Targeting the PI3K/Akt/mTOR pathway in castration-resistant prostate cancer

Bitting, Rhonda L.; Armstrong, Andrew J.

doi:10.1530/erc-12-0394

Cited by 278 publications

(257 citation statements)

References 126 publications

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“…The AR signaling pathway has been shown to cross-talk with many other cell signaling pathways in prostate cancer, including an array of growth factor signal transduction events, MAPK, and PI3K/Akt pathways (43)(44)(45). In addition, Akt was proved as a downstream target of the Notch signaling pathway in affecting cell growth and apoptosis in prostate cancer cells (46).…”

Section: Discussionmentioning

confidence: 99%

Androgen Receptor Promotes the Oncogenic Function of Overexpressed Jagged1 in Prostate Cancer by Enhancing Cyclin B1 Expression via Akt Phosphorylation

Yan¹,

Guan

Huang³

et al. 2014

Molecular Cancer Research

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The Jagged1, a Notch signaling pathway ligand, had been shown to have a positive correlation with prostate cancer development. Our study for Jagged1 expression in 218 prostate cancer tissue samples also supports this conclusion. However, the detailed molecular mechanism of Jagged1 in promoting the progression of prostate cancer is still unclear. Through cell proliferation examination, androgen receptor (AR) was found to promote the oncogenic function of Jagged1 to enhance the cell proliferation rate by comparing four prostate cancer cell lines, LNCaP, LAPC4, DU145, and PC3, which was further validated through analyzing the survival of 118 patients treated with androgen-deprivation therapy (ADT) with different expression levels of Jagged1 and AR. More importantly, our data showed that Jagged1 combined with AR could increase the phosphorylation level of Akt and, in turn, phosphorylated Akt plays an important role in regulating the expression level of cyclin B1 by interacting with AR and increasing the transcriptional activity of AR. These data indicate that prostate cancer progression regulated by Jagged1 can be dramatically enhanced by combining with AR through promoting Akt activity.

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Section: Discussionmentioning

confidence: 99%

Androgen Receptor Promotes the Oncogenic Function of Overexpressed Jagged1 in Prostate Cancer by Enhancing Cyclin B1 Expression via Akt Phosphorylation

Yan¹,

Guan

Huang³

et al. 2014

Molecular Cancer Research

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“…The phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR pathway is a key signaling pathway in prostate cancer progression [35]. Rapamycin and its analogs (rapalogs) were the first identified inhibitors of the PI3K/Akt/mTOR pathway and were found to inhibit tumor growth in mouse xenograft models derived from PTEN −/− PC-3 and PTEN +/− DU145 cells [36].…”

Section: Discussionmentioning

confidence: 99%

Combined Effects of Fe3O4 Nanoparticles and Chemotherapeutic Agents on Prostate Cancer Cells In Vitro

et al. 2018

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Abstract:Patients with metastatic castration-resistant prostate cancer (mCRPC) have poor outcomes. Docetaxel (DTX)-based therapy is a current standard treatment for patients with mCRPC. Approaches combining conventional chemotherapeutic agents and nanoparticles (NPs), particularly iron oxide NPs, may overcome the serious side effects and drug resistance, resulting in the establishment of new therapeutic strategies. We previously reported the combined effects of

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“…30 PTEN pathway activation is associated with resistance to ADT, disease progression, and poor outcomes in men with prostate cancer. 31 The development and clinical utility of agents that block the interaction between …”

Section: Androgen Receptor Signaling and The Pi3k Pathway And Pten Lomentioning

confidence: 99%

The Changing Therapeutic Landscape in Metastatic Prostate Cancer

Koletsky¹

2017

Oncology &Amp; Hematology Review (US)

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Over the past several years a number of novel and diverse agents have provided a significant clinical benefit for patients with metastatic castration-resistant prostate cancer including abiraterone, enzalutamide, sipuleucel-T, cabazitaxel, and radium-223. The early use of docetaxel or abiraterone at initiation of standard androgen deprivation therapy in patients with metastatic hormone-sensitive prostate cancer has also led to substantial improvements in overall survival. The identification of a truncating mutation in the androgen receptor (ARV7), a biomarker of resistance, may help clarify a more optimal sequencing of hormonal and chemotherapy-based therapies for patients with metastatic disease. The genomic landscape of both primary and metastatic prostate cancer has been an important focal point of translational research. The most widely studied pathways that affect tumorigenesis are the phosphoinositide 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/protein kinase B (AKT) and poly ADP ribose polymerase (PARP) and DNA repair pathways. This review will highlight recent clinical trials which have had a major impact on the management of patients with metastatic disease with an emphasis on treatments driven by common genomic aberrations present in advanced prostate cancer.

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Targeting the PI3K/Akt/mTOR pathway in castration-resistant prostate cancer

Cited by 278 publications

References 126 publications

Androgen Receptor Promotes the Oncogenic Function of Overexpressed Jagged1 in Prostate Cancer by Enhancing Cyclin B1 Expression via Akt Phosphorylation

Androgen Receptor Promotes the Oncogenic Function of Overexpressed Jagged1 in Prostate Cancer by Enhancing Cyclin B1 Expression via Akt Phosphorylation

Combined Effects of Fe3O4 Nanoparticles and Chemotherapeutic Agents on Prostate Cancer Cells In Vitro

The Changing Therapeutic Landscape in Metastatic Prostate Cancer

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