Forkhead box K1 regulates the malignant behavior of gastric cancer by inhibiting autophagy
Identifieur interne : 000151 ( an2020/Analysis ); précédent : 000150; suivant : 000152Forkhead box K1 regulates the malignant behavior of gastric cancer by inhibiting autophagy
Auteurs : Yixuan Wang [République populaire de Chine] ; Wensheng Qiu [République populaire de Chine] ; Ning Liu [République populaire de Chine] ; Libin Sun [République populaire de Chine] ; Zhao Liu [République populaire de Chine] ; Shasha Wang [République populaire de Chine] ; Peng Wang ; Shihai Liu [République populaire de Chine] ; Jing Lv [République populaire de Chine]Source :
- Annals of Translational Medicine [ 2305-5839 ] ; 2020.
Abstract
Forkhead box K1 (FOXK1) is a transcription factor that contributes to cancer development, but it is unclear how FOXK1 regulates the proliferation and migration of gastric cancer (GC) cells. The purpose of this study was to investigate the clinical significance, biological function, and molecular mechanisms of FOXK1 in GC.
We conducted bioinformatics assays and western blotting to assess FOXK1 expression. Then, we performed immunohistochemistry (IHC) with tissue microarrays (TMAs) to assess FOXK1 expression in order to identify an association between FOXK1 expression levels and clinical parameters. We used 5-ethynyl-2’-deoxyuridine (EdU), wound healing and Transwell assays to determine whether FOXK1 promotes malignant behaviors in GC. Furthermore, immunofluorescence staining, transmission electron microscopy and western blotting were used to verify an association between FOXK1 and autophagy.
We observed high levels of FOXK1 expression in GC tissues, which were associated with the degree of malignancy in GC. FOXK1 promotes the malignant behavior of GC by regulating autophagy via activation of the class I phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway and inhibition of the expression of class III PI3K.
These findings provide a new target for the comprehensive treatment of GC by highlighting the relationship between FOXK1 and malignant behaviors in GC.
Url:
DOI: 10.21037/atm.2019.12.123
PubMed: 32175400
PubMed Central: 7049027
Affiliations:
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PMC:7049027Le document en format XML
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>Forkhead box K1 (FOXK1) is a transcription factor that contributes to cancer development, but it is unclear how FOXK1 regulates the proliferation and migration of gastric cancer (GC) cells. The purpose of this study was to investigate the clinical significance, biological function, and molecular mechanisms of FOXK1 in GC.</p>
</sec>
<sec><title>Methods</title>
<p>We conducted bioinformatics assays and western blotting to assess FOXK1 expression. Then, we performed immunohistochemistry (IHC) with tissue microarrays (TMAs) to assess FOXK1 expression in order to identify an association between FOXK1 expression levels and clinical parameters. We used 5-ethynyl-2’-deoxyuridine (EdU), wound healing and Transwell assays to determine whether FOXK1 promotes malignant behaviors in GC. Furthermore, immunofluorescence staining, transmission electron microscopy and western blotting were used to verify an association between FOXK1 and autophagy.</p>
</sec>
<sec><title>Results</title>
<p>We observed high levels of FOXK1 expression in GC tissues, which were associated with the degree of malignancy in GC. FOXK1 promotes the malignant behavior of GC by regulating autophagy via activation of the class I phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway and inhibition of the expression of class III PI3K.</p>
</sec>
<sec><title>Conclusions</title>
<p>These findings provide a new target for the comprehensive treatment of GC by highlighting the relationship between FOXK1 and malignant behaviors in GC.</p>
</sec>
</div>
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