Cellular Distribution of Retinoic Acid Receptor&amp;ndash;&amp;alpha; in Benign Hyperplastic and Malignant Human Prostates: Comparison with Androgen, Estrogen and Progesterone Receptor Status

Gyftopoulos, Kostis; Sotiropoulou, Georgia; Varakis, Ioannis; Barbalias, George A.

doi:10.1159/000020301

Cited by 14 publications

(9 citation statements)

References 36 publications

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“…The results of an elevated PPAR γ in postinitiation phase in the current study are contrary to other reports which have revealed a decreased expression of PPAR γ in cancer [42, 43]. However, in the presence of mutation in APC gene, PPAR γ has been reported to be elevated in the later stages and promote the progression of colon cancer [44, 45]. It has been documented earlier also that PPAR γ can act as a tumour promoter, only in the presence of APC mutation or aberrant Wnt signaling pathway which indeed is the observation in the current study [46].…”

Section: Discussioncontrasting

confidence: 99%

Alterations in Lipid Mediated Signaling and Wnt/β-Catenin Signaling in DMH Induced Colon Cancer on Supplementation of Fish Oil

Kansal

Vaiphei

Agnihotri

2014

BioMed Research International

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Ceramide mediates inhibition of cyclooxygenase-2 (COX-2) which catalyzes formation of prostaglandin further activating peroxisome proliferator-activated receptorγ (PPARγ) and Wnt/β-catenin pathway; and hence plays a critical role in cancer. Therefore, in current study, ceramide, COX-2, 15-deoxy prostaglandin J2(15-deoxy PGJ2), PPARγ, and β-catenin were estimated to evaluate the effect of fish oil on lipid mediated and Wnt/β-catenin signaling in colon carcinoma. Male Wistar rats in Group I received purified diet while Groups II and III received modified diet supplemented with FO : CO(1 : 1) and FO : CO(2.5 : 1), respectively. These were further subdivided into controls receiving ethylenediaminetetraacetic acid and treated groups receiving dimethylhydrazine dihydrochloride (DMH)/week for 4 weeks. Animals sacrificed 48 hours after last injection constituted initiation phase and those sacrificed after 16 weeks constituted postinitiation phase. Decreased ceramide and increased PPARγ were observed in postinitiation phase only. On receiving FO+CO(1 : 1)+DMH and FO+CO(2.5 : 1)+DMH in both phases, ceramide was augmented whereas COX-2, 15-deoxy PGJ2, and nuclear translocation of β-catenin were reduced with respect to cancerous animals. Decrease was more significant in postinitiation phase with FO+CO(2.5 : 1)+DMH. Treatment with oils increased PPARγ in initiation phase but decreased it in postinitiation phase. Hence, fish oil altered lipid mediated signalling in a dose and time dependent manner so as to inhibit progression of colon cancer.

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Section: Discussioncontrasting

confidence: 99%

Alterations in Lipid Mediated Signaling and Wnt/β-Catenin Signaling in DMH Induced Colon Cancer on Supplementation of Fish Oil

Kansal

Vaiphei

Agnihotri

2014

BioMed Research International

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“…The presence of RAR-␣ in normal epithelium with relatively weak nuclear localization suggests that perhaps a minimal RAR-␣ signaling is sufficient for normal epithelial functions. The frequent appearance of granular RAR-␣ at the luminal edge of the epithelium might be due to the crowding of the epithelium and has been reported previously (Gyftopoulos et al, 2000b). On the contrary, increases in nuclear RAR-␣ in epithelial cells that were associated with BPH, PIN and various grades of cancer imply that RAR-␣ signaling events might have been exaggerated in these cells.…”

Section: Discussionsupporting

confidence: 62%

Immunohistochemical Localization of the Retinoic Acid Receptors in Human Prostate

RICHTER,

JOYCE,

FROMOWITZ

et al. 2002

Journal of Andrology

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Retinoic acid receptors (RARs) are nuclear transcription factors that mediate the effects of retinoids. Aberrant expression and regulation of RARs have been linked to various malignancies, including steroid‐related breast and cervical cancers. Our previous results also suggest that prostate cancer is associated with altered RAR signaling. To understand the relationship between RAR signaling and prostate cancer, the current study examined the cellular distribution of RAR‐α,‐β, and ‐γ in human prostate tissues exhibiting different pathologic conditions. In histologically normal epithelium, both RAR‐α and ‐γ were present throughout the epithelium with minimal nuclear accumulation. RAR‐β was present only in basal epithelial nuclei. On the contrary, RAR‐α was significantly increased in the nuclei of luminal epithelial cells, and both RAR‐β and ‐γ were increased in basal and luminal epithelial nuclei in glands exhibiting benign prostatic hyperplasia (BPH). RAR‐α was also increased in luminal epithelial nuclei in glands exhibiting prostatic intra‐epithelial neoplasia (PIN). In these glands, RAR‐β was persisting in basal epithelial nuclei that were also RAR‐γ positive. In low‐ and intermediate‐grade cancerous glands, RAR‐α was also significantly increased in luminal epithelial nuclei, and a strong RAR‐γ signal was seen in some cells. RAR‐β was absent in these glands. Both RAR‐α and ‐γ were also increased in high‐grade cancer cells. In conclusion, current results demonstrated changes in cellular distribution of RAR‐α and ‐γ in human prostate tissues exhibiting different pathologies. These results suggest links between altered RAR signaling and deregulated cell growth and/or tumorigenic transformation of prostate epithelial cells.

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“…RARB is a member of thyroid-steroid hormone receptor superfamily (Fig. 1b) and both genes are known to play a powerful role in the inhibition of proliferation and stimulation of cellular differentiation [15]. Artificial Neural Network (ANN) analysis [16] of the data sets revealed a strong positive correlation with several retinoic acid receptors (RARB, RXRB, and RXRG) all of which bind the biologically active form of vitamin A and PGR (Fig.…”

Section: Resultsmentioning

confidence: 99%

Mitochondrial dysfunction is a key determinant of the rare disease lymphangioleiomyomatosis and provides a novel therapeutic target

et al. 2018

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Lymphangioleiomyomatosis (LAM) is a rare and progressive systemic disease affecting mainly young women of childbearing age. A deterioration in lung function is driven by neoplastic growth of atypical smooth muscle-like LAM cells in the pulmonary interstitial space that leads to cystic lung destruction and spontaneous pneumothoraces. Therapeutic options for preventing disease progression are limited and often end with lung transplantation temporarily delaying an inevitable decline. To identify new therapeutic strategies for this crippling orphan disease, we have performed array based and metabolic molecular analysis on patient-derived cell lines. Our results point to the conclusion that mitochondrial biogenesis and mitochondrial dysfunction in LAM cells provide a novel target for treatment.

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Cellular Distribution of Retinoic Acid Receptor–α in Benign Hyperplastic and Malignant Human Prostates: Comparison with Androgen, Estrogen and Progesterone Receptor Status

Cited by 14 publications

References 36 publications

Alterations in Lipid Mediated Signaling and Wnt/β-Catenin Signaling in DMH Induced Colon Cancer on Supplementation of Fish Oil

Alterations in Lipid Mediated Signaling and Wnt/β-Catenin Signaling in DMH Induced Colon Cancer on Supplementation of Fish Oil

Immunohistochemical Localization of the Retinoic Acid Receptors in Human Prostate

Mitochondrial dysfunction is a key determinant of the rare disease lymphangioleiomyomatosis and provides a novel therapeutic target

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