Retinoic Acid Receptor β: A Potential Therapeutic Target in Retinoic Acid Treatment of Endometrial Cancer

Tsuji, Kiichiro; Utsunomiya, Hiroki; Miki, Yasuhiro; Hanihara, Mayu; Fue, Misaki; Takagi, Kiyoshi; Nishimoto, Masashi; Suzuki, Fujio; Yaegashi, Nobuo; Suzuki, Takashi; Itō, Kiyoshi

doi:10.1097/igc.0000000000000995

Cited by 7 publications

(11 citation statements)

References 25 publications

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“…It causes apoptosis by arresting the cell cycle in the G1/S phase [ 62 ]. Recent studies showed that retinoic acid (RA) has anticancer properties, including the suppression of cell proliferation and invasion in EC cells [ 63 ]. Because all-trans-retinoic acid (ATRA) is an analog of RA, it could be used to treat EC.…”

Section: Discussionmentioning

confidence: 99%

[Retracted] Ferroptosis‐Related lncRNA for the Establishment of Novel Prognostic Signature and Therapeutic Response Prediction to Endometrial Carcinoma

Zhou

Dai

et al. 2022

BioMed Research International

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Background. Ferroptosis is a recently described form of intentional cellular damage that is iron-dependent and separate from apoptosis, cellular necrosis, and autophagy. It has been demonstrated to be adequately regulated by long noncoding RNAs (lncRNAs) in various cancers. However, the predictive profile of ferroptosis-related lncRNAs (FRLs) in endometrial carcinoma (EC) is unknown. Herein, FRLs associated with uterine corpus endometrial carcinoma (UCEC) prognosis were screened to predict treatment response in EC. Methods. Samples of EC and adjacent normal tissues were obtained from The Cancer Genome Atlas (TCGA) dataset repository. Limma and survival packages in R software were used to screen FRLs associated with the prognosis of EC. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) chord and circle plots of FRLs were also plotted. Next, FRLs screened by the least absolute shrinkage and selection operator (LASSO) method were applied to construct and validate a multivariate Cox proportional risk regression model. Nomogram plots were created to forecast the outcome of UCEC patients, and gene set enrichment analysis (GSEA), principal component analysis (PCA), and immunoassays were performed on the prognostic models. Finally, limma, ggpubr, pRRophetic, and ggplot2 programs were used for drug sensitivity analysis of the prognostic models. Results. A signature based on nine FRLs (CFAP58-DT, LINC00443, EMSLR, HYI-AS1, ADIRF-AS1, LINC02474, CDKN2B-AS1, LINC01629, and LINC00942) was constructed. The developed FRL prognostic model effectively discriminated UCEC patients into low-risk and high-risk groups. Immunological checkpoints CD80 and CD40 were strongly expressed in the high-risk group. In addition, the nine FRLs were all more expressed in the high-risk group compared to the low-risk group. Conclusion. These findings significantly contribute to the understanding of the function of FRLs in UCEC and provide promising therapeutic strategies for UCEC.

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Section: Discussionmentioning

confidence: 99%

[Retracted] Ferroptosis‐Related lncRNA for the Establishment of Novel Prognostic Signature and Therapeutic Response Prediction to Endometrial Carcinoma

Zhou

Dai

et al. 2022

BioMed Research International

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“…Cells were cultured in 96-well plates at a density of 8000 cells/well and treated with NOMAC (0.3, 1, 3, 10, 30, or 100 μmol/L) or DMSO for 24, 48, and 72 h. Cell proliferation was determined using the CCK-8 Assay Kit (Dojindo Molecular Technologies, Kumamoto, Japan). We added 10 μL of CCK-8 solution to each well and incubated the cells at 37 °C for 2 h. The absorbance (optical density) was read with a spectrophotometric plate reader (Bio-Tek ELX-800, Winooski, VT, USA) at 450 nm to determine cell viability [ 41 ]. The results are presented as the percentage of cell growth inhibition (%), the half-maximal inhibitory concentration (IC 50 ), and the corresponding 95% CI [ 41 ].…”

Section: Methodsmentioning

confidence: 99%

“…We added 10 μL of CCK-8 solution to each well and incubated the cells at 37 °C for 2 h. The absorbance (optical density) was read with a spectrophotometric plate reader (Bio-Tek ELX-800, Winooski, VT, USA) at 450 nm to determine cell viability [ 41 ]. The results are presented as the percentage of cell growth inhibition (%), the half-maximal inhibitory concentration (IC 50 ), and the corresponding 95% CI [ 41 ]. The cell growth inhibition rate (%) was calculated using the following equation: (1 − OD of NOMAC-treated wells/OD of control wells) × 100% [ 42 ].…”

Section: Methodsmentioning

confidence: 99%

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Nomegestrol Acetate Suppresses Human Endometrial Cancer RL95-2 Cells Proliferation In Vitro and In Vivo Possibly Related to Upregulating Expression of SUFU and Wnt7a

