Krüppel-Like Factor 7 is a Marker of Aggressive Gastric Cancer and Poor Prognosis

Jiang, Zhonghua; Yu, Tingting; Fan, Zhining; Yang, Hongmei; Lin, Xin

doi:10.1159/000481748

Cited by 34 publications

(33 citation statements)

References 26 publications

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“…To explore TCGA datasets, we used cBioPortal (http://www.cbioportal. org/index.do) to find pathways of interest in one or more cancer types [16][17][18]. Sequencing of the dataset was based on the Illumina HiSeq platform [19].…”

Section: Patient Samplesmentioning

confidence: 99%

PGK1 is a Potential Survival Biomarker and Invasion Promoter by Regulating the HIF-1α–Mediated Epithelial-Mesenchymal Transition Process in Breast Cancer

Wei

et al. 2018

Cell Physiol Biochem

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Background/Aims: Glycolysis, a multi-step enzymatic reaction, is considered to be the root of cancer development and progression. The aim of this study is to figure out which glycolysis enzyme participates in the progression of breast cancer and its possible mechanisms. Materials: We firstly screened out PGK1 by performing an RT-PCR array of glycolysis-related genes in three paired breast cancer samples, and further investigated PGK1 using TCGA and our own database. The effect and mechanism of PGK1 on cell invasion was further explored both in vitro and using patient samples. Results: PGK1 was most upregulated in T3N0 with distant metastases compared to those with no metastases. In the TCGA database, high PGK1 expression predicted poor overall survival (OS) in breast cancer and some other cancers (P< 0.001). In the validation cohort, high PGK1 expression was significantly correlated with larger tumor size (P=0.011) and advanced TNM stage (P=0.033), and PGK1 expression was an independent prognostic factor for OS and disease free survival (DFS) in both univariate and multivariate regression analyses (P< 0.05). Functional studies indicated that knockdown of PGK1 expression significantly inhibited invasion and reversed the epithelial-mesenchymal transition process in breast cancer cells (P< 0.05). Mechanistically, PGK1 increased HRE luciferase activity in a dose-dependent manner, while silencing PGK1 expression decreased HRE activity. Conclusion: High PGK1 expression was associated with poor prognosis in breast cancer, because PGK1 and HIF-1α formed a positive feed-forward loop and thus stimulated breast cancer progression and metastases. Based on these results, PGK1 may serve as a promising biomarker and target therapy for breast cancer.

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Section: Patient Samplesmentioning

confidence: 99%

PGK1 is a Potential Survival Biomarker and Invasion Promoter by Regulating the HIF-1α–Mediated Epithelial-Mesenchymal Transition Process in Breast Cancer

Wei

et al. 2018

Cell Physiol Biochem

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“…Bioinformatics analysis speculated that miR-450b-3p might target Krüppel-like factor 7 (KLF7). KLF7, also referred to as ubiquitous Krüppel-like factor, is expressed at high levels in numerous human tissues [19,20]. In addition, KLF7 could effectively destroy the histological barrier that blocks tumor, and eventually cause tumor cells to detach from the primary site with complete structure to damage surrounding tissues [20].…”

Section: Introductionmentioning

confidence: 99%

“…KLF7, also referred to as ubiquitous Krüppel-like factor, is expressed at high levels in numerous human tissues [19,20]. In addition, KLF7 could effectively destroy the histological barrier that blocks tumor, and eventually cause tumor cells to detach from the primary site with complete structure to damage surrounding tissues [20]. Based on above, this study intended to investigate the biological function of miR-450b-3p in the malignant progression of GC, as well as analyze the correlations between the expression of miR-450b-3p and the clinical characteristics of GC patients.…”

Section: Introductionmentioning

confidence: 99%

miR-450b-3p inhibited the proliferation of gastric cancer via regulating KLF7

et al. 2020

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Background: This study aimed to investigate the clinical characteristics of miR-450b-3p in the patients of gastric cancer (GC), and further explore whether miR-450b-3p could inhibit the proliferation of GC cells via regulating KLF7. Methods:Real-time quantitative PCR (qRT-PCR) was performed to detect the expression level of miR-450b-3p in 48 GC patients of tumor tissue and paracancerous tissue specimens collected, and the associations between miR-450b-3p and the clinical characteristics of GC patients were analyzed. Meanwhile, the expression of miR-450b-3p in GC cell lines was verified using qRT-PCR. miR-450b-3p overexpression vectors was constructed in GC cell lines including AGS and BGC-823, and then CCK-8 cell proliferation assay, Plate colony formation assay and EdU assay were applied to analyze the biological function of miR-450b-3p in GC cell lines. Results:The results of qRT-PCR showed that the expression level of miR-450b-3p in GC tissues was lower than that in paracancerous tissues, and the difference was statistically significant. Compared with GC patients with high-miR-450b-3p expression, these GC patients with low-miR-450b-3p expression had a higher pathological stage and tumor size. Subsequently, the proliferation ability of GC cells in miR-450b-3p mimic was significantly decreased when comparing with the NC mimic. In addition, qRT-PCR indicated that the expression level of KLF7 significantly decreased after miR-450b-3p mimic. Therefore, it was demonstrated that miR-450b-3p might inhibit the malignant progression of GC via modulating KLF7. Bioinformatics analysis and dual luciferase reporter suggested miR-450b-3p was bound to KLF7. Finally, the results of the reverse experiment confirmed that overexpression of KLF7 could reverse miR-450b-3p mimic induced-inhibition of GC malignant progression. Conclusions:Generally, miR-450b-3p significantly down-regulated in GC tissues and cell lines, and was associated with the pathological stage and tumor size of GC patients. Meanwhile, miR-450b-3p inhibited cell proliferation in GC via modulating KLF7.

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“…KLF7 was also found to activate the TLR4/NF-kB/IL-6 pathway in adipocytes [96]. Finally, KLF7 has recently been also been found to be elevated in gastric cancers in patient samples in some populations and has been suggested to be a possible biomarker for the disease [97].…”

Section: Krüppel-like Factormentioning

confidence: 90%

Transcriptional and Epigenetic Regulation of Krüppel-Like Transcription Factors

Salmon¹

2020

Gene Expression and Phenotypic Traits

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Krüppel-like factors (KLFs) are a family of zinc finger transcription factors (ZF-TF) that are now known to be involved in complex biological processes including cancer, proliferation, and cardiovascular disease as well as developmental processes. KLFs first gained notoriety when it became known that they are crucial for promoting and maintenance of stem cell pluripotency. Over the past 20 years since the discovery of Krüppel-like factor 1 (KLF1), this transcription factor family has grown to include 18 members and 7 closely related members of the specificity protein 1 (Sp1) family. In the present study, we review the mechanisms related to regulation of KLFs by direct promoter activation or repression. We will also review and discuss some mechanisms of posttranslational modifications that could affect KLF function. We seek to understand how these transcriptional regulators are themselves regulated and how that regulation could become aberrant during various disease processes.

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Krüppel-Like Factor 7 is a Marker of Aggressive Gastric Cancer and Poor Prognosis

Cited by 34 publications

References 26 publications

PGK1 is a Potential Survival Biomarker and Invasion Promoter by Regulating the HIF-1α–Mediated Epithelial-Mesenchymal Transition Process in Breast Cancer

PGK1 is a Potential Survival Biomarker and Invasion Promoter by Regulating the HIF-1α–Mediated Epithelial-Mesenchymal Transition Process in Breast Cancer

miR-450b-3p inhibited the proliferation of gastric cancer via regulating KLF7

Transcriptional and Epigenetic Regulation of Krüppel-Like Transcription Factors

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