Nuclear estrogen receptor-mediated Notch signaling and GPR30-mediated PI3K/AKT signaling in the regulation of endometrial cancer cell proliferation

Ye, Wei; Zhang, Zhenbo; Liao, Hong; Wu, Ling; Wu, Xiaomei; Zhou, Dongmei; Xi, Xiaowei; Zhu, Yue; Feng, Yi

doi:10.3892/or.2011.1536

Cited by 35 publications

(24 citation statements)

References 24 publications

(29 reference statements)

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“…The combination of ligand and receptor activated Notch signaling and receptor was cleaved into NICD by γ-secreatase. NICD interacted with HES1 or other signaling such as Ras and PI3K/Akt and played an oncogenic role in ovarian cancer [20, 21]. Notch pathway cannot be triggered as carcinogenesis without the combination of ligand and Notch receptor.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of gamma-secretase in Notch1 signaling pathway as a novel treatment for ovarian cancer

Feng

Zhang

et al. 2016

Oncotarget

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Epithelial ovarian cancer (EOC) is the leading cause of death for gynecological cancer. Most patients are not diagnosed until the cancer is at an advanced stage with poor prognosis. Notch1 signaling pathway plays an oncogenic role in EOC. There have been few studies on enzymatic activity of γ-secretase and the mechanism of how γ-secretase inhibitor works on cancer cell. Here, we show that Jagged1 and NICD were highly expressed in ovarian carcinoma. The expressions of Notch1, Jagged1 and NICD in Notch1 pathway did not correlate with outcome in ovarian cancer. The enzymatic activity of γ-secretase in ovarian cancer cell lines SKOV3, CAOV3 and ES2 is significantly higher than in normal ovarian epithelial cell line T29. DAPT (a γ-secretase inhibitor) reduced the enzymatic activity of γ-secretase, inhibited the proliferation, and increased the apoptosis in ovarian cancer cell lines. Hence, γ-secretase inhibitor may become a highly promising novel therapeutic strategy against ovarian cancer in the field of precision medicine.

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Section: Discussionmentioning

confidence: 99%

Inhibition of gamma-secretase in Notch1 signaling pathway as a novel treatment for ovarian cancer

Feng

Zhang

et al. 2016

Oncotarget

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“…Western blotting was performed as previously described [57]. Briefly, 60 μg protein was separated by SDS-PAGE and transferred to a polyvinylidene fluoride membrane.…”

Section: Methodsmentioning

confidence: 99%

LSD1 binds to HPV16 E7 and promotes the epithelial-mesenchymal transition in cervical cancer by demethylating histones at the Vimentin promoter

et al. 2016

Self Cite

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Lysine-specific demethylase 1 (LSD1), which specifically demethylates histone H3 lysine 4 (H3K4) and lysine 9 (H3K9), is dysregulated in several cancers. We found that ectopic expression of LSD1 in cervical cancer cells promoted invasion and metastasis in vitro and in vivo, reduced the expression of the epithelial marker E-cadherin, and induced the expression of the mesenchymal marker, Vimentin. By contrast, LSD1 knockdown had the opposite effect and attenuated the HPV16 E7-induced epithelial-mesenchymal transition (EMT). We proposed a novel mechanism, whereby LSD1 is recruited to the Vimentin promoter and demethylates H3K4me1 and H3K4me2. Notably, HPV16 E7 enhanced the expression of LSD1, formed a complex with LSD1, and suppressed LSD1 demethylase activity by hindering the recruitment of LSD1 to the Vimentin promoter. Thus, LSD1 is a primary and positive regulator of the HPV16 E7-induced EMT and an attractive therapeutic target for alleviating HPV16 E7-induced EMT and tumor metastasis.

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“…In addition to E2, TAM as well as its metabolite, 4-OH-TAM, have also high-affinity binding to GPER and can activate the receptor [104,105,106,107], thus inducing rapid cellular signaling, including ERK activation, PI3K activation, calcium mobilization and cAMP production in breast cancer cells [98,105] (Figure 5). …”

Section: Tam Resistancementioning

confidence: 99%

Tamoxifen Resistance: Emerging Molecular Targets

Rondón-Lagos

Villegas

Rangel

et al. 2016

IJMS

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17β-Estradiol (E2) plays a pivotal role in the development and progression of breast cancer. As a result, blockade of the E2 signal through either tamoxifen (TAM) or aromatase inhibitors is an important therapeutic strategy to treat or prevent estrogen receptor (ER) positive breast cancer. However, resistance to TAM is the major obstacle in endocrine therapy. This resistance occurs either de novo or is acquired after an initial beneficial response. The underlying mechanisms for TAM resistance are probably multifactorial and remain largely unknown. Considering that breast cancer is a very heterogeneous disease and patients respond differently to treatment, the molecular analysis of TAM’s biological activity could provide the necessary framework to understand the complex effects of this drug in target cells. Moreover, this could explain, at least in part, the development of resistance and indicate an optimal therapeutic option. This review highlights the implications of TAM in breast cancer as well as the role of receptors/signal pathways recently suggested to be involved in the development of TAM resistance. G protein—coupled estrogen receptor, Androgen Receptor and Hedgehog signaling pathways are emerging as novel therapeutic targets and prognostic indicators for breast cancer, based on their ability to mediate estrogenic signaling in ERα-positive or -negative breast cancer.

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Nuclear estrogen receptor-mediated Notch signaling and GPR30-mediated PI3K/AKT signaling in the regulation of endometrial cancer cell proliferation

Abstract: Abstract.To elucidate the mechanisms of nuclear estrogen receptor (ER)-mediated and G protein-coupled receptor 30

Cited by 35 publications

References 24 publications

Inhibition of gamma-secretase in Notch1 signaling pathway as a novel treatment for ovarian cancer

Inhibition of gamma-secretase in Notch1 signaling pathway as a novel treatment for ovarian cancer

LSD1 binds to HPV16 E7 and promotes the epithelial-mesenchymal transition in cervical cancer by demethylating histones at the Vimentin promoter

Tamoxifen Resistance: Emerging Molecular Targets

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