Xie

Zhou

et al. 2017

IJMS

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Nomegestrol acetate (NOMAC) has been successfully used for the treatment of some gynecological disorders, and as a combined oral contraceptive with approval in many countries. In this study, we investigated the effects of NOMAC on human endometrial cancer cells in vitro and in vivo. The proliferation of human endometrial cancer cells (RL95-2 and KLE) were assessed using CCK-8 and EdU incorporation assays. Whole-genome cDNA microarray analysis was used to identify the effects of NOMAC on gene expression profiles in RL95-2 cells. RL95-2 xenograft nude mice were treated with NOMAC (50, 100, and 200 mg/kg) or medroxyprogesterone acetate (MPA; 100 and 200 mg/kg) for 28 consecutive days. The results showed that NOMAC significantly inhibited the growth of RL95-2 cells in a concentration-dependent manner, but not in KLE cells. Further investigation demonstrated that NOMAC produced a stronger inhibition of tumor growth (inhibition rates for 50, 100, and 200 mg/kg NOMAC were 24.74%, 47.04%, and 58.06%, respectively) than did MPA (inhibition rates for 100 and 200 mg/kg MPA were 41.06% and 27.01%, respectively) in the nude mice bearing the cell line of RL95-2. NOMAC altered the expression of several genes related to cancer cell proliferation, including SUFU and Wnt7a. The upregulation of SUFU and Wnt7a was confirmed using real-time quantitative polymerase chain reaction and Western blotting in RL95-2 cells and RL95-2 xenograft tumor tissues, but not in KLE cells. These data indicate that NOMAC can inhibit the proliferation of RL95-2 cell in vitro and suppress the growth of xenografts in the nude mice bearing the cell line of RL95-2 in vivo. This effect could be related to the upregulating expression of SUFU and Wnt7a.

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“…PRAME may therefore have predictive value in identifying patients likely to benefit from retinoid therapy, which promotes RAR signaling. Notably, retinoic acid has shown promise in preclinical studies of endometrial carcinoma, inhibiting cell growth and inducing differentiation both in vitro and in vivo (25)(26)(27).…”

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confidence: 99%

PRAME Expression in Endometrioid and Serous Endometrial Carcinoma: A Potential Immunotherapeutic Target and Possible Diagnostic Pitfall

Coppock

Gradecki

Mills

2022

International Journal of Gynecological Pathology

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Preferentially expressed antigen in melanoma (PRAME) is a cancer testes antigen initially employed as a diagnostic marker for melanoma. Although negative in most normal tissues, its expression has been reported in benign endometrial glands. Additionally, PRAME expression has been identified in a growing list of solid and hematologic malignancies and is of interest as a predictive biomarker, as cancer vaccination strategies and adoptive T-cell transfer targeting this molecule are under clinical investigation; additionally, PRAME may identify candidates for retinoid therapy. However, expression of PRAME has not been well-studied in endometrial cancers. We herein evaluate PRAME expression in endometrial carcinomas to better characterize its limitations as a diagnostic melanoma marker as well as its potential as a predictive biomarker in endometrial carcinomas. PRAME expression was evaluated in 256 endometrioid (n = 235) and serous (n = 21) endometrial carcinomas via tissue microarray. In all, 89% (227/256) demonstrated some degree of nuclear PRAME expression, including 88% (207/235) of endometrioid carcinomas and 95% (20/21) of serous carcinomas. Diffuse ( > 50%) expression was observed in 70% (179/256) of all cases, including 69% (163/235) of endometrioid carcinomas and 76% (16/21) of serous carcinomas. There was no association between degree of expression and grade, mismatch repair protein status, or stage. The widespread expression of PRAME in endometrial carcinomas suggests this marker should not be interpreted as specific for melanoma in this context. However PRAME may have utility as a predictive biomarker in endometrial cancer, and expansion of testing of PRAME-based therapies to endometrioid and serous endometrial carcinomas may lead to new therapeutic options for these endometrial cancer subtypes.

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Retinoic Acid Receptor β: A Potential Therapeutic Target in Retinoic Acid Treatment of Endometrial Cancer

Abstract: Retinoic acid might have multiple antitumor effects, and RARβ may be a potent therapeutic target in RA treatment for endometrial cancers.

Cited by 7 publications

References 25 publications

[Retracted] Ferroptosis‐Related lncRNA for the Establishment of Novel Prognostic Signature and Therapeutic Response Prediction to Endometrial Carcinoma

[Retracted] Ferroptosis‐Related lncRNA for the Establishment of Novel Prognostic Signature and Therapeutic Response Prediction to Endometrial Carcinoma

Nomegestrol Acetate Suppresses Human Endometrial Cancer RL95-2 Cells Proliferation In Vitro and In Vivo Possibly Related to Upregulating Expression of SUFU and Wnt7a

PRAME Expression in Endometrioid and Serous Endometrial Carcinoma: A Potential Immunotherapeutic Target and Possible Diagnostic Pitfall

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