Androgen Receptor Coregulator CTBP1-AS Is Associated With Polycystic Ovary Syndrome in Chinese Women: A Preliminary Study

Liu, Zhenteng; Hao, Cuifang; Song, Dehua; Zhang, Ning; Bao, Hongchu; Qu, Qinglan

doi:10.1177/1933719114565037

Cited by 36 publications

(29 citation statements)

References 57 publications

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“…In accordance with this hypothesis, it has been suggested that aberrant cofactor activity due to mutations or altered expression levels may be a contributing factor to PCa progression. In this situation, we speculate whether PCA3 could behave as an AR modulator, by affecting AR activity, AR and their cofactor interactions, or the expression patterns of AR cofactors, as has been proposed for the CTBP1-AS lncRNAs [38]. In support of our proposals, other authors have reported that ncRNAs are able to modulate AR signaling through their cofactors, such as miR-125b [39].…”

Section: Discussionsupporting

confidence: 84%

PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells

et al. 2016

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Prostate cancer antigen 3 (PCA3) is a prostate-specific long noncoding RNA (lncRNA) involved in the control of prostate cancer (PCa) cell survival, through modulating androgen receptor (AR) signaling. To further comprehend the mechanisms by which PCA3 modulates LNCaP cell survival, we characterized the expression patterns of several cancer-related genes, including those involved in epithelial-mesenchymal transition (EMT) and AR cofactors in response to PCA3 silencing. We also aimed to develop a strategy to stably silence PCA3. Small interfering RNA (siRNA) or short hairpin RNA (shRNA) was used to knock down PCA3 in LNCaP cells. The expression of 84 cancer-related genes, as well as those coding for AR cofactors and EMT markers, was analyzed by quantitative real-time PCR (qRT-PCR). LNCaP-PCA3 silenced cells differentially expressed 16 of the 84 cancer genes tested, mainly those involved in gene expression control and cell signaling. PCA3 knockdown also induced the upregulation of several transcripts coding for AR cofactors and modulated the expression of EMT markers. LNCaP cells transduced with lentivirus vectors carrying an shRNA sequence targeting PCA3 stably downregulated PCA3 expression, causing a significant drop (60 %) in the proportion of LNCaP cells expressing the transgene. In conclusion, our data provide evidence that PCA3 silencing modulates the expression of key cancer-related genes, including those coding for AR cofactors and EMT markers. Transducing LNCaP cells with an shRNA sequence targeting PCA3 led to loss of viability of the cells, supporting the proposal of PCA3 knockdown as a putative therapeutic approach to inhibit PCa growth.

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Section: Discussionsupporting

confidence: 84%

PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells

et al. 2016

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“…Also a novel lncRNA, namely C-Terminal binding protein 1 antisense(CTBP1-AS), which is known to be a regulator of androgen receptor expression was found to be increased in peripheral blood leukocytes of PCOS women. Its overexpression was correlated with high testosterone and HOMA-IR values (198).…”

Section: Non-coding Rnasas Additional Epigenetic Regulators In Pcosmentioning

confidence: 90%

Pathomechanisms of polycystic ovary syndrome Multidimensional approaches

2018

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Polycystic ovary syndrome is a complex endocrine disorder affecting numerous women of reproductive age across the globe. Characterized mainly by irregular menses, hirsutism, skewed LH: FSH ratios and bulky polycystic ovaries, this multifactorial endocrinopathy results in unfavorable reproductive and metabolic sequelae, including anovulatory infertility, type 2 diabetes, metabolic syndrome and cardiovascular disease in later years. Increasing evidence has shown that the manifestation of polycystic ovary syndrome (PCOS) is attributable to a cumulative impact of altered genetic, epigenetic and protein profiles which bring about a systemic dysfunction. While genetic approaches help ascertain role of causal variants in its etiology, tissue-specific epigenetic patterns help in deciphering the auxiliary role of environmental, nutritional and behavioral factors. Proteomics is advantageous, linking both genotype and phenotype and contributing to biomarker discovery. Investigating molecular mechanism underlying PCOS is imperative in order to gain insight into the pathophysiology of PCOS and formulate novel diagnostic and treatment strategies. In this review we have summarized these three aspects, which have been successfully utilized to delineate the pathomechanisms of PCOS.

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“…Total RNA was extracted from tissues using an RNeasy Mini kit (Qiagen, Inc., Valencia, CA, USA), as described previously (26). A BioWaveII spectrophotometer (Biochrom, Ltd., Cambridge, UK) was used to evaluate the concentration and purity of the RNA (A260:A280 ratio).…”

Section: Reverse Transcription-quantitative Polymerase Chain Reactionmentioning

confidence: 99%

Effects of hypoxia‑inducible factor‑1α on endometrial receptivity of women with polycystic ovary syndrome

Dai

Liu

et al. 2017

Mol Med Report

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Embryo implantation is associated with an hypoxic endometrial microenvironment. Hypoxia‑inducible factor‑1α (HIF‑1α) is activated under hypoxic conditions. In the present study, the expression pattern of HIF‑1α in endometrial tissue was investigated and its effects on endometrial receptivity in patients with polycystic ovary syndrome (PCOS) were examined. A total of 81 patients were enrolled for in vitro fertilization and embryo transfer. They were divided into PCOS (n=40) and Control groups (n=41); both groups were further divided based on body weight (overweight and normal weight subgroups). The expressions of HIF‑1α, vascular endothelial growth factor (VEGF) and glucose transporter protein (GLUT)‑1 and GLUT4 were determined by reverse transcription‑quantitative polymerase chain reaction and immunohistochemistry. The results demonstrated that mRNA and protein expression levels of HIF‑1α and VEGF in the PCOS group were significantly lower compared with expression levels in the Control group. However, there were no statistically significant differences in the expression levels of GLUT1 and GLUT4 between groups. In patients with PCOS, GLUT1 and GLUT4 were mainly localized in the nuclei and cytoplasm, but not in the cell membrane. Overweight patients had the lowest expression levels of HIF‑1α, VEGF and GLUT1 expression compared with normal weight patients. In conclusion, HIF‑1α may be involved in the molecular mechanisms of endometrial dysfunction in women with PCOS, particularly in those who are overweight. HIF‑1α might therefore be a novel target for improving the endometrial receptivity and successful embryo implantation in PCOS women.

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Androgen Receptor Coregulator CTBP1-AS Is Associated With Polycystic Ovary Syndrome in Chinese Women: A Preliminary Study

Cited by 36 publications

References 57 publications

PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells

PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells

Pathomechanisms of polycystic ovary syndrome Multidimensional approaches

Effects of hypoxia‑inducible factor‑1α on endometrial receptivity of women with polycystic ovary syndrome

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