HER2 drives Mucin-like 1 to control proliferation in breast cancer cells

Conley, R. Scott; Bosco, Emily E.; Tice, David A.; Hollingsworth, Robert E.; Herbst, Roy S.; Zhang, Xiao

doi:10.1038/onc.2015.487

Cited by 37 publications

(36 citation statements)

References 23 publications

(25 reference statements)

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“…In accordance with our results, it was previously shown that human monocyte-derived DC increased expression of Cyp24a1 in response to vitamin D3 [24]. Mucl1 has previously been identified as breast cancer-specific gene whose product Mucin-like protein 1 controls proliferation in breast cancer cells [25]. The protein is present intracellularly or secreted from the cancer cells.…”

Section: Comparison Of the Selected Gene Expression In DC Obtained Frsupporting

confidence: 92%

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Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats

et al. 2019

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List of abbreviations AO -Albino Oxford; CDcluster of differentiation; CNS -central nervous system; DA -Dark Agouti; DCdendritic cells; EAE -experimental autoimmune encephalomyelitis; FCS -fetal calf serum; GM-CSF -granulocyte-macrophage colony-stimulating factor; iDCimmature DC; IFN -interferon; IL -interleukin; LNC -lymph node cells; LPSlipopolysaccharide; mDCmature DC; PBS -phosphate buffer saline; SD -standard deviation; Th -T helper; TNFtumor necrosis factor; tolDCtolerogenic DC. 4 Abstract Dendritic cells (DC) are responsible for the initiation and shaping of the adaptive immune response and are in the focus of autoimmunity research. We were interested in comparison of DC obtained from autoimmunity-prone Dark Agouti (DA) rats and autoimmunity-resistant Albino Oxford (AO) rats. DC were generated from bone marrow precursors and matured (mDC) by lipopolysaccharide. Tolerogenic DC (tolDC) obtained by vitamin D3 treatment were studied in parallel. Profile of cytokine production was different in AO and DA mDC and tolDC. Expression of MHC class II molecules and CD86 were higher in DA DC, while vitamin D3 reduced their expression in dendritic cells of both strains. Allogeneic proliferation of CD4 + T cells was reduced by AO tolDC, but not with DA tolDC in comparison to respective mDC. Finally, expression of various genes identified as differentially expressed in human mDC and tolDC was also analyzed in AO and DA DC. Again, AO and DA DC differed in the expression of the analyzed genes. To conclude, AO and DA DC differ in production of cytokines, expression of antigen presentation-related molecules and in regulation of CD4 + T proliferation. The difference is valuable for understanding the divergence of the strains in their susceptibility to autoimmunity.

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Section: Comparison Of the Selected Gene Expression In DC Obtained Frsupporting

confidence: 92%

“…The protein is present intracellularly or secreted from the cancer cells. FAK/JNK pathway was identified as the downstream effector of MUCL1 signaling [25]. High expression of MUCL1 in human and rat tolDC implies that this protein might play an important role in tolerogenic activity of DC.…”

Section: Comparison Of the Selected Gene Expression In DC Obtained Frmentioning

confidence: 99%

Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats

et al. 2019

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“…BC has been recognized to be immunogenic, which has involved multiple putative tumor-associated antigens (TAAs), such as HER-2 and Mucin 1 (MUC1) [30,31]. Note worthily, these TAAs have been treated as the targets for developing new cancer vaccine and bispeci c antibody (bsAbs) over the past decade, among which, some have been translated into tumor-speci c immune responses and have been veri ed to be clinically bene cial [32].…”

