Role of Transcriptional Corepressor CtBP1 in Prostate Cancer Progression

Wang, Rui; Asangani, Irfan A.; Chakravarthi, Balabhadrapatruni V. S. K.; Ateeq, Bushra; Lonigro, Robert J.; Cao, Qi; Mani, Ram S.; Camacho, Daniel F.; McGregor, Natalie; Schumann, Taibriana; Jing, Xiaojun; Menawat, Radhika; Tomlins, Scott A.; Zheng, Heng; Otte, Arie P.; Mehra, Rohit; Siddiqui, Javed; Dhanasekaran, Saravana M.; Nyati, Mukesh K.; Pienta, Kenneth J.; Palanisamy, Nallasivam; Kunju, Lakshmi P.; Rubin, Mark A.; Chinnaiyan, Arul M.; Varambally, Sooryanarayana

doi:10.1593/neo.121192

Cited by 65 publications

(88 citation statements)

References 35 publications

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“…Our data also showed that restoration of miR-188-5p can promote PC-3 cells' sensitivity to adriamycin via the suppression of LAPTM4B. Previous study demonstrated that LAPTM4B can motivate multidrug resistance of cancer cells by promoting drug efflux and anti-apoptosis by activating PI3K/AKT signaling [15,16,32]. Collectively, these results indicated that restoration of miR-188-5p suppressed PI3K/AKT signaling pathway by targeting LAPTM4B.…”

Section: Discussionsupporting

confidence: 72%

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miR-188-5p inhibits tumour growth and metastasis in prostate cancer by repressing LAPTM4B expression

Zhang

et al. 2015

Oncotarget

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Elucidation of the molecular targets and pathways regulated by the tumour-suppressive miRNAs can shed light on the oncogenic and metastatic processes in prostate cancer (PCa). Using miRNA profiling analysis, we find that miR-188-5p was significantly down-regulated in metastatic PCa. Down-regulation of miR-188-5p is an independent prognostic factor for poor overall and biochemical recurrence-free survival. Restoration of miR-188-5p in PCa cells (PC-3 and LNCaP) significantly suppresses proliferation, migration and invasion in vitro and inhibits tumour growth and metastasis in vivo. We also find overexpression of miR-188-5p in PC-3 cells can significantly enhance the cells' chemosensitivity to adriamycin. LAPTM4B is subsequently identified as a direct target of miR-188-5p in PCa, and is found to be significantly over-expressed in PCa. Knockdown of LAPTM4B phenotypically copies miR-188-5p-induced phenotypes, whereas ectopic expression of LAPTM4B reverses the effects of miR-188-5p. We also find that restoration of miR-188-5p can inhibit the PI3K/AKT signaling pathway via the suppression of LAPTM4B. Taken together, this is the first report unveils that miR-188-5p acts as a tumour suppressor in PCa and may therefore serve as a useful therapeutic target for the development of new anticancer therapy.

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Section: Discussionsupporting

confidence: 72%

“…Proliferation and metastasis, two hallmarks of malignancy, are the leading causes for the cancer-related death [32,33]. Ectopic miR-188-5p expression significantly repressed the proliferation, migration and invasion of PC-3 and LNCaP cells in vitro , and tumour growth and metastasis in vivo .…”

Section: Discussionmentioning

confidence: 99%

miR-188-5p inhibits tumour growth and metastasis in prostate cancer by repressing LAPTM4B expression

Zhang

et al. 2015

Oncotarget

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“…Increased expression and mislocalization of CtBP is evident in prostate cancer cells. Furthermore, knockdown of CtBP in prostate cancer cell lines inhibited cell invasion (140). In melanoma, CtBPs are shown to repress BRCA1 and p16INK4a (141).…”

Section: Other Regulators Of Ctbp In Cancermentioning

confidence: 98%

C-terminal binding proteins: central players in development and disease

Stankiewicz¹,

Gray²,

Winter

et al. 2014

Biomolecular Concepts

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C-terminal binding proteins (CtBPs) were initially identified as binding partners for the E1A-transforming proteins. Although the invertebrate genome encodes one CtBP protein, two CtBPs (CtBP1 and CtBP2) are encoded by the vertebrate genome and perform both unique and duplicative functions. CtBP1 and CtBP2 are closely related and act as transcriptional corepressors when activated by nicotinamide adenine dinucleotide binding to their dehydrogenase domains. CtBPs exert transcriptional repression primarily via recruitment of a corepressor complex to DNA that consists of histone deacetylases (HDACs) and histone methyltransferases, although CtBPs can also repress transcription through HDAC-independent mechanisms. More recent studies have demonstrated a critical function for CtBPs in the transcriptional repression of pro-apoptotic genes such as Bax, Puma, Bik, and Noxa. Nonetheless, although recent efforts have characterized the essential involvement of CtBPs in promoting cellular survival, the dysregulation of CtBPs in both neurodegenerative disease and cancers remains to be fully elucidated.

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“…3A shows that CTBP1, a well-recognized EMT regulator [18], was up-regulated in endometrial carcinoma cells following BTR treatment. To confirm whether CTBP1 is involved in BTR-induced EMT, we suppressed endogenous CTBP1 levels using CTBP1-siRNA [27]. Western blotting showed that the expression level of CTBP1 was significantly inhibited by CTBP1-siRNA, and the BTR-induced up-regulation of N-cadherin/Vimentin and down-regulation of E-cadherin were reversed by CTBP1-siRNA (Fig.…”

Section: Resultsmentioning

confidence: 99%

Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition

Wang

Dai

Zhou

et al. 2017

Cell Physiol Biochem

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Background/Aims: Benzotriazole (BTR) and its derivatives, such as intermediates and UV stabilizers, are important man-made organic chemicals found in everyday life that have been recently identified as environmental toxins and a threat to female reproductive health. Previous studies have shown that BTR could act as a carcinogen by mimicking estrogen. Environmental estrogen mimics could promote the initiation and development of female cancers, such as endometrial carcinoma, a type of estrogenic-sensitive malignancy. However, there is little information on the relationship between BTR and endometrial carcinoma. In this study, we aimed to demonstrate the biological function of BTR in endometrial carcinoma and explored the underlying mechanism. Methods: The CCK-8 assay was performed to detect cell viability; transwell-filter assay was used to assess cell invasion; gene microarray analysis was employed to determine gene expression patterns in response to BTR treatment; western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were carried out to detect the expression levels of BTR-related genes. Results: Our data showed that BTR could induce the invasion and migration of endometrial carcinoma cells (Ishikawa and HEC-1-B). In addition, BTR increased the expression level of CTBP1, which could enhance the epithelial-mesenchymal transition (EMT) in cancer cells. Moreover, CTBP1 silencing reversed the effect of BTR on EMT progression in endometrial carcinoma cells. Conclusion: This study indicates that BTR could act as a carcinogen to promote the development of endometrial carcinoma mainly through CTBP1-mediated EMT, which deserves more attention.

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Role of Transcriptional Corepressor CtBP1 in Prostate Cancer Progression

Cited by 65 publications

References 35 publications

miR-188-5p inhibits tumour growth and metastasis in prostate cancer by repressing LAPTM4B expression

miR-188-5p inhibits tumour growth and metastasis in prostate cancer by repressing LAPTM4B expression

C-terminal binding proteins: central players in development and disease

Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition

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