LXR Agonist Regulates the Carcinogenesis of PCa via the SOCS3 Pathway

Fu, Weihua; Yao, Jiwei; Huang, Yan; Li, Qianwei; Li, Weibing; Chen, Zhiwen; He, Fengtian; Zhou, Zhansong; Yan, Jing

doi:10.1159/000356662

Cited by 46 publications

(23 citation statements)

References 35 publications

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“…Several studies have been conducted on the pharmacological potentialities of different NRs, including cancer research, neurodegenerative disorders, and acute brain injury, among others (Aleshin et al, 2013; Fu et al, 2014; Garattini et al, 2014). Among the NR superfamily, PPARs are the most studied ones (Aleshin et al, 2013).…”

Section: Nuclear Receptors (Nrs): Ppars and Their Potential Role In Amentioning

confidence: 99%

Alzheimerâ€™s disease: relevant molecular and physiopathological events affecting amyloid-Î² brain balance and the putative role of PPARs

Zolezzi

Bastías-Candia

Santos

et al. 2014

Front. Aging Neurosci.

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Alzheimer’s disease (AD) is the most common form of age-related dementia. With the expected aging of the human population, the estimated morbidity of AD suggests a critical upcoming health problem. Several lines of research are focused on understanding AD pathophysiology, and although the etiology of the disease remains a matter of intense debate, increased brain levels of amyloid-β (Aβ) appear to be a critical event in triggering a wide range of molecular alterations leading to AD. It has become evident in recent years that an altered balance between production and clearance is responsible for the accumulation of brain Aβ. Moreover, Aβ clearance is a complex event that involves more than neurons and microglia. The status of the blood-brain barrier (BBB) and choroid plexus, along with hepatic functionality, should be considered when Aβ balance is addressed. Furthermore, it has been proposed that exposure to sub-toxic concentrations of metals, such as copper, could both directly affect these secondary structures and act as a seeding or nucleation core that facilitates Aβ aggregation. Recently, we have addressed peroxisomal proliferator-activated receptors (PPARs)-related mechanisms, including the direct modulation of mitochondrial dynamics through the PPARγ-coactivator-1α (PGC-1α) axis and the crosstalk with critical aging- and neurodegenerative-related cellular pathways. In the present review, we revise the current knowledge regarding the molecular aspects of Aβ production and clearance and provide a physiological context that gives a more complete view of this issue. Additionally, we consider the different structures involved in AD-altered Aβ brain balance, which could be directly or indirectly affected by a nuclear receptor (NR)/PPAR-related mechanism.

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Section: Nuclear Receptors (Nrs): Ppars and Their Potential Role In Amentioning

confidence: 99%

Alzheimerâ€™s disease: relevant molecular and physiopathological events affecting amyloid-Î² brain balance and the putative role of PPARs

Zolezzi

Bastías-Candia

Santos

et al. 2014

Front. Aging Neurosci.

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“…Prostate cancer is one of the most commonly diagnosed cancer and the second most common cause of cancer death in men in the US [1,2,3]. About one million new cases are diagnosed with prostate cancer every year and it accounts for nearly 10% of all new cancer cases in men worldwide [4,5].…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA MEG3 Inhibits Cell Proliferation and Induces Apoptosis in Prostate Cancer

Luo

Wang

et al. 2015

Cell Physiol Biochem

158

128

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Background/Aims: Long non-coding RNAs (lncRNAs) play important roles in diverse biological processes, such as cell growth, apoptosis and migration. Although downregulation of lncRNA maternally expressed gene 3 (MEG3) has been identified in several cancers, little is known about its role in prostate cancer progression. The aim of this study was to detect MEG3 expression in clinical prostate cancer tissues, investigate its biological functions in the development of prostate cancer and the underlying mechanism. Methods: MEG3 expression levels were detected by qRT-PCR in both tumor tissues and adjacent non-tumor tissues from 21 prostate cancer patients. The effects of MEG3 on PC3 and DU145 cells were assessed by MTT assay, colony formation assay, western blot and flow cytometry. Transfected PC3 cells were transplanted into nude mice, and the tumor growth curves were determined. Results: MEG3 decreased significantly in prostate cancer tissues relative to adjacent normal tissues. MEG3 inhibited intrinsic cell survival pathway in vitro and in vivo by reducing the protein expression of Bcl-2, enhancing Bax and activating caspase 3. We further demonstrated that MEG3 inhibited the expression of cell cycle regulatory protein Cyclin D1 and induced cell cycle arrest in G0/G1 phase. Conclusions: Our study presents an important role of MEG3 in the molecular etiology of prostate cancer and implicates the potential application of MEG3 in prostate cancer therapy.

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“…Suppressor of cytokine signaling 3 (SOCS3) inhibits PCa cell growth and migration mediated by the JAK/STAT and MAPK pathways [51,52], and becomes an even more critical negative regulator when PTEN and p53 are inactivated [53], as they are in PC3M. SOCS3 downregulation in concert with CXCL1 and CXCR4 induction and IGFBP3 suppression could produce additive or synergistic motogenic signaling.…”

Section: Analysis Of Hgf Motogenic Signaling By Gene Expression Profimentioning

confidence: 99%

Expression array analysis of the hepatocyte growth factor invasive program

Cecchi

Lih

Lee

et al. 2015

Clin Exp Metastasis

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Signaling by human hepatocyte growth factor (hHGF) via its cell surface receptor (MET) drives mitogenesis, motogenesis and morphogenesis in a wide spectrum of target cell types and embryologic, developmental and homeostatic contexts. Oncogenic pathway activation also contributes to tumorigenesis and cancer progression, including tumor angiogenesis and metastasis, in several prevalent malignancies. The HGF gene encodes full-length hHGF and two truncated isoforms known as NK1 and NK2. NK1 induces all three HGF activities at modestly reduced potency, whereas NK2 stimulates only motogenesis and enhances HGF-driven tumor metastasis in transgenic mice. Prior studies have shown that mouse HGF (mHGF) also binds with high affinity to human MET. Here we show that, like NK2, mHGF stimulates cell motility, invasion and spontaneous metastasis of PC3M human prostate adenocarcinoma cells in mice through human MET. To identify target genes and signaling pathways associated with motogenic and metastatic HGF signaling, i.e., the HGF invasive program, gene expression profiling was performed using PC3M cells treated with hHGF, NK2 or mHGF. Results obtained using Ingenuity Pathway Analysis software showed significant overlap with networks and pathways involved in cell movement and metastasis. Interrogating The Cancer Genome Atlas project also identified a subset of 23 gene expression changes in PC3M with a strong tendency for co-occurrence in prostate cancer patients that were associated with significantly decreased disease-free survival.

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LXR Agonist Regulates the Carcinogenesis of PCa via the SOCS3 Pathway

Cited by 46 publications

References 35 publications

Alzheimerâ€™s disease: relevant molecular and physiopathological events affecting amyloid-Î² brain balance and the putative role of PPARs

Alzheimerâ€™s disease: relevant molecular and physiopathological events affecting amyloid-Î² brain balance and the putative role of PPARs

Long Non-Coding RNA MEG3 Inhibits Cell Proliferation and Induces Apoptosis in Prostate Cancer

Expression array analysis of the hepatocyte growth factor invasive program

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