scholarly journals Retinoblastoma protein expression and its predictors in triple-negative breast cancer

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Jaymin M. Patel ◽  
Andrew Goss ◽  
Judy E. Garber ◽  
Vanda Torous ◽  
Edward T. Richardson ◽  
...  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Anna E. M. Bastiaansen ◽  
A. Mieke Timmermans ◽  
Marcel Smid ◽  
Carolien H. M. van Deurzen ◽  
Esther S. P. Hulsenboom ◽  
...  

AbstractNew therapies are an urgent medical need in all breast cancer subgroups. Metabotropic glutamate receptor 1 (mGluR1) is suggested as a potential new molecular target. We examined the prevalence mGluR1 expression in different clinically relevant breast cancer subgroups and determined its association with prognosis. In this retrospective cohort, 394 consecutive primary breast cancer tissues were incorporated into a tissue microarray and immunohistochemically stained for mGluR1. The prevalence of mGluR1 protein expression in different breast cancer subgroups was evaluated and correlated with metastasis-free survival (MFS) and overall survival (OS). In total, 56% (n = 219) breast cancer tissues had mGluR1 expression. In estrogen receptor (ER)-negative tumors, 31% (n = 18/58) had mGluR1 expression that was significantly associated with MFS (HR 5.00, 95% CI 1.03–24.35, p = 0.046) in multivariate analysis, independently from other prognostic factors. Of the 44 triple-negative breast cancer (TNBC), 25% (n = 11) expressed mGluR1. mGluR1 expression in TNBC was significantly associated with shorter MFS (HR 8.60, 95% CI 1.06–20.39, p = 0.044) and with poor OS (HR 16.07, 95% CI 1.16–223.10, p = 0.039). In conclusion, mGluR1 is frequently expressed in breast cancer. In ER-negative breast cancer and in TNBC mGluR1 protein expression is an unfavorable prognostic marker. This study provides rationale to explore mGluR1 as a novel target for breast cancer treatment, especially for the more aggressive TNBC.


2012 ◽  
Vol 12 (5) ◽  
pp. 581-584 ◽  
Author(s):  
Jimmy Jacob ◽  
Adam E Frampton ◽  
Leandro Castellano ◽  
Justin Stebbing ◽  
Jonathan Krell

PLoS ONE ◽  
2019 ◽  
Vol 14 (12) ◽  
pp. e0227068
Author(s):  
Fabiola Giudici ◽  
Elisabetta Petracci ◽  
Oriana Nanni ◽  
Cristina Bottin ◽  
Maurizio Pinamonti ◽  
...  

2012 ◽  
Vol 17 (6) ◽  
pp. 766-774 ◽  
Author(s):  
Chandra Bartholomeusz ◽  
Ana M. Gonzalez‐Angulo ◽  
Ping Liu ◽  
Naoki Hayashi ◽  
Ana Lluch ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e102176 ◽  
Author(s):  
Sara Jansson ◽  
Pär-Ola Bendahl ◽  
Dorthe Aamand Grabau ◽  
Anna-Karin Falck ◽  
Mårten Fernö ◽  
...  

2021 ◽  
Author(s):  
Xiao Tong ◽  
Jiani Xing ◽  
Haizhou Liu ◽  
Shunheng Zhou ◽  
Yue Huang ◽  
...  

Abstract Background Long non-coding RNAs (lncRNAs) is widely described as a class of RNA longer than 200 nucleotides without encoding capability. But recent years, more and more open reading frames (ORFs) have been found in lncRNAs which indicate they have coding capacity. But the mechanisms of the encoding products in cancer are mostly unknown. We have previously shown lncRNA HCP5 is an oncogene in triple negative breast cancer (TNBC), and the aim of the current study was to investigate if lncRNA HCP5 encoding protein promotes TNBC by regulating ferroptosis. Methods We use bioinformatics to predict coding capacity. Molecular biology experiments and the xenograft assay in nude mice to study the mechanism of lncRNA HCP5 encoding protein. And the protein expression was evaluated in a tissue microarray of 140 invasive breast tumors and 45 pared precancerous breast tissues. Association between the protein expression and clinicopathologic features of breast cancer patients was analyzed. Results In this study, we identify that ORF in lncRNA HCP5 can encode a conserved protein with 132-amino acid. The protein, which is named HCP5-132aa, promotes TNBC growth. Mechanistically, the HCP5-132aa regulates GPX4 expression and lipid ROS level through ferroptosis pathway to promote TNBC progression. HCP5-132aa ORF knockdown synergizes with ferroptosis activators in vitro and in vivo. Breast cancer patients with high levels of HCP5-132aa have poorer prognosis. Conclusions Our study indicates that overexpression of lncRNA HCP5 encoding protein is a critical oncogenic event in TNBC. Our findings uncover a regulatory mechanism of ferroptosis in TNBC orchestrated by a protein encoded by an lncRNA.


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