Mutations and Krüppel-like factor 6 (KLF6) expression levels in breast cancer

Özdemir, Filiz; Koksal, Mehtap Gulcihan Cinar; Özmen, Vahit; Aydın, İbrahim; Buyru, Nur

doi:10.1007/s13277-014-1678-6

Cited by 16 publications

(17 citation statements)

References 40 publications

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“…KLF6 is a member of the KLF family that consists of four exons and encodes a nuclear core promoter element-binding protein [32]. KLF6 is a tumor suppressor based on its inactivation and somatic mutations in a variety of cancers such as prostate [20], gastric [21], ovarian [24], breast [27], liver [25,26], and colorectal cancer [22,23]. KLF6 ’s growth-suppressive activity is linked to p53-independent transactivation of p21 [20] and inhibition of the Cyclin D1/CDK4 complex [28].…”

Section: Discussionmentioning

confidence: 99%

“…In addition to gastric cancer [21], functional inactivation of KLF6 was observed in a number of other human cancers including prostate [20], colorectal [22,23], ovarian [24], liver [25,26], and breast cancer [27]. With different cell types and contexts, KLF6 exhibits growth inhibition activity through several major cancer pathways such as p53-independent up-regulation of p21 [20], disruption of Cyclin D1 and CDK4 interaction [28] and induction of apoptosis [23].…”

Section: Introductionmentioning

confidence: 99%

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The Growth of SGC-7901 Tumor Xenografts Was Suppressed by Chinese Bayberry Anthocyanin Extract through Upregulating KLF6 Gene Expression

et al. 2016

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To investigate the antitumor effect of anthocyanins extracted from Chinese bayberry fruit (Myrica rubra Sieb. et Zucc.), a nude mouse tumor xenograft model was established. Treatments with C3G (cyanidin-3-glucoside, an anthocyanin) significantly suppressed the growth of SGC-7901 tumor xenografts in a dose-dependent manner. Immunohistochemical staining showed a significant increase in p21 expression, indicating that the cell cycle of tumor xenografts was inhibited. qPCR screening showed that C3G treatment up-regulated the expression of the KLF6 gene, which is an important tumor suppressor gene inactivated in many human cancers. Western blot showed that C3G treatments markedly increased KLF6 and p21 protein levels, inhibited CDK4 and Cyclin D1 expression, but did not notably change the expression of p53. These results indicated that KLF6 up-regulates p21 in a p53-independent manner and significantly reduces tumor proliferation. This study provides important information for the possible mechanism of C3G-induced antitumor activity against gastric adenocarcinoma in vivo.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Growth of SGC-7901 Tumor Xenografts Was Suppressed by Chinese Bayberry Anthocyanin Extract through Upregulating KLF6 Gene Expression

et al. 2016

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“…It actually breaks the function of kinase dependent on cyclin D1 and causes the cell cycle to stop in the G1 stage. Furthermore, KLF6 acts as an inhibitor of cell proliferation against C-Jun oncoprotein [53,54]. Down-regulation of KLF6 may contribute to the development of solid human cancers, and inactivating it may result in the development of colorectal cancer as a primary or common occurrence.…”

Section: Epigenetic and Cancermentioning

confidence: 99%

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer

Babaei¹,

Khaksar²,

Zeinali³

et al. 2019

BioMedicine

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Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.

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“…In this study, CPBP, NF‐AT1, and miR‐30c‐5p were located in the central hub of our TF–miRNA–gene network, highlighting their importance in esophageal carcinoma. As a tumor suppressor downregulated and frequently mutated in various cancers, CPBP can increase the transcription of genes with specific promoters approximately fourfold . KLF6‐SV1, an oncogenic splice variant of CPBP, is implicated as a key driver of cancer metastasis and is a potential target for treatment .…”

Section: Discussionmentioning

confidence: 99%

Landscape of expression profiles in esophageal carcinoma by The Cancer Genome Atlas data

Zhan

Wang

et al. 2015

Dis Esophagus

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In this study, we explored the gene and microRNA (miRNA) expressions profile of esophageal carcinoma. The expression data for messenger RNAs and miRNAs in normal and cancerous esophageal tissues were obtained from the Cancer Genome Atlas database and then the differentially expressed genes and miRNAs were identified. As a result, we identified 2962 genes and 45 miRNAs differentially expressed in esophageal carcinoma compared with normal esophageal tissues. Subsequently, the altered gene functions and signaling pathways were investigated using gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, and these differentially expressed genes were significantly enriched in the cell cycle, cell migration, mitogen-activated protein kinase (MAPK) and toll-like receptor signaling pathway, and so on. Then the regulatory relationships between the differentially expressed miRNAs and genes were examined with Targetscan and Miranda, and the potential target sites of transcription factors (TFs) in the promoter regions of these miRNAs and genes were identified using the TRANSFAC database. Finally the TF-miRNA-gene network in esophageal cancer was established, summarizing the regulatory links among the TFs, differentially expressed miRNAs and differentially expressed genes. Factors such as core promoter-binding protein (CPBP), nuclear factor of activated T-cells 1 (NFAT-1), miR-30c-5p, were located in the central hub of this network, highlighting their vital roles in esophageal tumorigenesis. These findings may extend our understanding of the molecular mechanisms underlying esophageal carcinoma and promote new perspectives for prevention, diagnosis and treatment.

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Mutations and Krüppel-like factor 6 (KLF6) expression levels in breast cancer

Cited by 16 publications

References 40 publications

The Growth of SGC-7901 Tumor Xenografts Was Suppressed by Chinese Bayberry Anthocyanin Extract through Upregulating KLF6 Gene Expression

The Growth of SGC-7901 Tumor Xenografts Was Suppressed by Chinese Bayberry Anthocyanin Extract through Upregulating KLF6 Gene Expression

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer

Landscape of expression profiles in esophageal carcinoma by The Cancer Genome Atlas data

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