Expression of estrogen receptor α, retinoic acid receptor α and cellular retinoic acid binding protein II genes is coordinately regulated in human breast cancer cells

Lü, Min; Mira-y-Lopez, Rafael; Nakajo, Shigeo; Nakaya, Kazuyasu; Jing, Yongkui

doi:10.1038/sj.onc.1208661

Cited by 60 publications

(55 citation statements)

References 43 publications

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“…Consistent with the present study, previous studies have reported that RARα was also involved in the regulation of the cell cycle in breast cancer (13). Retinoic acid, a ligand of RARα, inhibited the growth of breast cancer cells through the induction of cell cycle arrest at the G1 phase and cell apoptosis (13). The mechanism of RARα in the regulation of the development of LSCC is the focus of a number of studies; it has been reported that there are genomic and non-genomic influences (20).…”

Section: Discussionsupporting

confidence: 82%

“…It was indicated that the overexpression of RARα served an important function in the development of LSCC. Consistent with the present study, previous studies have reported that RARα was also involved in the regulation of the cell cycle in breast cancer (13). Retinoic acid, a ligand of RARα, inhibited the growth of breast cancer cells through the induction of cell cycle arrest at the G1 phase and cell apoptosis (13).…”

Section: Discussionsupporting

confidence: 80%

“…The contribution of RARα to the development of hepatocellular carcinoma was associated with its regulation of cytochrome P450 family 1 subfamily A member 1 expression (10,11). RARα is also involved in the development of breast cancer and prostate carcinoma (12)(13)(14). However, little is known about the expression and function of RARα in human LSCC.…”

Section: Introductionmentioning

confidence: 99%

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An oncogenic function of retinoic acid receptor‑α in the development of laryngeal squamous cell carcinoma

et al. 2017

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Abstract. The aberrant expression of retinoic acid receptor-α (RARα) has been reported in various types of cancer. However, its association with the prognosis and development of laryngeal squamous cell carcinoma (LSCC) has not yet been determined. Therefore, the present study aimed to examine the expression and function of RARα in patients with LSCC. The expression of RARα in LSCC tissues was investigated using immunostaining. An MTT assay and flow cytometry analysis were also performed to investigate the function of RARα in the proliferation and cell cycle of LSCC cells. The expression of RARα was significantly elevated in LSCC tissues compared with adjacent noncancerous tissues (78.1 vs. 6.3%, P<0.05). The overexpression of RARα was associated with poorly differentiated features of LSCC (P<0.05). Furthermore, the downregulation of RARα inhibited the proliferation of LSCC cells, and arrested the cell cycle at the G1 phase via upregulation of cyclin dependent kinase inhibitor 1A, which may be associated with inhibition of the protein kinase B signaling pathway. Therefore, the overexpression of RARα may contribute to the development of LSCC through the regulation of the cell cycle. The results of the present study provide evidence that RARα serves an important function in LSCC development and may be a potential therapeutic target or prognostic predictor for LSCC.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

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An oncogenic function of retinoic acid receptor‑α in the development of laryngeal squamous cell carcinoma

et al. 2017

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“…30). The pCH110 plasmid that codes h-galactosidase was cotransfected into PC-3 and LNCaP cells using Lipofectmine 2000 (31). The cells were treated with or without AKBA (10 Ag/mL) for 24 h and then harvested for luciferase activity assay.…”

