Repression of NR4A1 by a chromatin modifier promotes docetaxel resistance in PC‐3 human prostate cancer cells

Liang, Yong; Su, Yansheng; Zhao, Jie; Wang, He; Li, Wei

doi:10.1016/j.febslet.2013.06.029

Cited by 45 publications

(25 citation statements)

References 41 publications

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“…In prostate cancer cells, NGFI-B can mediate apoptosis via direct transactivation of E2F1 transcription factor [95], direct interaction with anti-apoptotic protein Bcl-B in mitochondria [96], and nucleus-mitochondria translocation [97]. Moreover, overexpression of NGFI-B can enhance chemo-sensitivity of docetaxel in chemo-resistant prostate cancer sublines PC-3R [98]. Since NGFI-B expression can be induced by some pro-apoptotic agents, like calcium ionophore/etoposide [94], PKC-inducer TPA [95] and analogs of gonadotropin-releasing hormone (GnRH) [99] in prostate cancer cells, NGFI-B could be a potential drug target for this cancer.…”

Section: Ngfi-bsmentioning

confidence: 99%

The emerging roles of orphan nuclear receptors in prostate cancer

Cheung

Wang

et al. 2016

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Orphan nuclear receptors are members of the nuclear receptor (NR) superfamily and are so named because their endogenous physiological ligands are either unknown or may not exist. Because of their important regulatory roles in many key physiological processes, dysregulation of signalings controlled by these receptors is associated with many diseases including cancer. Over years, studies of orphan NRs have become an area of great interest because their specific physiological and pathological roles have not been well-defined, and some of them are promising drug targets for diseases. The recently identified synthetic small molecule ligands, acting as agonists or antagonists, to these orphan NRs not only help to understand better their functional roles but also highlight that the signalings mediated by these ligand-independent NRs in diseases could be therapeutically intervened. This review is a summary of the recent advances in elucidating the emerging functional roles of orphan NRs in cancers, especially prostate cancer. In particular, some orphan NRs, RORγ, TR2, TR4, COUP-IFII, ERRα, DAX1 and SHP, exhibit crosstalk or interference with androgen receptor (AR) signaling in either normal or malignant prostatic cells, highlighting their involvement in prostate cancer progression as androgen and AR signaling pathway play critical roles in this process. We also propose that a better understanding of the mechanism of actions of these orphan NRs in prostate gland or prostate cancer could help to evaluate their potential value as therapeutic targets for prostate cancer.

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Section: Ngfi-bsmentioning

confidence: 99%

The emerging roles of orphan nuclear receptors in prostate cancer

Cheung

Wang

et al. 2016

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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“…The upregulation of MTA1 expression contributes to cell transformation, the epithelial-mesenchymal transition (EMT), cell proliferation, anchorageindependent cell growth, cell metastatic ability, angiogenesis, survival, and drug resistance. These effects lead to a higher pathological stage, higher depth of invasion, higher degree of lymph node metastasis, and a poor cancer prognosis [4,8,12,73,74]. …”

Section: The Expression and Roles Of Mta1 In Malignant Tumorsmentioning

confidence: 99%

Subcellular localization of MTA proteins in normal and cancer cells

Liu

Wang

Huang

et al. 2014

Cancer Metastasis Rev

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The subcellular localization of a protein is closely linked to and indicates its function. The metastatic tumor antigen (MTA) family has been under continuous investigation since its identification two decades ago. MTA1, MTA2, and MTA3 are the main members of the MTA family. MTA1, as the representative member of this family, has been shown to be widely expressed in both embryonic and adult tissues, as well as in normal and cancerous conditions, indicating that MTA1 has functions both in physiological and pathological contexts. MTA1 is expressed at a higher level in most cancers than in their normal tissue counterparts. Even in normal cells, MTA1 levels vary a great deal from tissue to tissue. Importantly, MTA1 shows a multiple localization pattern in the cell, as do MTA2 and MTA3. Different MTA components in different subcellular compartments may exert different molecular functions in the cell. Previous studies revealed that MTA1 and MTA2 are predominately localized to the nucleus, while MTA3 is observed in both the nucleus and cytoplasm. Recent studies have reported that MTA1 is located in the nucleus, cytoplasm, and the nuclear envelope. In the nucleus, MTA1 dynamically interacts with chromatin in a MTA1-K532 methylation-dependent manner, whereas cytoplasmic MTA1 binds to the microtubule skeleton. MTA1 also shows a dynamic distribution during the cell cycle. Further investigations are needed to identify the exact subcellular localizations of MTA proteins. We review the sub-cellular localization patterns of the MTA family members and give a comprehensive overview of their respective molecular activities in multiple contexts.

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“…Anchorage-dependent clonogenic ability was assessed as described previously (Yu et al 2013). Approximately 400 cells (transformed with the pCMV6-XL5-PROS1 or vector)/10 cm plastic dish (Falcon; Becton Dickinson, Lincoln Park, NJ, USA) were cultured in media containing either 10% fetal bovine serum (FBS) or 10% FBS-CS at 37°C in a humidified atmosphere of 5% CO 2 and 95% air.…”

Section: Colony Formation Assaymentioning

confidence: 99%

“…RT-PCR was performed as described previously (Yu et al 2013). Amplification of 18S served as the internal control.…”

Section: Reverse Transcription-quantitative Polymerase Chain Reactionmentioning

confidence: 99%

Role of protein S in castration-resistant prostate cancer-like cells

Ning¹,

Zhong²,

Jiang³

et al. 2016

Endocrine-Related Cancer

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Understanding how castration-resistant prostate cancer (CRPC) cells survive the androgen-deprivation condition is crucial for treatment of this advanced prostate cancer (PCa). Here, we reported for the first time the up-regulation of protein S (PROS), an anticoagulant plasma glycoprotein with multiple biological functions, in androgen-insensitive PCa cells and in experimentally induced castration-resistant PCa cells. Overexpression of exogenous PROS in LNCaP cells reduced androgen deprivation-induced apoptosis and enhanced anchorage-dependent clonogenic ability under androgen deprivation condition. Reciprocally, PROS1 knockdown inhibited cell invasiveness and migration, caused the growth inhibition of castration-resistant tumor xenograft under androgen-depleted conditions, and potentiated Taxol (a widely prescribed anti-neoplastic agent)-mediated cell death in PC3 cells. Furthermore, PROS overexpression significantly stimulated AKT activation but failed to evoke oxidative stress in LNCaP cells under normal condition, suggesting that the malignance-promoting effects of the above-mentioned pathway may occur in the order of oxidative stress/PROS/AKT. The potential mechanism may be due to control of oxidative stress-elicited activation of PI3K-AKT-mTOR pathway. Taken together, our gain-of-function, loss-of-function analyses suggest that PROS may facilitate cell proliferation and promote castration resistance in human castration-resistant PCa-like cells via its apoptosis-regulating property. Future study emphasizing on delineating how PROS regulate cellular processes controlling transformation during the development of castration resistance should open new doors for the development of novel therapeutic targets for CRPC.

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Repression of NR4A1 by a chromatin modifier promotes docetaxel resistance in PC‐3 human prostate cancer cells

Cited by 45 publications

References 41 publications

The emerging roles of orphan nuclear receptors in prostate cancer

The emerging roles of orphan nuclear receptors in prostate cancer

Subcellular localization of MTA proteins in normal and cancer cells

Role of protein S in castration-resistant prostate cancer-like cells

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