&lt;p&gt;Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion&lt;/p&gt;

Wu, Rongting; Yun, Qiang; Zhang, Jianping; Bao, Jingang

doi:10.2147/ott.s188270

Cited by 16 publications

(16 citation statements)

References 37 publications

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“…Nevertheless, the role of miR-125-5p and its mechanism of action in osteosarcoma via zinc-finger transcription factor, Kruppel-like factor 13 (KLF13) are elusive. KLF13 is known for its tumor promotive role and has been shown to affect cell differentiation, proliferation, cell cycle and apoptosis (Wu et al 2019). The present study showed that miR-125 has sufficient downregulation in osteosarcoma and directly targets KLF13 to regulate the growth and viability of osteosarcoma cells.…”

Section: Introductionsupporting

confidence: 53%

MicroRNA-125-5p targets Kruppel-like factor 13 (KLF13) to regulate the proliferation, migration, and invasion of human osteosarcoma cells*

Yang

Jin

et al. 2021

All Life

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Section: Introductionsupporting

confidence: 53%

MicroRNA-125-5p targets Kruppel-like factor 13 (KLF13) to regulate the proliferation, migration, and invasion of human osteosarcoma cells*

Yang

Jin

et al. 2021

All Life

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“…DNMT1, along with DNMT2, DNMT3A, DNMT3B, and DNMT3L, belongs to DNA methyl transferase family, which regulate target gene expression by the CpG island methylation (Wu et al, 2019). Aberrant methylation, particularly in the promoter regions of tumor suppressor genes, inhibits gene expression and can facilitate human tumorigenesis (Zhou et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

LncRNA NEAT1 Interacted With DNMT1 to Regulate Malignant Phenotype of Cancer Cell and Cytotoxic T Cell Infiltration via Epigenetic Inhibition of p53, cGAS, and STING in Lung Cancer

Lei

Ding

et al. 2020

Front. Genet.

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Purpose: Lung cancer is the main cause of cancer-related mortality worldwide. We report here the biological role of nuclear paraspeckle assembly transcript 1 (NEAT1) in the pathogenesis of lung cancer and the underlying mechanisms. Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting analysis were used to evaluate expression of mRNA and protein. RNA immunoprecipitation (RIP) assay, chromatin immunoprecipitation followed by qPCR analysis, and reporter assay were used to detect DNA/RNA and protein binding. Tumorinfiltrating lymphocytes were assessed with hematoxylin-eosin staining. Cytotoxic T cell infiltration was evaluated with flow cytometric analysis and immunohistochemistry (IHC) staining. The changes of cell viability and cell invasive and migratory ability were analyzed by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), colony formation, and Transwell assays, respectively. Syngeneic tumor model was set up to evaluate antitumor effect. Results: The results showed that NEAT1 was overexpressed in lung cancer tissues and cancer cell lines. This aberrant expression was closely related with tumor stage and lymph node metastasis. Tumor sample with high CD8 + showed lower NEAT1 expression. In vitro studies displayed that inhibition of NEAT1 with shRNA resulted in suppression of survival and migration/invasion of lung cancer cells. On the other side, NEAT1 was found to promote tumor growth via inhibiting cytotoxic T cell immunity in syngeneic models. Finally, NEAT1 was found to interact with DNMT1, which in turn inhibited P53 and cyclic GMP-AMP synthase stimulator of interferon genes (cGAS/STING) expression. Conclusion: Our findings demonstrated that NEAT1 interacted with DNMT1 to regulate cytotoxic T cell infiltration in lung cancer via inhibition of cGAS/STING pathway. The results provided the novel mechanistic insight into the pathogenesis of lung cancer.

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“…30 DNMT1-mediated KLF13 epigenetic silencing plays a role in regulating glioma cell proliferation and invasion, and the upregulation of KLF13 may be found to be a new treatment. 31 However, the exact function of KLF13 in HCC remains to be explored. Here, we found that KLF13 was a tumor promoter in HCC.…”

Section: Discussionmentioning

confidence: 99%

Krüppel-like Factor 13 Promotes HCC Progression by Transcriptional Regulation of HMGCS1-mediated Cholesterol Synthesis

Chen¹,

Xie²,

Zhao³

et al. 2022

J Clin Transl Hepatol

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Background and Aims: Krüppel-like factor (KLF) has a role in the occurrence, development and metabolism of cancer. We aimed to explore the role and potential molecular mechanism of KLF13 in the growth and migration of liver cancer cells. Methods: The expression of KLF13 in hepatocellular carcinoma (HCC) tissues was higher than that in normal tissues according to analysis of The Cancer Genome Atlas (TCGA) database. Lentiviral plasmids were used for overexpression and plasmid knockdown of KLF13. Real-time quantitative polymerase chain reaction (qPCR) and western blotting were used to detect mRNA and protein expression in HCC tissues and cells. Cell counting kit-8 (CCK-8), colony formation, cell migration and invasion, and flow cytometry assays were used to assess the in vitro function of KLF13 in HCC cells. The effect of KLF13 on xenograft tumor growth in vivo was evaluated. The cholesterol content of HCC cells was determined by an indicator kit. A dual-luciferase reporter assay and chromatin immunoprecipitation sequencing (ChIPseq) revealed the binding relationship between KLF13 and HMGCS1. Results: The expression of KLF13 was upregulated in HCC tissues and TCGA database. KLF13 knockdown inhibited the proliferation, migration and invasion of HepG2 and Huh7 cells and increased the apoptosis of Huh7 cells. The opposite effects were observed with the overexpression of KLF13 in SK-Hep1 and MHCC-97H cells. The overexpression of KLF13 promoted the growth of HCC in nude mice and KLF13 transcription promoted the expression of HMGCS1 and the biosynthesis of cholesterol. KLF13 knockdown inhibited cholesterol biosynthesis mediated by HMGCS1 and inhibited the growth and metastasis of HCC cells. Conclusions: KLF13 acted as a tumor promoter in HCC by positively regulating HMGCS1-mediated cholesterol biosynthesis.

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<p>Downregulation of KLF13 through DNMT1-mediated hypermethylation promotes glioma cell proliferation and invasion</p>

Cited by 16 publications

References 37 publications

MicroRNA-125-5p targets Kruppel-like factor 13 (KLF13) to regulate the proliferation, migration, and invasion of human osteosarcoma cells*

MicroRNA-125-5p targets Kruppel-like factor 13 (KLF13) to regulate the proliferation, migration, and invasion of human osteosarcoma cells*

LncRNA NEAT1 Interacted With DNMT1 to Regulate Malignant Phenotype of Cancer Cell and Cytotoxic T Cell Infiltration via Epigenetic Inhibition of p53, cGAS, and STING in Lung Cancer

Krüppel-like Factor 13 Promotes HCC Progression by Transcriptional Regulation of HMGCS1-mediated Cholesterol Synthesis

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