Section: Introductionmentioning

confidence: 99%

Acetyl-Keto-β-Boswellic Acid Induces Apoptosis through a Death Receptor 5–Mediated Pathway in Prostate Cancer Cells

et al. 2008

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Acetyl-keto-B-boswellic acid (AKBA), a triterpenoid isolated from Boswellia carterri Birdw and Boswellia serrata, has been found to inhibit tumor cell growth and to induce apoptosis. The apoptotic effects and the mechanisms of action of AKBA were studied in LNCaP and PC-3 human prostate cancer cells. AKBA induced apoptosis in both cell lines at concentrations above 10 Mg/mL. AKBA-induced apoptosis was correlated with the activation of caspase-3 and caspase-8 as well as with poly(ADP)ribose polymerase (PARP) cleavage. The activation of caspase-8 was correlated with increased levels of death receptor (DR) 5 but not of Fas or DR4. AKBA-induced apoptosis, caspase-8 activation, and PARP cleavage were inhibited by knocking down DR5 using a small hairpin RNA. AKBA treatment increased the levels of CAAT/enhancer binding protein homologous protein (CHOP) and activated a DR5 promoter reporter but did not activate a DR5 promoter reporter with the mutant CHOP binding site. These results suggest that AKBA induces apoptosis in prostate cancer cells through a DR5-mediated pathway, which probably involves the induced expression of CHOP.

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“…Previous studies on MCF-cells support our data that RARα is the primer target of atRA (6). The decrease of RARα expression may affect RARβ2 transcription and further sensitivity of tumor cells to retinoids (7,34,35). Interestingly, BCA-2 cells constitutively expressed RARβ5, but not RARα, RARβ2, or RARγ proteins, suggesting significant post-translational defects in RAR signaling that correlated with cell resistance to retinoids both in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Early in vitro passages of breast cancer cells are differentially susceptible to retinoids and differentially express RARβ isoforms

Christov

2011

Int J Oncol

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Abstract. The effect of retinoids on breast cancer has been predominantly studied in vitro, on established cell lines, which in biology differ significantly from primary tumor cells. Little is known on whether early in vitro passages of breast cancer cells (EPBCCs) are differentially sensitive to retinoids and differentially express retinoid acid receptors (RARs) and retinoid X receptors (RXRs). We have previously identified a novel RARβ isoform (RARβ5) and hypothesized that it may serve as a potential target of retinoids in EPBCCs. Breast cancer cells isolated from primary tumors were cultured in vitro for 6-12 passages (EPBCCs) and their epithelial origin was confirmed by a cocktail of antibodies against cytokeratins. EPBCCs were treated for 4 days with 1.0 µM of all-trans retinoic acid (atRA), 9-cis retinoic acid (9cRA) or 4-hydroxy-phenylretinamide (4-HPR) and their viability determined by MTT assay. Among nine EPBCCs consistently grown in vitro, three were resistant to the above retinoids, five were susceptible to atRA, four to 4-HPR and two to 9cRA, suggesting that patients with breast carcinomas may differentially respond to various retinoids. All EPBBCs differentially expressed RARα, RARγ, RXRα, RXRβ proteins and RARβ5 and RARβ2 mRNAs. However, only one EPBCC (BCA-2) expressed RARβ5 at mRNA and protein level and it was resistant to retinoids, both in vitro and in a xenograft tumor assay. RARβ5 suppression by siRNA in BCA-2 cells increased their susceptibility to atRA. No correlation was found between sensitivity of EPBCCs to the above retinoids and RARβ5 and RARβ2 mRNA expression. atRA reduced RARβ expression in most EPBCCs suggesting that this retinoid receptor is most probably the prime target of retinoids in breast cancer. These data may have clinical implication in selecting patients with breast cancer that would benefit the most from clinical trials with retinoids.

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Expression of estrogen receptor α, retinoic acid receptor α and cellular retinoic acid binding protein II genes is coordinately regulated in human breast cancer cells

Cited by 60 publications

References 43 publications

An oncogenic function of retinoic acid receptor‑α in the development of laryngeal squamous cell carcinoma

An oncogenic function of retinoic acid receptor‑α in the development of laryngeal squamous cell carcinoma

Acetyl-Keto-β-Boswellic Acid Induces Apoptosis through a Death Receptor 5–Mediated Pathway in Prostate Cancer Cells

Early in vitro passages of breast cancer cells are differentially susceptible to retinoids and differentially express RARβ isoforms

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