Role of EZH2 in the Growth of Prostate Cancer Stem Cells Isolated from LNCaP Cells

Li, Kuiqing; Liu, Cheng; Zhou, Bangfen; Bi, Liangkuan; Huang, Hai; Lin, Tianxin; Xu, Kecheng

doi:10.3390/ijms140611981

Cited by 46 publications

(36 citation statements)

References 35 publications

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“…This demonstrated that OCT4 has a close relationship with TNM staging, consistent with previously published research (Kregel et al, 2013). In addition, in line with a report by Li et al (2013), we also found that OCT4 expression rates of tissues at different degrees of differentiation were similar, suggesting that OCT4 expression has no close relationship with prostate cancer differentiation.…”

Section: Discussionsupporting

confidence: 92%

Expression and significance of S100P, CD147, and OCT4 in different prostate cancer tissue TNM stages

Wang¹,

Zhang²,

Wang³

2015

Genet. Mol. Res.

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ABSTRACT. The aim of this project was to investigate the expression and significance of S100P, CD147, and OCT4 in prostate cancer tissue at different TNM stages. We enrolled 54 patients with prostate cancer, 40 with benign prostatic hyperplasia, and 20 subjects with normal prostates. S100P, CD147, and OCT4 were detected by immunohistochemistry. The positive rate of S100P detection was 18.52% in prostate cancer tissues, significantly lower than in normal and benign prostate hyperplasia tissues (P ˂ 0.05). The positive expression rate of CD147 and OCT4 were 100 and 77.38% in prostate cancer tissue, respectively, both markedly higher than in normal and benign prostate hyperplasia tissue (P ˂ 0.05). The positive rate of S100P in stage V was 0, which was significantly lower than in stages I (37.50%) and II (35.71%) (P ˂ 0.05). OCT4 expression in stages III (86.67%) and V (94.12%) was higher than in stage I (37.50%). The positive rate of S100P in patients with distant metastasis was 4%, which was significantly lower than that in patients without metastases 6845 S100P, CD147, and OCT4 in prostate cancer ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 6844-6851 (2015) (P ˂ 0.05). In contrast, the positive rate of OCT4 in patients with distant metastasis was 92%. S100P, CD147, and OCT4 expression in prostate cancer patients with different degrees of differentiation had no significant difference (P > 0.05). Overall, our results demonstrated that S100P expression in prostate cancer tissue was significantly decreased, whereas CD147 and OCT4 expression was increased. Their expression levels were closely associated with TNM stage and distant metastasis, but were not related to the degree of differentiation.

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Section: Discussionsupporting

confidence: 92%

Expression and significance of S100P, CD147, and OCT4 in different prostate cancer tissue TNM stages

Wang¹,

Zhang²,

Wang³

2015

Genet. Mol. Res.

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“…The histone deacetylase EZH2 is highly expressed in NEPC, and its increased expression in clinically localized prostate tumors is associated with poorer prognosis [6, 37, 38]. In PC3, prostate cancer cells with high metastatic potential and neuroendocrine properties, as well as in LNCaP cells, which have lower metastatic potential, EZH2 was found to be upregulated selectively within the CD44 + /CD133 + population [39], and inducing its degradation using DZNep (both a S -adenosyl-homocysteine synthesis inhibitor, and a histone methyl-transferase EZH2 inhibitor), significantly diminished the number of tumor-initiating cells, as well as attenuated the growth of AR -/low DU145 cells [40]. Studies using patient-derived xenografts revealed that in NEPC, the AR promoter is enriched in silencing histone modifications such as H3K27me3 [41].…”

Section: Role Of Tumor Plasticity In Neuroendocrine Trans-differentiamentioning

confidence: 99%

EMT, stemness and tumor plasticity in aggressive variant neuroendocrine prostate cancers

Soundararajan

Paranjape

Maity

et al. 2018

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Neuroendocrine/Aggressive Variant Prostate Cancers are lethal variants of the disease, with an aggressive clinical course and very short responses to conventional therapy. The age-adjusted incidence rate for this tumor sub-type has steadily increased over the past 20 years in the United States, with no reduction in the associated mortality rate. The molecular networks fueling its emergence and sustenance are still obscure; however, many factors have been associated with the onset and progression of neuroendocrine differentiation in clinically typical adenocarcinomas including loss of androgen-receptor expression and/or signaling, conventional therapy, and dysregulated cytokine function. "Tumor-plasticity" and the ability to dedifferentiate into alternate cell lineages are central to this process. Epithelial-to-mesenchymal (EMT) signaling pathways are major promoters of stem-cell properties in prostate tumor cells. In this review, we examine the contributions of EMT-induced cellular-plasticity and stem-cell signaling pathways to the progression of Neuroendocrine/Aggressive Variant Prostate Cancers in the light of potential therapeutic opportunities.

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“…EZH2 is overexpressed in various cancers such as ovarian carcinoma [8] and prostate cancer [9] and it predicts poor prognosis, high tumor grade and high clinical stage [10]. Pre-clinical studies showed that EZH2 is able to silence several anti-metastatic genes (E-cadherin and tissue inhibitors of metalloproteinases), thereby favoring cell invasion and anchorage-independent growth [10].…”

Section: Ezh2 and Dznepmentioning

confidence: 99%

EZH2 as a Therapeutic Target in Glioblastoma: A Cellular and Molecular Study

Rosa¹,

Iraburu²,

Oller³

et al. 2016

J Carcinog Mutagen

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Glioblastoma is the most common malignant brain tumor in adults and it is currently treated with a combination of surgery, radiotherapy and chemotherapy with temozolomide (TMZ). Many patients show resistance to TMZ, which is a challenge in the treatment of this type of brain cancer. New strategies are being tested, like the inhibition of EZH2, a histone methyltransferase which is overexpressed in cancer cells, leading to angiogenesis and metastasis. In this work, the EZH2 inhibitor DZNeP was tested in A172 glioblastoma cells and in A172-TMZ-resistant glioblastoma cells. Inhibition of cell proliferation, adhesion, colony formation, and migration was noted in control and TMZresistant glioblastoma cells after DZNeP treatment. At the level of EZH2 target gene expression, DZNeP decreased EZH2 expression, and increased the expression of its target genes (E-cadherin and TIMP3), which might probably contribute to inhibiting the development of a cancer metastatic phenotype. Finally, DZNeP negatively regulated the TGFβ pathway. In conclusion, we propose that inhibition of EZH2 might be considered as a therapeutic strategy against glioblastoma.

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Role of EZH2 in the Growth of Prostate Cancer Stem Cells Isolated from LNCaP Cells

Cited by 46 publications

References 35 publications

Expression and significance of S100P, CD147, and OCT4 in different prostate cancer tissue TNM stages

Expression and significance of S100P, CD147, and OCT4 in different prostate cancer tissue TNM stages

EMT, stemness and tumor plasticity in aggressive variant neuroendocrine prostate cancers

EZH2 as a Therapeutic Target in Glioblastoma: A Cellular and Molecular Study

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