Expression of estrogen receptors‐α and ‐β in bladder cancer cell lines and human bladder tumor tissue

Shen, Steven S.; Smith, Carolyn L.; Hsieh, Jer‐Tsong; Yu, Jiang; Kim, Isaac Y.; Jian, Weiguo; Sonpavde, Guru; Ayala, Gustavo; Younes, Mamoun; Lerner, Seth P.

doi:10.1002/cncr.21945

Cited by 183 publications

(170 citation statements)

References 23 publications

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“…Our finding that immortalized and tumor urothelial cells also express significantly higher levels of PCNA than primary cells supports the concept that immortalization, malignant transformation, recurrence, and the development of muscle invasion of human bladder tumor are accompanied by increased expression of PCNA (Syrigos et al 2004). One study reported that bladder cancers express high levels of ERb but low levels of ERa; however, this report considered tumors with 10% or fewer cells expressing ERa as negative for ERa (Shen et al 2006). Thus, low expression of ERa was equaled with no expression.…”

Section: Discussionsupporting

confidence: 81%

Roles of estrogen receptor and in modulating urothelial cell proliferation

Teng¹,

Wang²,

Jarrard³

et al. 2008

Endocrine Related Cancer

108

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We reported previously that both subtypes of estrogen receptors, ERa and ERb, are expressed by human urothelial cells and mediate estrogen-induced cell proliferation in these cells. The aim of this study was to determine the extent to which each ER subtype contributes to urothelial cell proliferation and their possible involvement in the regulation of the cell cycle. We compared the expression of ERa and ERb mRNAs and protein quantitatively in primarily cultured human bladder urothelial cells obtained from six individuals with three immortalized urothelial (E6, E7, and UROtsa) and two bladder cancer cell lines (HTB-9 and T24). We found that all these cells express similar levels of ERb, but immortalized and cancer cells express much higher amounts of ERa than primary cells. Higher levels of ERa mRNA were also observed in the biopsies of bladder transitional cell carcinoma compared with sample from the same bladder unaffected by tumor. Using the ERaselective agonist PPT, the ERb-selective agonist DPN, and specific small interfering RNA against ERa or ERb, we found that ERb predominantly mediates estrogen-induced G1/S transition and cell proliferation in the primary urothelial cells. By contrast, ERa predominantly mediates estrogeninduced G1/S transition and cell proliferation in bladder cancer cell lines. Furthermore, we found that 17b-estradiol (E 2 ) rapidly induces phosphorylation of extracellular signal-regulated kinases, but U0126, a mitogen-activated protein kinase kinase (MEK) inhibitor, does not affect E 2 -induced urothelial cell proliferation. E 2 up-regulated cyclin D1 and cyclin E expression in both the primary and bladder cancer cells, and the cancer cells have higher cyclin D1 and cyclin E expression during G0/G1 phases. Our data suggest that estrogen exerts its effects through different ER subtypes in urothelial cells. Increased expression of ERa may contribute to early induction of cyclin D1 and cyclin E during the cell cycle in bladder cancer cells.

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Section: Discussionsupporting

confidence: 81%

Roles of estrogen receptor and in modulating urothelial cell proliferation

Teng¹,

Wang²,

Jarrard³

et al. 2008

Endocrine Related Cancer

108

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“…They share several functionally conserved structural domains such as the regions responsible for DNA binding, dimerization, ligand binding and ligand-dependent transactivation of gene expression. 72 ERa and ERb have different transcriptional activities in certain ligand, cell type and promoter contexts and also exhibit distinct tissue-and cell type-specific expression patterns. ERa is found predominantly in the normal pituitary, breast, uterus, vagina, testis, liver and kidney, whereas ERb is mainly expressed in thyroid, ovary, prostate, skin, bladder, lungs, gastrointestinal tract, bone and cartilage.…”

mentioning

confidence: 99%

Targeting molecular signaling pathways of Schistosoma haemotobium infection in bladder cancer

et al. 2011

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“…In addition, FHL1 interacts with estrogen receptors and inhibits breast cancer cell growth (24,25). Moreover, estrogen receptors are highly expressed in BC and contribute to BC cell proliferation (26,27). Thus, previous and current findings lead us to think that FHL1 might have a tumor suppressive function through interaction with p21, c-myc, and estrogen receptors in BC.…”

Section: Discussionmentioning

confidence: 86%

CpG hypermethylation of human four-and-a-half LIM domains 1 contributes to migration and invasion activity of human bladder cancer

Matsumoto

Kawakami²,

Enokida³

et al. 2010

Int J Mol Med

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Abstract. We previously reported a simple technique that combines microarray data from clinical bladder cancer (BC) specimens with those from a BC cell line (BOY) treated with a pharmacologic demethylating agent (5-aza-dC). We focused on the human four-and-a-half LIM domains 1 (FHL1) gene which was selected on the basis of previous microarray data analysis. Because LIM domains provide protein-protein binding interfaces, FHL genes play an important role in cellular events, such as focal adhesion and differentiation, by interacting with the target protein as either a repressor or activator. We hypothesized that inactivation of the FHL1 gene through CpG methylation contributes to cell viability including migration and invasion activity of human BC. After 5-aza-dC treatment, the expression levels of FHL1 mRNA transcript markedly increased in all cell lines tested, as shown by real-time reverse transcription-polymerase chain reaction (RT-PCR). The methylation index of FHL1 in our samples was significantly higher in 70 BC specimens than in 10 normal bladder epithelium (NBE) specimens (63.9±25.5 and 0.3±0.2, respectively; p=0.0066). Conversely, FHL1 mRNA expression was significantly lower in the BC specimens than in the NBE ones (0.331±0.12 and 2.498±0.61, respectively; p=0.0011). In addition, significant inhibitions of wound healing (45.78±6.2, and 100±0, respectively; p=0.009) and of cell invasion (18.5±2.3 and 95.2±2.4, respectively; p=0.02) were observed in stable FHL1-transfected cells than in the control BC cells. In conclusion, we found that the mechanism of FHL1 down-regulation in BC is through CpG hypermethylation of the promoter region. FHL1 gene inactivation by CpG hypermethylation may thus contribute to migration and invasion activity of BC.

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Expression of estrogen receptors‐α and ‐β in bladder cancer cell lines and human bladder tumor tissue

Abstract: We report a case of a newborn infant who had simultaneous sialoblastoma and hepatoblastoma tumours at birth. The diagnoses were made on post mortem examination. Both of these are rare tumours in the neonatal period. Pediatr Blood Cancer 2009;52:883–885. © 2009 Wiley‐Liss, Inc.

Cited by 183 publications

References 23 publications

Roles of estrogen receptor and in modulating urothelial cell proliferation

Roles of estrogen receptor and in modulating urothelial cell proliferation

Targeting molecular signaling pathways of Schistosoma haemotobium infection in bladder cancer

CpG hypermethylation of human four-and-a-half LIM domains 1 contributes to migration and invasion activity of human bladder cancer

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