Increased Expression of Estrogen Receptor a-36 by Breast Cancer Oncogene IKKe Promotes Growth of ER-Negative Breast Cancer Cells

Li, Qihong; Sun, Haiyan; Zou, Jie; Cheng, Ge; Yu, Kaitao; Cao, Yuan; Qin, Hong

doi:10.1159/000350101

Cited by 10 publications

(6 citation statements)

References 25 publications

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“…It has been reported that wtERa functions as a tumor suppressor gene in some cancers including HCC [21]. Though the function of ERa36 in HCC has not yet been defined, it is known to promote the growth of other cancers such as breast cancer cells [27]. The fact that wtERa is reduced in HCC and wtERa functions as a tumor suppressor may well explained the failure of early trial of tamoxifen, as wtER antagonist, to treat HCC [6, 28].…”

Section: Discussionmentioning

confidence: 99%

Alternative splicing of estrogen receptor alpha in hepatocellular carcinoma

et al. 2016

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BackgroundThe role of estrogen receptor alpha (ERa), estrogen receptor beta (ERb) and ERa36 signaling in hepatocellular carcinoma (HCC) is not fully addressed.MethodsIn this study, three cohorts were included: (i) primary HCC patients (N = 76, cohort P), (ii) colorectal liver metastasis (mCRC) (N = 32, cohort S), and (iii) HCC from The Cancer Genome Atlas (TCGA) (N = 121). The levels of ERa36 and wtER36 were measured and their correlation with clinicopathologic features was determined.ResultsWtERa was downregulated and that ERa36 was upregulated in tumor tissues in both cohort P and TCGA data set. ERa36 was downregulated in tumor tissues in cohort S. In cohort P, wtERa was differentially expressed in gender (P < 0.000), age (P = 0.004), tumor number (P = 0.043), tumor size (P = 0.002), intrahepatic recurrence (P = 0.054). ERa36 was unequally expressed in different non-tumor liver status (P = 0.040). WtERa was negatively associated with overall survival (OS) and disease free survival (DFS) in cohort P. Compared with non-tumor tissues, the expression of ERa36 was increased in primary HCC but decreased in secondary HCC, showing opposite expression patterns of ERa36 between primary HCC and secondary HCC.ConclusionsPrimary HCC is associated with the decreased WtERa but increased ERa36. The expression pattern of ERa36 is different between primary HCC and secondary HCC, as the former with the increased ERa36 but the latter with the decreased ERa36. Therefore, the expression of ERa36 may be used to differentiate the primary HCC and the secondary one.

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Section: Discussionmentioning

confidence: 99%

Alternative splicing of estrogen receptor alpha in hepatocellular carcinoma

et al. 2016

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“…Triple-negative breast cancers (TNBCs) are a heterogeneous set of tumors defined by an absence of actionable therapeutic targets (ER, PR, and HER-2) [36,37]. TNBCs are generally associated with an aggressive clinical course and where targeted therapies are currently limited [38].…”

Section: Discussionmentioning

confidence: 99%

Comparative Profiling of Triple-Negative Breast Carcinomas Tissue Glycoproteome by Sequential Purification of Glycoproteins and Stable Isotope Labeling

Chen

Huang

et al. 2016

Cell Physiol Biochem

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Background: Women with triple negative breast cancers (TNBCs) have a poor prognosis due to lack of suitable targeted therapies. Changes in the protein glycosylation are increasingly being recognized as an important modification associated with cancer etiology. Methods: In an attempt to identify TNBC biomarkers with greater diagnostic and prognostic capabilities, hydrazide- based chemistry method combined with LC-MS/MS were used to purify and identify N-linked glycopeptides or glycoproteins of tissues from TNBC patients. Results: A total of 550 unique N-linked glycoproteins were identified, among these proteins, 72 unique N-linked glycoproteins were significantly regulated in tumor tissues, of which 56 proteins were upregulated and 16 proteins were downregulated. To assess the validity of the results, three selected proteins including Vascular endothelial growth factor receptor 1, Insulin receptor, Tissue factor pathway inhibitor were selected for western blot analysis, and these proteins were found as potential biomarkers of TNBC. The top three pathways of differentially expressed glycoproteins participated in were caveolar-mediated endocytosis signaling, agrin interactions at neuromuscular junction and LXR/RXR activation. Conclusion: This work provides potential glycoprotein markers to function as a novel tissue-based biomarker for TNBC.

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“…[42] The identification of novel molecules that can inhibit IKKε is currently underway as a means to inflammatory processes associated with cancer progression. [47] Moreover, if DADS can reduce IKKε, this could also prevent events downstream to IKKε over expression such as activation of p52 NF-κB dimers [48], [49] estrogen receptor ERα activation, upregulation of cyclin D1 and chemotherapy resistance in breast cancer cells in particular to tamoxifen [50]. In the current study we were focused on IKKi/IKKε because it plays an important role in TNFα signaling.…”

Section: Discussionmentioning

confidence: 99%

Diallyl disulfide inhibits TNFα induced CCL2 release through MAPK/ERK and NF-Kappa-B signaling

et al. 2015

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TNFα receptors are constitutively overexpressed in tumor cells, correlating to sustain elevated NFκB and monocyte chemotactic protein-1 (MCP-1/CCL2) expression. The elevation of CCL2 evokes aggressive forms of malignant tumors marked by tumor associated macrophage (TAM) recruitment, cell proliferation, invasion and angiogenesis. Previously, we have shown that the organo-sulfur compound diallyl disulfide (DADS) found in garlic (Allium sativum) attenuates TNFα induced CCL2 production in MDA-MB-231 cells. In the current study, we explored the signaling pathways responsible for DADS suppressive effect on TNFα mediated CCL2 release using PCR Arrays, RT-PCR and western blots. The data in this study show that TNFα initiates a rise in NFκB mRNA, which is not reversed by DADS. However, TNFα induced heightened expression of IKKε and phosphorylated ERK. The expression of these proteins corresponds to increased CCL2 release that can be attenuated by DADS. CCL2 induction by TNFα was also lessened by inhibitors of p38 (SB202190) and MEK (U0126) but not JNK (SP 600125), all of which were suppressed by DADS. In conclusion, the obtained results indicate that DADS down regulates TNFα invoked CCL2 production primarily through reduction of IKKε and phosphorylated-ERK, thereby impairing MAPK/ERK, and NFκB pathway signaling. Future research will be required to evaluate the effects of DADS on the function and expression of TNFα surface receptors.

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Increased Expression of Estrogen Receptor a-36 by Breast Cancer Oncogene IKKe Promotes Growth of ER-Negative Breast Cancer Cells

Cited by 10 publications

References 25 publications

Alternative splicing of estrogen receptor alpha in hepatocellular carcinoma

Alternative splicing of estrogen receptor alpha in hepatocellular carcinoma

Comparative Profiling of Triple-Negative Breast Carcinomas Tissue Glycoproteome by Sequential Purification of Glycoproteins and Stable Isotope Labeling

Diallyl disulfide inhibits TNFα induced CCL2 release through MAPK/ERK and NF-Kappa-B signaling

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