The role of NANOG transcriptional factor in the development of malignant phenotype of cancer cells

Gawlik-Rzemieniewska, Natalia; Bednarek, Ilona

doi:10.1080/15384047.2015.1121348

Cited by 111 publications

(79 citation statements)

References 70 publications

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“…Reportedly, Nanog is an example of a gene induced by Tet1 expression. Not only does Nanog have a role in the maintenance of mouse ES cells (20), but also in the maintenance of cancer stem cells, suppression of apoptosis, promotion of cancer progression and metastasis, and angiogenesis (21). These findings suggest that PTEN deficiency drives TET1 and TET1-gene regulation during carcinogenesis; however, the underlying reasons for an increase in the TET1 expression in PTEN deficiency remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Generation of PTEN‑knockout (‑/‑) murine prostate cancer cells using the CRISPR/Cas9 system and comprehensive gene expression profiling

et al. 2018

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Phosphatase and tensin homolog (PTEN) deficiency is associated with development, progression, and metastasis of various cancers. However, changes in gene expression associated with PTEN deficiency have not been fully characterized. To explore genes with altered expression in PTEN‑deficient cells, the present study generated a PTEN‑knockout cell line (ΔPTEN) from a mouse prostate cancer‑derived cell line using the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR‑associated protein 9 (CRISPR/Cas9) gene editing system. Following transfection of the CRISPR/Cas9 construct, DNA sequencing was performed to identify deletion of the Pten locus and PTEN inactivation was verified by western blotting. The ΔPTEN cell line exhibited enhanced RAC‑alpha serine/threonine‑protein kinase phosphorylation and cyclin D1 expression. In addition, an increase in cell proliferation and colony formation was observed in the ΔPTEN cell line. Gene expression profiling experiments were analyzed with microarray and microRNA (miRNA) arrays. In the microarray analysis, 111 genes exhibited ≥10‑fold increased expression compared with the parent strain and mock cell line and 23 genes were downregulated. The only miRNA with increased expression of 10‑fold or more was mmu‑miR‑210‑3p. Genes with enhanced expression included genes involved in the development, progression, and metastasis of cancer such as Tet methylcytosine dioxygenase 1, twist family BHLH transcription factor 2, C‑fos‑induced growth factor and Wingless‑Type MMTV Integration Site Family, Member 3, and genes involved in immunosuppression such as Arginase 1. The results of the present study suggest that PTEN deficiency mobilizes a variety of genes critical for cancer cell survival and host immune evasion.

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Section: Discussionmentioning

confidence: 99%

Generation of PTEN‑knockout (‑/‑) murine prostate cancer cells using the CRISPR/Cas9 system and comprehensive gene expression profiling

et al. 2018

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“…The results of agar colony formation rate assay showed that the supernatants of 1-2F monoclonal cells with different dilution ratios reduced the rate of HUSSLCs agar colony formation in concentration-dependent manner, indicating that 1-2F monoclonal antibodies can inhibit anchorage-independent growth of HUSSLCs and has tumorigenic effect. ABCG2 overexpression contributes to and maintains multidrug resistance of tumor stem cells [35][36][37][38] ; Abnormal expression of Bmi1 contributes to and maintains the self-renewal, unrestricted proliferation and multidrug resistance properties [39][40][41][42] of tumor stem cells; Nanog abnormal expression and functional effect of self-renewal and unrestricted proliferation [43][44][45][46]…”

Section: Discussionmentioning

confidence: 99%

Study on Functional Monoclonal Antibodies of Anti-Human Uterine Sarcoma Stem Cell-Like Cells