Section: Discussionmentioning

confidence: 99%

Immune-related Gene Data-based Molecular Subtyping Related to the Prognosis for Breast Cancer Patients

et al. 2020

Preprint

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Background Breast cancer (BC), the most frequently seen malignant tumor in female, is associated with increasing morbidity and mortality year by year. Generally, the available treatments for BC include surgery, chemotherapy, radiotherapy, endocrinotherapy and molecular targeted therapy. Typically, as molecular biology, immunology and pharmacogenomics develop, a growing amount of evidence has suggested that immunocyte infiltration into tumor microenvironment, together with the immunophenotype of tumor cells, would remarkably influence the development and malignant transformation of tumor; as a result, immunotherapy has become a promising therapy for treating BC, which would also affect patient prognosis.Methods In this study, samples collected from TCGA and ImmPort database would be analyzed to search for specific immune-related genes affecting BC patient prognosis. A total of 64 immune-related genes with significant correlation with patient prognosis had been screened and performed shrinkage estimate, among which, 29 most representative ones with significant correlation with patient prognosis had been selected and utilized to establish the prognosis prediction model for BC patients (as referred to as the RiskScore equation). Thereafter, samples in both training set and test set would be substituted into the model, respectively; meanwhile, BC patients would also be divided based on the median RiskScore to assess the efficiency, accuracy and stability of the model in predicting and classifying patient prognosis. Subsequently, functional annotations, GO and KEGG signaling pathway enrichment analysis would be carried out among the 29 as-screened immune-related genes.Results The results found that, these 29 genes could be mainly enriched to numerous BC- and immune microenvironment-related pathways. Eventually, the relationship between RiskScore and the sample clinical features as well as the signaling pathways would be analyzed.Conclusions Our findings indicate that, the prognosis prediction model RiskScore established on the basis of the expression profiles of 29 immune-related genes has displayed high prediction accuracy and stability in identifying the immune features, which can guide the clinicians to diagnose and predict the prognosis for different immunophenotypes, in the meantime of offering numerous therapeutic targets for precisely treating BC in clinic using the identified subtype-specific immune molecules.

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“…In addition, various autoantibodies against membranous and serum proteins, which are easily bound by autoAbs, are frequent in sarcoidosis patient sera. These antibodies (autoAbs against tumor necrosis factor receptor superfamily member 14 (TNFRSF14) [57], growth differentiation factor 10 {GDF10 (BMP3)} [58], mucin-like protein 1 (MUCL1) [59], ring finger and SPRY domain containing 1 (RSPRY1) [60], RRAD and GEM like GTPase 1 (REM1) [61], and gametocyte-specific factor 1-like (GTSF1L) may be modulators of the disease course. These results suggest that autoAbs reflect the ongoing pathophysiology of the disease itself.…”

Section: Sarcoidosismentioning

confidence: 99%

Natural Autoantibodies in Chronic Pulmonary Diseases

Fukushima

Tsujino

Futami

et al. 2020

IJMS

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In autoantibody-mediated autoimmune diseases, pathogenic autoantibodies generated by a failure of central or peripheral tolerance, have different effects mediated by a variety of mechanisms. Interestingly, even non-autoimmune chronic diseases have a set of disease-specific natural autoantibodies that are maintained for a long time. Because most of these natural autoantibodies target intracellular proteins or long non-coding RNAs, they are speculated to be non-pathological and have some important as yet unrecognized physiological functions such as debris clearance. Recently, we revealed a set of disease-specific natural autoantibodies of chronic pulmonary diseases with unknown etiology by protein arrays that enable detection of specific autoantibodies against >8000 targets. Surprisingly, some of the targeted antigens of disease-specific autoantibodies were subsequently reported by other laboratories as strongly associated with the disease, suggesting that these antigens reflect the pathology of each disease. Furthermore, some of these autoantibodies that target extracellular antigens might modify the original course of each disease. Here, we review the disease-specific natural autoantibodies of chronic pulmonary diseases, including chronic fibrosing idiopathic interstitial pneumonias, sarcoidosis, and autoimmune pulmonary alveolar proteinosis, and discuss their utility and effects.

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HER2 drives Mucin-like 1 to control proliferation in breast cancer cells

Cited by 37 publications

References 23 publications

Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats

Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats

Immune-related Gene Data-based Molecular Subtyping Related to the Prognosis for Breast Cancer Patients

Natural Autoantibodies in Chronic Pulmonary Diseases

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