Glucocorticoid Receptor: A Multifaceted Actor in Breast Cancer

Noureddine, Lara Malik; Trédan, Olivier; Hussein, Nader; Badran, Bassam; Romancer, Muriel Le; Poulard, Coralie

doi:10.3390/ijms22094446

Cited by 38 publications

(44 citation statements)

References 153 publications

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“…For example, in ovarian and endometrial cancer cells, increased GR expression has been associated with poor prognoses [83,84]. GR expression is also correlated with a poor prognosis in estrogen receptor alpha (ERα)-negative breast cancer; however, it is correlated with a good prognosis in ERα-positive breast cancer [85]. An increase in stress-driven GCs has been associated with breast cancer progression [85,86].…”

Section: Glucocorticoids and Cancermentioning

confidence: 99%

“…GR expression is also correlated with a poor prognosis in estrogen receptor alpha (ERα)-negative breast cancer; however, it is correlated with a good prognosis in ERα-positive breast cancer [85]. An increase in stress-driven GCs has been associated with breast cancer progression [85,86]. In contrast, an in vitro study using cancerous epithelial prostrate cells observed a favorable prognosis for non-small cell lung cancers expressing GR, suggesting that GR may function as a tumor suppressor in these contexts [87,88].…”

Section: Glucocorticoids and Cancermentioning

confidence: 99%

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Glucocorticoid and PD-1 Cross-Talk: Does the Immune System Become Confused?

Adorisio

Cannarile

Delfino

et al. 2021

Cells

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Programmed cell death protein 1 (PD-1) and its ligands, PD-L1/2, control T cell activation and tolerance. While PD-1 expression is induced upon T cell receptor (TCR) activation or cytokine signaling, PD-L1 is expressed on B cells, antigen presenting cells, and on non-immune tissues, including cancer cells. Importantly, PD-L1 binding inhibits T cell activation. Therefore, the modulation of PD-1/PD-L1 expression on immune cells, both circulating or in a tumor microenvironment and/or on the tumor cell surface, is one mechanism of cancer immune evasion. Therapies that target PD-1/PD-L1, blocking the T cell-cancer cell interaction, have been successful in patients with various types of cancer. Glucocorticoids (GCs) are often administered to manage the side effects of chemo- or immuno-therapy, exerting a wide range of immunosuppressive and anti-inflammatory effects. However, GCs may also have tumor-promoting effects, interfering with therapy. In this review, we examine GC signaling and how it intersects with PD-1/PD-L1 pathways, including a discussion on the potential for GC- and PD-1/PD-L1-targeted therapies to “confuse” the immune system, leading to a cancer cell advantage that counteracts anti-cancer immunotherapy. Therefore, combination therapies should be utilized with an awareness of the potential for opposing effects on the immune system.

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Section: Glucocorticoids and Cancermentioning

confidence: 99%

Section: Glucocorticoids and Cancermentioning

confidence: 99%

Glucocorticoid and PD-1 Cross-Talk: Does the Immune System Become Confused?

Adorisio

Cannarile

Delfino

et al. 2021

Cells

View full text Add to dashboard Cite

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“…Clinically, synthetic glucocorticoids (GR agonists) such as dexamethasone are ubiquitously used in breast cancer in conjunction with chemotherapy to mitigate hypersensitivity reactions, and for their antiemetic, anti-inflammatory, as well as orexigenic properties. However, dexamethasone triggers different effects depending on the breast cancer subtype [ 149 ].…”

Section: Glucocorticoid Receptor Signallingmentioning

confidence: 99%

Type 1 Nuclear Receptor Activity in Breast Cancer: Translating Preclinical Insights to the Clinic

Kumar

Freelander

Lim

2021

Cancers

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The nuclear receptor (NR) family of transcription factors is intimately associated with the development, progression and treatment of breast cancer. They are used diagnostically and prognostically, and crosstalk between nuclear receptor pathways and growth factor signalling has been demonstrated in all major subtypes of breast cancer. The majority of breast cancers are driven by estrogen receptor α (ER), and anti-estrogenic therapies remain the backbone of treatment, leading to clinically impactful improvements in patient outcomes. This serves as a blueprint for the development of therapies targeting other nuclear receptors. More recently, pivotal findings into modulating the progesterone (PR) and androgen receptors (AR), with accompanying mechanistic insights into NR crosstalk and interactions with other proliferative pathways, have led to clinical trials in all of the major breast cancer subtypes. A growing body of evidence now supports targeting other Type 1 nuclear receptors such as the glucocorticoid receptor (GR), as well as Type 2 NRs such as the vitamin D receptor (VDR). Here, we reviewed the existing preclinical insights into nuclear receptor activity in breast cancer, with a focus on Type 1 NRs. We also discussed the potential to translate these findings into improving patient outcomes.

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“…[3]. Кроме того, в зависимости от подтипа РМЖ, GC могут значительно способствовать прогрессированию опухоли [2,4].…”

Section: Introductionunclassified

In vitro screening of effectiveness and antiproliferative effects of potential ddit4 inhibitors for breast cancer cell lines

et al. 2022

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Objective: screening of previously selected DDIT4 inhibitors by their ability to suppress basal and glucocorticoid-induced expression of this gene in breast cancer (BC) cells, as well as evaluation of antiproliferative and cytotoxic effects of the studied drug combinations the antiproliferative and proapoptotic effects of studied drug combinations. Material and Methods. Breast cancer cells of the luminal, HER2- positive and triple negative subtypes were used. The effects of drugs (rapamycin, wortmannin, LY-294002, apigenin, resveratrol, curcumin, CGP-60474, and emetine) on the basal and glucocorticoid-induced levels of expression of the DDIT4 gene and its protein product were evaluated by qPCR and Western blotting assays. Results. Emetine, rapamycin, wortmannin, LY-294002 and CGP-60474 demonstrated DDIT4-inhibition activity. Glucocorticoid dexamethasone showed cytotoxic effects and antiproliferative activity in combination with emetine, CGP-60474 (C protein kinase inhibitor), resveratrol and curcumin. Conclusion. Novel inhibitors of DDIT4 in breast cancer model cells in vitro were found. Emetine and CGP-60474 are the most promising drugs for further research.

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Glucocorticoid Receptor: A Multifaceted Actor in Breast Cancer

Cited by 38 publications

References 153 publications

Glucocorticoid and PD-1 Cross-Talk: Does the Immune System Become Confused?

Glucocorticoid and PD-1 Cross-Talk: Does the Immune System Become Confused?

Type 1 Nuclear Receptor Activity in Breast Cancer: Translating Preclinical Insights to the Clinic

In vitro screening of effectiveness and antiproliferative effects of potential ddit4 inhibitors for breast cancer cell lines

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