Retinoic Acid Affects the EGF-R Signaling Pathway during Differentiation Induction of Human Endometrial Adenocarcinoma Cells

Carter, Charleata A.; Shaw, Benjamin L.

doi:10.1006/exmp.2000.2301

Cited by 7 publications

(4 citation statements)

References 52 publications

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“…Studies from Carter et al (1996) and Carter & Madden (2000) have demonstrated that RA could induce differentiation of human endometrial adenocarcinoma cell lines (CAC-1 and RL-95 cells). Further studies indicated that phosphatidylinositol 3-kinase and epidermal growth factor receptor cell signaling pathways were involved in RA-induced cell differentiation of human endometrial adenocarcinoma cells (Carter & Shaw 2000, Carter 2003). Saidi et al (2006) have recently reported that PPARα agonist (Fenofibrate) inhibits proliferation and induces apoptosis in endometrial cancer cells in vitro , and these effects are potentiated by RA.…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid inhibits endometrial cancer cell growth via multiple genomic mechanisms

Cheng¹,

Utsunomiya²,

Pavone³

et al. 2011

Journal of Molecular Endocrinology

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Previous studies have indicated that retinoic acid (RA) may be therapeutic for endometrial cancer. However, the downstream target genes and pathways triggered by ligand-activated RA receptor α (RARα) in endometrial cancer cells are largely unknown. In this study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and immunoblotting assays were used to assess the roles of RA and the RA agonist (AM580) in the growth of endometrial cancer cells. Illumina-based microarray expression profiling of endometrial Ishikawa cells incubated with and without AM580 for 1, 3, and 6 h was performed. We found that both RA and AM580 markedly inhibited endometrial cancer cell proliferation, while knockdown of RARα could block AM580 inhibition. Knockdown of RARα significantly increased proliferating cell nuclear antigen and BCL2 protein levels. Incubation of Ishikawa cells with or without AM580 followed by microarray expression profiling showed that 12 768 genes out of 47 296 gene probes were differentially expressed with significant P values. We found that 90 genes were the most regulated genes with the most significant P value (P<0.0001) using F-test. We selected four highly regulated genes with diverse functions, namely G0S2, TNFAIP2, SMAD3, and NRIP1. Real-time PCR verified that AM580 highly regulated these genes, whereas chromatin immunoprecipitation-PCR assay demonstrated that ligand-activated RARα interacted with the promoter of these genes in intact endometrial cancer cells. AM580 also significantly altered 18 pathways including those related to cell growth, differentiation, and apoptosis. In conclusion, AM580 treatment of Ishikawa cells causes the differential expression of a number of RARα target genes and activation of signaling pathways. These pathways could, therefore, mediate the carcinogenesis of human endometrial cancer.

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Section: Introductionmentioning

confidence: 99%

Retinoic acid inhibits endometrial cancer cell growth via multiple genomic mechanisms

Cheng¹,

Utsunomiya²,

Pavone³

et al. 2011

Journal of Molecular Endocrinology

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“…The authors were able to conclude that retinoic acid induced differentiation in this tumor cell line via interference with the EGF-R signaling pathway. 23 Additionally, human skin fibroblasts show no change in the EGF-R number or affinity with use of retinoic acid. 24 Based on this reasoning, we attempted the use of low-dose isotretinoin in our patient with excellent clinical results.…”

Section: Discussionmentioning

confidence: 99%

Acneiform eruptions associated with epidermal growth factor receptor–targeted chemotherapy

DeWitt

Siroy

Stone

2007

Journal of the American Academy of Dermatology

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“…Isotretinoin may be used as chemoprevention for cutaneous and head and neck squamous cell carcinomas 43,44 . On a molecular level, Carter et al demonstrate down regulation of EGFR signaling in endometrial adenocarcinoma cell lines treated with isotretinoin 45 …”

Section: Discussionmentioning

confidence: 99%

A systematic review of oral retinoids for treatment of acneiform eruptions induced by epidermal growth factor receptor inhibitors

Rachel

Lam

Pehr

2022

Dermatologic Therapy

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Epidermal growth factor receptor inhibitors (EGFRi) are now standard of care in patients with EGFR mutations in non-small cell lung cancer (NSCLC) and are increasingly being used in other EGFR mutated cancers, including gastrointestinal, and head and neck. However, EGFRi are well known to cause acneiform eruptions, which are shown to positively correlate with tumor response to treatment, but may be severe enough to cause interruption of their treatment. Although most guidelines call for the use of tetracyclines to treat these acneiform eruptions, there is mounting evidence for the use of systemic retinoids instead. The objective of this review is to summarize available data on the use of systemic retinoids for management of acneiform eruptions on EGFRi. This study was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. MEDLINE and EMBASE were searched from database inception until December 10th, 2021. All articles were screened and relevant data extracted independently in duplicate by two reviewers. In total, 16 case reports, case series and retrospective reviews were included. Forty-three patients were treated with retinoids for their acneiform eruption due to EGFRi. The majority (77%) noted moderate to significant improvement after treatment initiation with minimal adverse events (16%).The findings of this systematic review suggest that systemic retinoids are a safe and effective therapy for the management of acneiform eruptions induced by EGFRi.

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Retinoic Acid Affects the EGF-R Signaling Pathway during Differentiation Induction of Human Endometrial Adenocarcinoma Cells

Cited by 7 publications

References 52 publications

Retinoic acid inhibits endometrial cancer cell growth via multiple genomic mechanisms

Retinoic acid inhibits endometrial cancer cell growth via multiple genomic mechanisms

Acneiform eruptions associated with epidermal growth factor receptor–targeted chemotherapy

A systematic review of oral retinoids for treatment of acneiform eruptions induced by epidermal growth factor receptor inhibitors

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