An androgen receptor regulated gene score is associated with epithelial to mesenchymal transition features in triple negative breast cancers

Rajarajan, Savitha; Snijesh, V.P; Anupama, C.E; Nair, Madhumathy G; Mavatkar, Apoorva D; Naidu, Chandrakala M; Patil, Sharada; Nimbalkar, Vidya P; Alexander, Annie; Pillai, Maalavika; Jolly, Mohit Kumar; Sabarinathan, Radhakrishnan; Ramesh, Rakesh S; BS, Srinath; Prabhu, Jyothi S

doi:10.1016/j.tranon.2023.101761

Cited by 5 publications

(2 citation statements)

References 73 publications

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“…Our finding revealed that the group identified as high-risk group exhibited heightened sensitivity to medications such as bicalutamide, dasatinib, and lapatinib. Of these, bicalutamide can reverse the decrease in E-cadherin in TNBC, thereby reversing EMT [ 59 ], which is associated with VM formation [ 60 ]. In TNBC, using functionalized vincristine plus dasatinib liposomes which have been tailored using the targeted molecule DSPE-PEG 2000 -c(RGDyK), both in vivo and in vitro can result in the nondetection of recognized VM channel markers.…”

Section: Discussionmentioning

confidence: 99%

Constructing a novel prognostic model for triple-negative breast cancer based on genes associated with vasculogenic mimicry

Ren,

Feng,

Tan

et al. 2024

Aging

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Background: Research has shown a connection between vasculogenic mimicry (VM) and cancer progression. However, the functions of genes related to VM in the emergence and progression of TNBC have not been completely elucidated. Methods: A survival risk model was constructed by screening biomarkers using DESeq2 and WGCNA based on public TNBC transcriptome data. Furthermore, gene set enrichment analysis was performed, and tumor microenvironment and drug sensitivity were analyzed. The selected biomarkers were validated via quantitative PCR detection, immunohistochemical staining, and protein detection in breast cancer cell lines. Biomarkers related to the proliferation and migration of TNBC cells were validated via in vitro experiments. Results: The findings revealed that 235 target genes were connected to the complement and coagulation cascade pathways. The risk score was constructed using KCND2, NRP1, and VSTM4. The prognosis model using the risk score and pathological T stage yielded good validation results. The clinical risk of TNBC was associated with the angiogenesis signaling pathway, and the low-risk group exhibited better sensitivity to immunotherapy. Quantitative PCR and immunohistochemistry indicated that the expression levels of KCND2 in TNBC tissues were higher than those in adjacent nontumor tissues. In the TNBC cell line, the protein expression of KCND2 was increased. Knockdown of KCND2 and VSTM4 inhibited the proliferation and migration of TNBC cells in vitro . Conclusions: In this study, three VM-related biomarkers were identified, including KCND2, NRP1, and VSTM4. These findings are likely to aid in deepening our understanding of the regulatory mechanism of VM in TNBC.

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Section: Discussionmentioning

confidence: 99%

Constructing a novel prognostic model for triple-negative breast cancer based on genes associated with vasculogenic mimicry

Ren,

Feng,

Tan

et al. 2024

Aging

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“…AR has been related to promoting tumor proliferation when ERα is not expressed [16,18], as it has been studied that AR influences in PI3K/AKT pathways [41]. Also, AR expression has been associated with increased metastasis in TNBC by activation of ZEB-1 or the SRC/PI3K pathways [42]. Thus, AR could be an interesting therapeutic target in the Regarding anastrozole treatment, a generalized reduction in estrogen and DHT levels was found among cell lines, while T levels increased in some cell lines.…”

Section: Discussionmentioning

confidence: 99%

Androgen and Estrogen β Receptor Expression Enhances Efficacy of Antihormonal Treatments in Triple-Negative Breast Cancer Cell Lines

Crespo,

Illera,

Silvan

et al. 2024

IJMS

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The triple-negative breast cancer (TNBC) subtype is characterized by the lack of expression of ERα (estrogen receptor α), PR (progesterone receptor) and no overexpression of HER-2. However, TNBC can express the androgen receptor (AR) or estrogen receptor β (ERβ). Also, TNBC secretes steroid hormones and is influenced by hormonal fluctuations, so the steroid inhibition could exert a beneficial effect in TNBC treatment. The aim of this study was to evaluate the effect of dutasteride, anastrozole and ASP9521 in in vitro processes using human TNBC cell lines. For this, immunofluorescence, sensitivity, proliferation and wound healing assays were performed, and hormone concentrations were studied. Results revealed that all TNBC cell lines expressed AR and ERβ; the ones that expressed them most intensely were more sensitive to antihormonal treatments. All treatments reduced cell viability, highlighting MDA-MB-453 and SUM-159. Indeed, a decrease in androgen levels was observed in these cell lines, which could relate to a reduction in cell viability. In addition, MCF-7 and SUM-159 increased cell migration under treatments, increasing estrogen levels, which could favor cell migration. Thus, antihormonal treatments could be beneficial for TNBC therapies. This study clarifies the importance of steroid hormones in AR and ERβ-positive cell lines of TNBC.

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Differential role of glucocorticoid receptor based on its cell type specific expression on tumor cells and infiltrating lymphocytes

Snijesh,

Nimbalkar,

Patil

et al. 2024

Translational Oncology

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An androgen receptor regulated gene score is associated with epithelial to mesenchymal transition features in triple negative breast cancers

Cited by 5 publications

References 73 publications

Constructing a novel prognostic model for triple-negative breast cancer based on genes associated with vasculogenic mimicry

Constructing a novel prognostic model for triple-negative breast cancer based on genes associated with vasculogenic mimicry

Androgen and Estrogen β Receptor Expression Enhances Efficacy of Antihormonal Treatments in Triple-Negative Breast Cancer Cell Lines

Differential role of glucocorticoid receptor based on its cell type specific expression on tumor cells and infiltrating lymphocytes

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