Krüppel-like factor 4 mediates lysophosphatidic acid-stimulated migration and proliferation of PC3M prostate cancer cells

Shin, Sang Hun; Kwon, Yang Woo; Heo, Soon Chul; Jeong, Geun Ok; Kim, Ba Reun; Seo, Eun Jin; Kim, Jae Ho

doi:10.1038/emm.2014.34

Cited by 21 publications

(20 citation statements)

References 36 publications

(51 reference statements)

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“…Moreover, KLF4 expression is markedly down-regulated in colon cancer, and the loss of KLF4 can serve as an independent predictor of its recurrence and survival [38]. However, KLF4 reportedly acts as an oncogene in melanoma and prostate cancer [39, 40]. The dual function of KLF4 in cancer biological behavior may shift depending on tumor type, tumor stage, and research approach.…”

Section: Discussionmentioning

confidence: 99%

Krüppel-Like Factor 4 Inhibits Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis by Down-Regulating Caveolin-1 Expression

Zhu

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Krüppel-like factor 4 (KLF4), a member of the KLF family of zinc finger transcription factors, has been identified as a tumor suppressor gene in a variety of tumors. However, the molecular mechanisms by which KLF4 inhibits epithelial-to-mesenchymal transition (EMT) and metastasis in pancreatic cancer remain unclear. Methods: KLF4 expression in pancreatic cancer was analyzed using public datasets (Oncomine and The Cancer Genome Atlas). The expression of KLF4, caveolin-1 (Cav-1), E-cadherin, and vimentin, and their correlations with clinicopathological characteristics were evaluated by immunohistochemistry in pancreatic cancer tissues. The biological functions and underlying mechanisms of KLF4 expression on EMT and metastasis were also investigated in vitro and in vivo. Results: Public datasets showed that KLF4 expression was significantly decreased in pancreatic cancer and correlated with the depth of invasion and disease stage. The expression of KLF4, Cav-1, E-cadherin, and vimentin protein in pancreatic cancer tissues was closely associated with pathological grade, disease stage, and metastasis. KLF4 expression was also positively correlated with E-cadherin expression and negatively correlated with vimentin expression, whereas Cav-1 expression was negatively associated with E-cadherin expression and positively correlated with vimentin expression. Knockdown of KLF4 expression promoted EMT and facilitated pancreatic cancer cell growth and metastasis in vitro and in vivo. In addition, immunohistochemistry (IHC) results indicated that KLF4 expression was negatively correlated with Cav-1 expression. Furthermore, down-regulating KLF4 expression increased Cav-1 and vimentin expression and decreased E-cadherin expression. Mechanistically, KLF4 could transcriptionally inhibit Cav-1 expression by binding directly to the promoter domain of Cav-1. Conclusions: KLF4 inhibits pancreatic cancer EMT and metastasis by down-regulating Cav-1 expression, suggesting that the KLF4/Cav-1 signaling pathway may be a novel diagnostic and therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Krüppel-Like Factor 4 Inhibits Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis by Down-Regulating Caveolin-1 Expression

Zhu

Wang

et al. 2018

Cell Physiol Biochem

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“…As several reports have shown, ZNF750 interacts with KLF4 to induce differentiation genes [14,25,26] . KLF4 is a member of the Krüppel-type zinc finger transcription factor family [27][28][29] . Ma et al [30] reported that expression of KLF4 was negatively correlated with lymph node metastasis and stage of progression in ESCC cases.…”

Section: Discussionmentioning

confidence: 99%

ZNF750 Expression as a Novel Candidate Biomarker of Chemoradiosensitivity in Esophageal Squamous Cell Carcinoma

