&lt;p&gt;Estrogen Receptor Beta Inhibits The Proliferation, Migration, And Angiogenesis Of Gastric Cancer Cells Through Inhibiting Nuclear Factor-Kappa B Signaling&lt;/p&gt;

Zhang, Yiping; Wu, Yahua; Zhou, Xinchun; Yi, Benyi; Wang, Lili

doi:10.2147/ott.s214529

Cited by 3 publications

(2 citation statements)

References 33 publications

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“…Previous studies have shown that ERβ can suppress canonical NFκB/p65 signaling in various cell and tissue types, however the mechanism(s) remains unclear and these effects have not been studied in TNBC 48 – 52 . Mechanistically, we provide evidence that ERβ does not alter the upstream signaling pathways required for p65 activation, nor does it impact p65 phosphorylation or nuclear localization.…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB/p65 signaling in triple negative breast cancer

et al. 2022

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Triple Negative Breast Cancer (TNBC) accounts for 15–20% of all breast cancer cases, yet is responsible for a disproportionately high percentage of breast cancer mortalities. Thus, there is an urgent need to identify novel biomarkers and therapeutic targets based on the molecular events driving TNBC pathobiology. Estrogen receptor beta (ERβ) is known to elicit anti-cancer effects in TNBC, however its mechanisms of action remain elusive. Here, we report the expression profiles of ERβ and its association with clinicopathological features and patient outcomes in the largest cohort of TNBC to date. In this cohort, ERβ was expressed in approximately 18% of TNBCs, and expression of ERβ was associated with favorable clinicopathological features, but correlated with different overall survival outcomes according to menopausal status. Mechanistically, ERβ formed a co-repressor complex involving enhancer of zeste homologue 2/polycomb repressive complex 2 (EZH2/PRC2) that functioned to suppress oncogenic NFκB/RELA (p65) activity. Importantly, p65 was shown to be required for formation of this complex and for ERβ-mediated suppression of TNBC. Our findings indicate that ERβ+ tumors exhibit different characteristics compared to ERβ− tumors and demonstrate that ERβ functions as a molecular switch for EZH2, repurposing it for tumor suppressive activities and repression of oncogenic p65 signaling.

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Section: Discussionmentioning

confidence: 99%

Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB/p65 signaling in triple negative breast cancer

et al. 2022

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“…Endothelial cell migration plays important roles in angiogenesis, wound healing, and endothelial injury healing. 45,51,52 Therefore, we studied the effects of OGD/R and apelin-13 on endothelial cell migration. In the early stage of reperfusion (R16 h and R24 h), OGD/R decreased the migration capacity of cells, suggesting that reperfusion injury prevents migration by endothelial cells at the early stage.…”

Section: Discussionmentioning

confidence: 99%

Apelin-13 prevents the effects of oxygen–glucose deprivation/reperfusion on bEnd.3 cells by inhibiting AKT–mTOR signaling

Zhang

Cheng

et al. 2022

Exp Biol Med (Maywood)

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Autophagy plays works by degrading misfolded proteins and dysfunctional organelles and maintains intracellular homeostasis. Apelin-13 has been investigated as an agent that might protect the blood–brain barrier (BBB) from cerebral ischemia/reperfusion (I/R) injury. In this study, we examined whether apelin-13 protects cerebral microvascular endothelial cells, important components of the BBB, from I/R injury by regulating autophagy. To mimic I/R injury, the mouse cerebral microvascular endothelia l cell line bEnd 3 undergoes the process of oxygen and glucose deprivation and re feeding in the process of culture. Cell viability was detected using a commercial kit, and cell migration was monitored by in vitro scratch assay. The tight junction (TJ) proteins ZO-1 and occludin; the autophagy markers LC3 II, beclin 1, and p62; and components of the AKT–mTOR signaling pathway were detected by Western blotting and immunofluorescence. To confirm the role of autophagy in OGD/R and the protective effect of apelin-13, we treated the cells with 3-methyladenine (3-MA), a pharmacological inhibitor of autophagy. Our results demonstrated that OGD/R increased autophagic activity but decreased viability, abundance of TJs, and migration. Viability and TJ abundance were further reduced when the OGD/R group was treated with 3-MA. These results indicated that bEnd.3 upregulates autophagy to ameliorate the effects of OGD/R injury on viability and TJs, but that the autophagy induced by OGD/R alone is not sufficient to protect against the effect on cell migration. Treatment of OGD/R samples with apelin-13 markedly increased viability, TJ abundance, and migration, as well as autophagic activity, whereas 3-MA inhibited this increase, suggesting that apelin-13 exerted its protective effects by upregulating autophagy.

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Missing link between tissue specific expressing pattern of ERβ and the clinical manifestations in LGBLEL

Zhang

Zhao

et al. 2023

Front. Med.

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PurposeLacrimal gland benign lymphoepithelial lesion (LGBLEL) is an IgG4-related disease of unknown etiology with a risk for malignant transformation. Estrogen is considered to be related to LGBLEL onset.MethodsSeventy-eight LGBLEL and 13 control clinical samples were collected and studied to determine the relationship between estrogen and its receptors and LGBLEL development.ResultsThe serological analysis revealed no significant differences in the levels of three estrogens be-tween the LGBLEL and control groups. However, immunohistochemical analyses indicated that the expression levels of ERβ and its downstream receptor RERG were relatively lower in LGBLEL samples than in control samples, with higher expression in the lacrimal gland and lower expression in the lymphocyte infiltration region. However, low expression of ERα was detected. The transcriptome sequence analysis revealed upregulated genes associated with LGBLEL enriched in lymphocyte proliferation and activation function; downregulated genes were enriched in epithelial and vascular proliferation functions. The key genes and gene networks were further analyzed. Interactions between B cells and epithelial cells were analyzed due to the identified involvement of leukocyte subsets and epithelial cells. B cell proliferation was found to potentially contribute to lacrimal gland apoptosis.ConclusionTherefore, the tissue-heterogeneous expression pattern of ERβ is potentially related to the clinical manifestations and progression of LGBLEL, although further investigations are required to confirm this finding.

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<p>Estrogen Receptor Beta Inhibits The Proliferation, Migration, And Angiogenesis Of Gastric Cancer Cells Through Inhibiting Nuclear Factor-Kappa B Signaling</p>

Cited by 3 publications

References 33 publications

Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB/p65 signaling in triple negative breast cancer

Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB/p65 signaling in triple negative breast cancer

Apelin-13 prevents the effects of oxygen–glucose deprivation/reperfusion on bEnd.3 cells by inhibiting AKT–mTOR signaling

Missing link between tissue specific expressing pattern of ERβ and the clinical manifestations in LGBLEL

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