KLF11 promotes gastric cancer invasion and migration by increasing Twist1 expression

Ji, Qiang; Li, Y; Zhao, Qun; Fan, Li; Tan, Bibo; Zhang, Z D; Zhao, Xiwa; Liu, Y; Wang, D; Nan, Jun

doi:10.4149/neo_2018_180325n201

Cited by 18 publications

(8 citation statements)

References 33 publications

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“…This is in line with our oncogenic phenotype of Cbt in fly gut. Similarly, high KLF11 expression has been associated with gastric and breast cancers (92,93). How these connections might play out in terms of cell cycle control is an interesting topic for future studies.…”

Section: Discussionmentioning

confidence: 99%

The Krüppel-like factor Cabut has cell cycle regulatory properties similar to E2F1

Zhang

Katzaroff

Buttitta

et al. 2021

Proc. Natl. Acad. Sci. U.S.A.

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Using a gain-of-function screen in Drosophila, we identified the Krüppel-like factor Cabut (Cbt) as a positive regulator of cell cycle gene expression and cell proliferation. Enforced cbt expression is sufficient to induce an extra cell division in the differentiating fly wing or eye, and also promotes intestinal stem cell divisions in the adult gut. Although inappropriate cell proliferation also results from forced expression of the E2f1 transcription factor or its target, Cyclin E, Cbt does not increase E2F1 or Cyclin E activity. Instead, Cbt regulates a large set of E2F1 target genes independently of E2F1, and our data suggest that Cbt acts via distinct binding sites in target gene promoters. Although Cbt was not required for cell proliferation during wing or eye development, Cbt is required for normal intestinal stem cell divisions in the midgut, which expresses E2F1 at relatively low levels. The E2F1-like functions of Cbt identify a distinct mechanism for cell cycle regulation that may be important in certain normal cell cycles, or in cells that cycle inappropriately, such as cancer cells.

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Section: Discussionmentioning

confidence: 99%

The Krüppel-like factor Cabut has cell cycle regulatory properties similar to E2F1

Zhang

Katzaroff

Buttitta

et al. 2021

Proc. Natl. Acad. Sci. U.S.A.

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“…KLF10 and KLF11 were originally introduced as transcriptional repressors, however several studies have shown that they can also function as transcriptional activators depending on the cellular context 23 . It has been described for example that KLF11 promotes invasion and migration in gastric cancer through activation of Twist1 24 .…”

Section: Discussionmentioning

confidence: 99%

Genome-wide aberrant methylation in primary metastatic UM and their matched metastases

Smit

Boers

Vaarwater

et al. 2022

Sci Rep

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Uveal melanoma (UM) is an aggressive intra-ocular cancer with a strong tendency to metastasize. Metastatic UM is associated with mutations in BAP1 and SF3B1, however only little is known about the epigenetic modifications that arise in metastatic UM. In this study we aim to unravel epigenetic changes contributing to UM metastasis using a new genome-wide methylation analysis technique that covers over 50% of all CpG’s. We identified aberrant methylation contributing to BAP1 and SF3B1-mediated UM metastasis. The methylation data was integrated with expression data and surveyed in matched UM metastases from the liver, skin and bone. UM metastases showed no commonly shared novel epigenetic modifications, implying that epigenetic changes contributing to metastatic spreading and colonization in distant tissues occur early in the development of UM and epigenetic changes that occur after metastasis are mainly patient-specific. Our findings reveal a plethora of epigenetic modifications in metastatic UM and its metastases, which could subsequently result in aberrant repression or activation of many tumor-related genes. This observation points towards additional layers of complexity at the level of gene expression regulation, which may explain the low mutational burden of UM.

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“…Although KLF11 expression is decreased in colon, kidney, lung, ovary, and pancreas cancers, 11 it is increased in gastric and breast cancers. 3 , 6 In the present study, we collected data from 116 glioma patients to detect KLF11 expression by IHC assay. KLF11 expression was increased in glioma tissues.…”

Section: Discussionmentioning

confidence: 99%

“… 4 Previous studies have shown that KLF11 can act as an oncogene in breast cancer, 3 but other studies demonstrated that KLF11 can play the role of a tumor suppressor gene in pancreatic, renal, lung, and gastric cancer. 5 , 6 There have been no reports about KLF11 in gliomas, so it is very interesting and important to clarify the role of KLF11 in glioma tissues. The purpose of this article is to determine whether KLF11 expression in glioma tissues is related to patient survival.…”

Section: Introductionmentioning

confidence: 99%

KLF11 Expression Predicts Poor Prognosis in Glioma Patients

Xi¹,

Zhang²,

Zhang³

et al. 2021

IJGM

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Purpose Glioma is a primary intracranial malignant tumor with high recurrence and mortality rates. It is very important to study the prognostic factors. KLF11 can function as an oncogene or a tumor suppressor, depending on the tumor and tissue types and the cancer stage. In this study, we aimed to determine whether KLF11 expression is related to the overall survival of glioma patients. Patients and Methods We investigated KLF11 expression in 116 glioma patients with different grades using Western blot and immunohistochemistry assay. We analyzed the patients with different glioma grades and KLF11 expression levels by Kaplan–Meier survival curves. Independent prognostic factors for poor overall survival were identified by univariate and multivariate analyses. Results There were 37 patients in KLF11 low expression group and 79 patients in high expression group. There was no difference in gender, age, tumor diameter or tumor location between two groups. The patients in KLF11 high expression group had higher ECOG score ( P =0.025) and higher WHO grades ( P =0.029). Western blot and immunohistochemistry assay showed KLF11 expression was significantly upregulated in glioma groups compared with normal brain tissues group ( P < 0.05), and the expression in grades III–IV was significantly higher than those in grades I–II ( P < 0.05). Kaplan–Meier survival curve analysis showed high KLF11 expression tended to reduce the overall survival ( P < 0.05). After univariate and multivariate analyses, KLF11 expression ( P =0.003) and age ( P =0.007) were independent prognostic factors for poor survival in glioma patients. Conclusion KLF11 expression was increased in glioma tissues, and high KLF11 expression was associated with poor prognosis. KLF11 expression was an independent prognostic factor for poor survival in glioma patients. KLF11 may serve as a novel prognostic marker for gliomas and as a novel treatment target.

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KLF11 promotes gastric cancer invasion and migration by increasing Twist1 expression

Cited by 18 publications

References 33 publications

The Krüppel-like factor Cabut has cell cycle regulatory properties similar to E2F1

The Krüppel-like factor Cabut has cell cycle regulatory properties similar to E2F1

Genome-wide aberrant methylation in primary metastatic UM and their matched metastases

KLF11 Expression Predicts Poor Prognosis in Glioma Patients

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