et al. 2017

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Objective: ZNF750, an epidermal differentiation regulator, has been suggested to act as a tumor suppressor of esophageal squamous cell carcinoma (ESCC). Although a correlation between the epidermal differentiation gene and resistance to chemoradiotherapy (CRT) has been posited, no data regarding the ZNF750 status in ESCC have been reported. The aim of the present study was to evaluate the relationship between ZNF750 expression and response to CRT in ESCC. Methods: Eighty-seven patients who had been pathologically diagnosed with ESCC were evaluated in the present study. All patients underwent neoadjuvant CRT, followed by curative esophagectomy. The expression of ZNF750 in pretreatment biopsy samples was immunohistochemically investigated and compared to the histopathological effectiveness of CRT in surgical specimens. Results: High expression of ZNF750 was closely correlated with good sensitivity to CRT (p = 0.016). A univariate analysis showed that high/intermediate expression of ZNF750 was a significant predictive factor for good sensitivity to CRT (p = 0.006). High/intermediate expression of ZNF750 (30% or more) remained an independent predictive factor for sensitivity to CRT in a multivariate analysis (p = 0.033). Conclusions: ZNF750 expression predicts sensitivity to CRT and can be a biomarker that reliably predicts the response of ESCC to CRT.

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“…For example, LINC00673 is overexpressed in both hepatocellular carcinoma and tongue squamous cell carcinoma (TSCC) and also associated with poor prognoses of these carcinomas. 12 DNA methylation is closely linked to numerous human cancers and KLF4, as readers of DNA methylation specific to sequence, also requires methylated cytosine-phosphate-guanine (CpG). 9 KLF4 belongs to the KLFs class of transcriptional mediators which can bind to DNA and are widely expressed in human cancers serving as oncogenes or tumour suppressors.…”

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confidence: 99%

Long non‐coding RNA LINC00673 silencing inhibits proliferation and drug resistance of prostate cancer cells via decreasing KLF4 promoter methylation

Jiang

Zhang

Chen

et al. 2019

J Cellular Molecular Medi

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| INTRODUC TI ONAs a non-skin tumour accompanied by variable natural history, prostate cancer is a highly prevalent malignancy and represents one of the leading causes of cancer-related deaths in the male populace. 1,2 Risk factors responsible for prostate cancer comprise smoking, alcohol consumption and levels of male androgens. 3 Paclitaxel is widely regarded as an essential important drug for prostate cancer treatment; however, paclitaxel resistance ensues in many prostate cancer patients, which highlights the significance of developing strategies AbstractProstate cancer is one of the major causes of cancer-related mortality in men across the world. Recently, long non-coding RNAs (lncRNAs) and Kruppel-like factor 4 (KLF4) have been reported to participate in the biology of multiple cancers including prostate cancer. Here, this study aimed to explore the possible role of LINC00673 in prostate cancer via KLF4 gene promoter methylation. Microarray-based gene expression profiling of prostate cancer was employed to identify differentially expressed lncRNAs and genes, after which the expression of LINC00673 and KLF4 in prostate cancer tissues was determined using RT-qPCR. Next, the relationship between LINC00673 and KLF4 was evaluated using in silico analysis. Further, the effect of LINC00673 and KLF4 on cell proliferation and drug resistance of transfected cells was examined with gain-and loss-of-function experimentation. It was found that LINC00673 was highly expressed, while KLF4 was poorly expressed in prostate cancer tissues. Additionally, LINC00673 could bind to KLF4 gene promoter region and recruit methyltransferase to the KLF4 gene promoter region. Moreover, LINC00673silencing was demonstrated to reduce methylation of the KLF4 gene promoter to elevate the expression of KLF4, thus suppressing the proliferation and drug resistance of prostate cancer cells. In summary, LINC00673 silencing could drive demethylation of the KLF4 gene promoter and thus inhibit the proliferation and drug resistance of prostate cancer cells, suggesting that silencing of LINC00673 and elevation of KLF4 could serve as tumour suppressors in prostate cancer.

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Krüppel-like factor 4 mediates lysophosphatidic acid-stimulated migration and proliferation of PC3M prostate cancer cells

Cited by 21 publications

References 36 publications

Krüppel-Like Factor 4 Inhibits Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis by Down-Regulating Caveolin-1 Expression

Krüppel-Like Factor 4 Inhibits Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis by Down-Regulating Caveolin-1 Expression

ZNF750 Expression as a Novel Candidate Biomarker of Chemoradiosensitivity in Esophageal Squamous Cell Carcinoma

Long non‐coding RNA LINC00673 silencing inhibits proliferation and drug resistance of prostate cancer cells via decreasing KLF4 promoter methylation

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