NANOG gene expression is regulated by the ETS transcription factor ETV4 in human embryonic carcinoma NCCIT cells

Park, Sung-Won; Do, Hyun-Jin; Choi, Wonbin; Song, Hyuk; Chung, Hak-Jae; Kim, Jaehwan

doi:10.1016/j.bbrc.2017.04.059

Cited by 9 publications

(6 citation statements)

References 45 publications

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“…Another Ets protein, Pea3/ETV4, was shown to regulate Nanog and Oct4 expression in pluripotent NCCIT embryonic carcinoma cells [37,38]. Interestingly, members of the Pea3 subfamily of ETS proteins, ETV4 and ETV5, were found to be expressed in undifferentiated ES cells, and suppression of Oct3/4 was found to result in downregulation of their expression, and ETV4 and ETV5 were found to be important for proliferation of undifferentiated ES cells through regulation of stem cell-related genes such as Tcf15, Gbx2, and Zic3 [39].…”

Section: Discussionmentioning

confidence: 99%

ETS-Domain Transcription Factor Elk-1 Regulates Stemness Genes in Brain Tumors and CD133+ BrainTumor-Initiating Cells

Söğüt

Venugopal

Kandemir

et al. 2021

JPM

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Elk-1, a member of the ternary complex factors (TCFs) within the ETS (E26 transformation-specific) domain superfamily, is a transcription factor implicated in neuroprotection, neurodegeneration, and brain tumor proliferation. Except for known targets, c-fos and egr-1, few targets of Elk-1 have been identified. Interestingly, SMN, SOD1, and PSEN1 promoters were shown to be regulated by Elk-1. On the other hand, Elk-1 was shown to regulate the CD133 gene, which is highly expressed in brain-tumor-initiating cells (BTICs) and used as a marker for separating this cancer stem cell population. In this study, we have carried out microarray analysis in SH-SY5Y cells overexpressing Elk-1-VP16, which has revealed a large number of genes significantly regulated by Elk-1 that function in nervous system development, embryonic development, pluripotency, apoptosis, survival, and proliferation. Among these, we have shown that genes related to pluripotency, such as Sox2, Nanog, and Oct4, were indeed regulated by Elk-1, and in the context of brain tumors, we further showed that Elk-1 overexpression in CD133+ BTIC population results in the upregulation of these genes. When Elk-1 expression is silenced, the expression of these stemness genes is decreased. We propose that Elk-1 is a transcription factor upstream of these genes, regulating the self-renewal of CD133+ BTICs.

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Section: Discussionmentioning

confidence: 99%

ETS-Domain Transcription Factor Elk-1 Regulates Stemness Genes in Brain Tumors and CD133+ BrainTumor-Initiating Cells

Söğüt

Venugopal

Kandemir

et al. 2021

JPM

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“…17 In addition, Nanog plays a crucial role in maintaining the stemness of cancer cells, such as self-renewal, recurrence and high tumorigenicity in various cancers. 18 Previous researches have reported that inhibition of Nanog functions was capable of suppressing cancer cell growth and inducing cancer cell apoptosis. 19 Thus, Nanog gene has been developed as a potential cancer target for genesilencing therapy.…”

Section: Introductionmentioning

confidence: 99%

Novel functionalized nanoparticles for tumor-targeting co-delivery of doxorubicin and siRNA to enhance cancer therapy

Xia

Wang

et al. 2017

IJN

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Human homeobox protein (Nanog) is highly expressed in most cancer cells and has gradually emerged as an excellent target in cancer therapy, owing to its regulation of cancer cell proliferation, metastasis and apoptosis. In this study, we prepared tumor-targeting functionalized selenium nanoparticles (RGDfC-SeNPs) to load chemotherapeutic doxorubicin (DOX) and Nanog siRNA. Herein, RGDfC peptide was used as a tumor-targeting moiety which could specifically bind to α v β 3 integrins overexpressed on various cancer cells. The sizes of RGDfC-SeNPs@DOX nanoparticles (~12 nm) were confirmed by both dynamic light scattering and transmission electron microscopy. The chemical structure of RGDfC-SeNPs@DOX was characterized via Fourier-transform infrared spectroscopy. The RGDfC-SeNPs@DOX was compacted with siRNA (anti-Nanog) by electrostatic interaction to fabricate the RGDfC-SeNPs@DOX/siRNA complex. The RGDfC-SeNPs@DOX/siRNA complex nanoparticles could efficiently enter into HepG2 cells via clathrin-associated endocytosis, and showed high gene transfection efficiency that resulted in enhanced gene silencing. The in vivo biodistribution experiment indicated that RGDfC-SeNPs@DOX/siRNA nanoparticles were capable of specifically accumulating in the tumor site. Furthermore, treatment with RGDfC-SeNPs@DOX/siRNA resulted in a more significant anticancer activity than the free DOX, RGDfC-SeNPs@DOX or RGDfC-SeNPs/siRNA in vitro and in vivo. In summary, this study shows a novel type of DOX and siRNA co-delivery system, thereby providing an alternative route for cancer treatment.

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“… 77 In embryonic carcinoma NCCIT cells, the pluripotency factor NANOG gene can be activated by ETV4 at the transcriptional level in a dose-dependent manner. 78 These results indicate that ETV4 has a tumor-promoting effect on some gynecological cancers, including ovarian cancer and endometrial cancer.…”

Section: Gynecological Cancersmentioning

confidence: 76%

E26 transformation-specific variant 4 as a tumor promotor in human cancers through specific molecular mechanisms

Jiang

Chen

et al. 2021

Molecular Therapy - Oncolytics

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E26 transformation-specific (ETS) variant 4 (ETV4) is an important transcription factor that belongs to the ETS transcription factor family and is essential for much cellular physiology. Recent evidence has revealed that ETV4 is aberrantly expressed in many types of tumors, and its overexpression is related to poor prognosis of cancer patients. Additionally, increasing studies have identified that ETV4 promotes cancer growth, invasion, metastasis, and drug resistance. Mechanistically, the level of ETV4 is regulated by some post-translation modulations in a broad spectrum of cancers. However, little progress has been made to comprehensively summarize the critical roles of ETV4 in different human cancers. Hence, this review mainly focuses on the physiological functions of ETV4 in various human tumors. In addition, the molecular mechanisms of ETV4-mediated cancer progression were elucidated, including how ETV4 modulates its downstream signaling pathways and how ETV4 is regulated by some factors. On this basis, the present review may provide a valuable therapeutics strategy for future cancer treatment by targeting ETV4-related pathways.

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NANOG gene expression is regulated by the ETS transcription factor ETV4 in human embryonic carcinoma NCCIT cells

Cited by 9 publications

References 45 publications

ETS-Domain Transcription Factor Elk-1 Regulates Stemness Genes in Brain Tumors and CD133+ BrainTumor-Initiating Cells

ETS-Domain Transcription Factor Elk-1 Regulates Stemness Genes in Brain Tumors and CD133+ BrainTumor-Initiating Cells

Novel functionalized nanoparticles for tumor-targeting co-delivery of doxorubicin and siRNA to enhance cancer therapy

E26 transformation-specific variant 4 as a tumor promotor in human cancers through specific molecular mechanisms

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