Kr üppel-like factor 1 serves as a facilitator in gastric cancer progression via activating the Wnt/β-catenin pathway

In this study, we explored the role and potential mechanism of KLF1 in GC progression by using a series of experimental methods including RT-qPCR, Western blot, CCK-8 assay, EdU staining, and cell cycle analysis. KLF1 was found to be elevated in GC tissues (n=415) compared with the normal tissues by applying UALCAN to analyze datasets from The Cancer Genome Atlas (TCGA). The upregulation of KLF1 was also validated in GC cell lines. Functional studies proved that RNA interference-mediated silencing of KLF1 inhibited GC cell growth, as evidenced by the decreased cell viability, DNA synthesis, and arrested cell cycle in G1 phase. Moreover, KLF1 knockdown exerted the inhibitory effects on cell migration and invasion as well as the epithelial-mesenchymal transition (EMT) in GC cells. Conversely, overexpression of KLF1 had the opposite effects on GC progression. Furthermore, we proved that the activation of Wnt/β-catenin pathway was markedly inhibited by KLF1 knockdown and promoted by KLF1 overexpression. The blockade of Wnt/β-catenin pathway rescued the effects of KLF1 overexpression. These results suggested that KLF1 promoted the growth, migration, invasion, and EMT process in GC cells, and this promotion was achieved by activating the Wnt/β-catenin pathway. This work will be helpful for searching the potential therapeutic targets for treatment of GC.PMID:34669363 | DOI:10.18388/abp.2020_5680
Source: Acta Biochim Pol - Category: Biochemistry Authors: Source Type: research

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Source: Inflammation - Category: Allergy & Immunology Source Type: research
In this study, we explored the role and potential mechanism of KLF1 in GC progression by using a series of experimental methods including RT-qPCR, Western blot, CCK-8 assay, EdU staining, and cell cycle analysis. KLF1 was found to be elevated in GC tissues (n=415) compared with the normal tissues by applying UALCAN to analyze datasets from The Cancer Genome Atlas (TCGA). The upregulation of KLF1 was also validated in GC cell lines. Functional studies proved that RNA interference-mediated silencing of KLF1 inhibited GC cell growth, as evidenced by the decreased cell viability, DNA synthesis, and arrested cell cycle in G1 ph...
Source: Acta Biochim Pol - Category: Biochemistry Authors: Source Type: research
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Source: Clinical Lung Cancer - Category: Cancer & Oncology Authors: Source Type: research
Condition:   Kita-kyushu Lung Cancer Antigen 1, Human Interventions:   Drug: IL-2 (Aldesleukin);   Drug: Cyclophosphamide;   Biological: KK-LC-1 TCR;   Drug: Fludarabine Sponsor:   National Cancer Institute (NCI) Not yet recruiting
Source: ClinicalTrials.gov - Category: Research Source Type: clinical trials
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