Differential expression of the klf6 tumor suppressor gene upon cell damaging treatments in cancer cells

Gehrau, Ricardo C.; D’Astolfo, Diego S.; Andreoli, Verónica; Bocco, José Luis; Koritschoner, Nicolás P.

doi:10.1016/j.mrfmmm.2010.12.002

Cited by 10 publications

(14 citation statements)

References 37 publications

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“…KLF6, a zinc finger transcription factor, is frequently downregulated in several types of human cancer, including lung (29), ovarian (30), prostate (31), glioma (32) and colorectal cancer (33). Previous studies have demonstrated that KLF6 contributes to the regulation of various biological processes, including cell proliferation, apoptosis, differentiation, invasion and metastasis (34,35). In GC, the expression level of KLF6 is decreased in tumor tissues compared with normal gastric mucosa (18).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑18b acts as an oncogene in gastric cancer by directly targeting Kruppel‑like factor 6

et al. 2019

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑18b acts as an oncogene in gastric cancer by directly targeting Kruppel‑like factor 6

et al. 2019

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“…Following cell loss or death, activation of cell proliferation and regeneration, combined with attenuation of growth suppressor activity within remnant liver tissue restores liver cell mass. Downregulation of KLF6, a tumor suppressor gene that inhibits proliferation through induction of p21 and in synergy with p53 8 , 10 , 12 has been observed in primary liver tumors and is associated with a worse outcome in cancer 1 , 11 , 33 . Following PHx in mice, hepatocyte-specific deletion of Klf6 accelerates cell proliferation at early time points after resection.…”

Section: Discussionmentioning

confidence: 99%

“…Krüppel-like factor 6 (KLF6) is a ubiquitously expressed zinc finger transcription factor, which contributes to cell proliferation, differentiation, cell death and signal transduction 1 . Hepatocyte expression of KLF6 regulates hepatic fatty acid and glucose metabolism via transcriptional activation of liver glucokinase and posttranscriptional regulation of the nuclear receptor peroxisome proliferator activated receptor alpha (PPARα) 2 , 3 .…”

Section: Introductionmentioning

confidence: 99%

Krüppel-like factor 6 is a transcriptional activator of autophagy in acute liver injury

Sydor

Manka

Best

et al. 2017

Sci Rep

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Krüppel-like factor 6 (KLF6) is a transcription factor and tumor suppressor. We previously identified KLF6 as mediator of hepatocyte glucose and lipid homeostasis. The loss or reduction of KLF6 is linked to the progression of hepatocellular carcinoma, but its contribution to liver regeneration and repair in acute liver injury are lacking so far. Here we explore the role of KLF6 in acute liver injury models in mice, and in patients with acute liver failure (ALF). KLF6 was induced in hepatocytes in ALF, and in both acetaminophen (APAP)- and carbon tetrachloride (CCl4)-treated mice. In mice with hepatocyte-specific Klf6 knockout (DeltaKlf6), cell proliferation following partial hepatectomy (PHx) was increased compared to controls. Interestingly, key autophagic markers and mediators LC3-II, Atg7 and Beclin1 were reduced in DeltaKlf6 mice livers. Using luciferase assay and ChIP, KLF6 was established as a direct transcriptional activator of ATG7 and BECLIN1, but was dependent on the presence of p53. Here we show, that KLF6 expression is induced in ALF and in the regenerating liver, where it activates autophagy by transcriptional induction of ATG7 and BECLIN1 in a p53-dependent manner. These findings couple the activity of an important growth inhibitor in liver to the induction of autophagy in hepatocytes.

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“…Thus, it is valuable to further explore the effect of KLF6 overexpression on xenograft tumor growth in vivo. The mean volume of tumors in the experimental mice before treatment was 57.23 ± 22.75 mm 3 . During the whole tumor growth period, the tumor growth activity was measured.…”

Section: The Effect Of Klf6 On Xenograft Tumor Growthmentioning

confidence: 99%

Kruppel-like factor 6 suppresses growth and invasion of hepatocellular carcinoma cells in vitro and in vivo

Wang

Zhang

Wang

et al. 2016

Int J Immunopathol Pharmacol

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Kruppel-like factor 6 (KLF6) as a novel tumor suppressive gene participates in multiple biological behaviors and plays an important role in regulating tumor cell growth and invasion. However, the functions of KLF6 in hepatocellular carcinoma (HCC) remain poorly understood. The expression level of KLF6 was examined by immunohistochemical assay in human HCC tissues, and KLF6-overexpressed HCC cells (SMCC-7721 and HepG2) were used for evaluating cell proliferation and invasion by MTT and Transwell assays. A subcutaneous HCC tumor model was established for assessing tumor growth in vivo. Our results showed that the expression of KLF6 was significantly downregulated in HCC tissues compared with the adjacent non-cancerous tissues (50.0% vs. 72.0%, P = 0.034) and negatively associated with the lymph-vascular space invasion (LVSI) in HCC patients (P = 0.003). Furthermore, overexpression of KLF6 reduced cell proliferation and weakened the cell invasive potential followed with the decreased expression of PCNA and MMP-9 in HCC cells. The in vivo experiment indicated that KLF6 overexpression suppressed the xenograft tumor growth. Therefore, our findings show that KLF6 suppresses growth and invasion of HCC cells in vitro and in vivo, suggesting a tumor suppressive function in HCC and provides the potential therapeutic target for the treatment of HCC.

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Differential expression of the klf6 tumor suppressor gene upon cell damaging treatments in cancer cells

Cited by 10 publications

References 37 publications

MicroRNA‑18b acts as an oncogene in gastric cancer by directly targeting Kruppel‑like factor 6

MicroRNA‑18b acts as an oncogene in gastric cancer by directly targeting Kruppel‑like factor 6

Krüppel-like factor 6 is a transcriptional activator of autophagy in acute liver injury

Kruppel-like factor 6 suppresses growth and invasion of hepatocellular carcinoma cells in vitro and in vivo

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