Cai

Gao

Zhang

et al. 2020

Preprint

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Background: To establish a functional monoclonal antibody library using Human Uterine Sarcoma Stem Cell-Like Cells (HUSSLCs) to screen and identify functional monoclonal antibodies that can recognize and inhibit HUSSLCs. Methods: B lymphocytes in proliferative state were prepared by using the second generation CD133+spheroid cells of SK-UT-1 cell line, i.e. HUSSLCs, as antigens; Spheroid formation, agar colony formation, wound healing, flow cytometry, and Western blotting were adopted to detect the effect of monoclonal antibodies with varied dilution ratios on HUSSLCs spheroid formation, agar colony formation, cell migration, CD133 expression, and expression of CD44, ABCG2, Bmi1, Nanog, Oct4 and ALDH1. Results: Myeloma cells of SP2/0 cell line can achieve 85% degrees of fusion and results of 1-2F monoclonal cell supernatants with different dilution ratios reduced HUSSLCs spheroid formation rate, agar colony formation rate, cell migration rate, CD133 positive cell expression and protein expression levels of CD44, ABCG2, Bmi1, Nanog, Oct4, and ALDH1 in concentration-dependent manner (P <0.05). Conclusion: The antibody valence produced by HUSSLCs-immunized mice reached the requirement for preparation of monoclonal antibody. Anti-HUSSLCs monoclonal antibodies feature functions of inhibiting the self-renewal, unrestricted proliferation, migration, invasion and multidrug resistance of HUSSLCs and functions characterized by tumor stem cells. Key words: uterine leiomyosarcoma; tumor stem cell; monoclonal antibody; self-renewal ability; infinite multiplication; drug resistance

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“…Given it is a transcription factor and one that has been shown to be adequate to reprogrammed induced pluripotent cells, it is not surprising that NANOG has a role in tumorigenesis across different cancers [15]. STAT3 seems to be an important downstream effector of NANOG overexpression in cancer cells [12,16].…”

Section: Discussionmentioning

confidence: 99%

NANOG regulates epithelial–mesenchymal transition and chemoresistance in ovarian cancer

Qin

Cao

et al. 2017

Bioscience Reports

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A key transcription factor associated with poor prognosis and resistance to chemotherapy in ovarian cancer is NANOG. However, the mechanism by which NANOG functions remains undefined. It has been suggested that epithelial-to-mesenchymal transition (EMT) also contributes to development of drug resistance in different cancers. We thus determined whether NANOG expression was associated with EMT and chemoresistance in epithelial ovarian cancer cells. NANOG expression was increased in epithelial ovarian cancer cell lines compared with its expression in normal epithelial ovarian cell lines. NANOG expression in SKOV-3 or OV2008 cells directly correlated with high expression of mesenchymal cell markers and inversely with low expression of epithelial cell marker. RNAi-mediated silencing of NANOG in SKOV-3 reversed the expression of mesenchymal cell markers and restored expression of E-cadherin. Reversibly, stable overexpression of NANOG in Moody cells increased expression of N-cadherin whereas down-regulating expression of E-cadherin, cumulatively indicating that NANOG plays an important role in maintaining the mesenchymal cell markers. Modulating NANOG expression did not have any effect on proliferation or colony formation. Susceptibility to cisplatin increased in SKOV-3 cells on down-regulating NANOG and reversible results were obtained in Moody cells post-overexpression of NANOG. NANOG silencing in SKOV-3 and OV2008 robustly attenuated in vitro migration and invasion. NANOG expression exhibited a biphasic pattern in patients with ovarian cancer and expression was directly correlated to chemoresistance retrospectively. Cumulatively, our data demonstrate that NANOG expression modulates chemosensitivity and EMT resistance in ovarian cancer.

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The role of NANOG transcriptional factor in the development of malignant phenotype of cancer cells

Cited by 111 publications

References 70 publications

Generation of PTEN‑knockout (‑/‑) murine prostate cancer cells using the CRISPR/Cas9 system and comprehensive gene expression profiling

Generation of PTEN‑knockout (‑/‑) murine prostate cancer cells using the CRISPR/Cas9 system and comprehensive gene expression profiling

Study on Functional Monoclonal Antibodies of Anti-Human Uterine Sarcoma Stem Cell-Like Cells

NANOG regulates epithelial–mesenchymal transition and chemoresistance in ovarian cancer

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