

et al. 2018

Artificial Cells, Nanomedicine, and Biotechnology

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Recently, long non-coding RNAs (lncRNAs) were involved in promoting gastric cancer (GC) initiation and progression. In the current study, we revealed that the expression level of LINC02163 was elevated in GC cell lines and tissues. Knockdown of LINC02163 inhibited GC cells growth and invasion both in vitro and in vivo. Mechanismly, LINC02163 exerted as a ceRNA and negatively regulated miR-593-3p expression. In addition, FOXK1 was identified as a down-stream target of miR-593-3p. The miR-593-3p/FOXK1 axis mediated LINC02163's effect on GC. To the best of our knowledge, our findings provided the first evidence that LINC02163 functioned as an oncogene in GC. LINC02163 may be a candidate prognostic biomarker and a target for new therapies in GC patients.

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FOXK1 plays an oncogenic role in the development of esophageal cancer

Cited by 38 publications

References 22 publications

WITHDRAWN: The LncRNA XIST Promotes Colorectal Cancer Cell Growth Through Regulating miR-497-5p/FOXK1 Axis

WITHDRAWN: The LncRNA XIST Promotes Colorectal Cancer Cell Growth Through Regulating miR-497-5p/FOXK1 Axis

<p>MicroRNA-652 suppresses malignant phenotypes in glioblastoma multiforme via FOXK1-mediated AKT/mTOR signaling pathway</p>

LINC02163 regulates growth and epithelial-to-mesenchymal transition phenotype via miR-593-3p/FOXK1 axis in gastric cancer cells

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