PI3K pathway in prostate cancer: All resistant roads lead to PI3K.

  title={PI3K pathway in prostate cancer: All resistant roads lead to PI3K.},
  author={Soonbum Park and Young Sik Kim and David Kim and Insuk So and Ju-Hong Jeon},
  journal={Biochimica et biophysica acta. Reviews on cancer},
  volume={1870 2},
PIM kinase inhibition: co-targeted therapeutic approaches in prostate cancer
The rationale and basis for co-targeting PIM with inhibitors of PI3K/mTOR/AKT, JAK/STAT, MYC, stemness, and RNA Polymerase I transcription, along with other therapies, including androgen deprivation, radiotherapy, chemotherapy, and immunotherapy are presented.
Co-targeting PIM and PI3K/mTOR using multikinase inhibitor AUM302 and a combination of AZD-1208 and BEZ235 in prostate cancer
The preclinical inhibitor AUM302, used at a lower dose, elicited a comparable or superior functional outcome compared with combined AZD-1208 + BEZ235, which have been investigated in clinical trials, and could help to reduce treatment toxicity in future trials.
Bloom Syndrome Protein Activates AKT and PRAS40 in Prostate Cancer Cells
It is demonstrated that Bloom syndrome protein activates AKT and PRAS40 to promote PC cell proliferation and survival and proposed that ROS act in concert with BLM to facilitate PC oncogenesis, potentially via further enhancing AKT signaling and downregulating PTEN expression.
Evolving Castration Resistance and Prostate Specific Membrane Antigen Expression: Implications for Patient Management
Simple Summary This review is a summary of recent findings on the role of prostate-specific membrane antigen (PSMA) in metastatic castration-resistant prostate cancer (mCRPC) and how they can be
Proteomic analysis of extracellular vesicles identified PI3K pathway as a potential therapeutic target for cabazitaxel‐resistant prostate cancer
This work aimed to identify candidate therapeutic targets for CBZ‐resistance by proteomic analysis of extracellular vesicles isolated from serum of DOC‐resistant PC patients who later developed CBZ•resistance as well as those harvested from culture medium of docetaxel‐ and CBZ-resistant PC cell lines.
Combined mTOR/MEK inhibition prevents proliferation and induces apoptosis in NF2-mutant tumors.
  • N. Li, X-Y Lu, W. Li
  • Biology, Medicine
    European review for medical and pharmacological sciences
  • 2019
It is found that PI3K/mTOR inhibitor could decrease the proliferation of NF-2 mutation tumor cell lines by enhancing apoptosis, while the combination of two drugs might have a better effect.
Cellular and Molecular Mechanisms Underlying Prostate Cancer Development: Therapeutic Implications
The ensemble of these molecular studies has led to suggest the existence of two main molecular groups of prostate cancers: one characterized by the presence of ERG rearrangements and by the frequent mutations in the E3 ubiquitin ligase adapter SPOP and/or deletion of CDH1, a chromatin remodeling factor.


The PI3K pathway as drug target in human cancer.
This review will discuss how PI3K signaling affects the growth and survival of tumor cells and consider how inhibitors of this pathway, either alone or in combination with other therapeutics, can be used for the treatment of cancer.
Inhibition of the PI3K/AKT/mTOR Pathway in Solid Tumors.
  • P. LoRusso
  • Biology
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • 2016
To maximize therapeutic benefit, drug combinations and schedules must be explored to identify those with the highest efficacy and lowest toxicity overlap, and defining appropriate patient subpopulations, for both monotherapy and drug combinations, will be important.
Targeting PI3K in Cancer: Impact on Tumor Cells, Their Protective Stroma, Angiogenesis, and Immunotherapy.
It is proposed that PI3K isoform-selective inhibitors may be exploited in the context of cancer immunotherapy and by targeting angiogenesis to improve drug and immune cell delivery.
Development of PI3K inhibitors: lessons learned from early clinical trials
This Review focuses on early clinical and translational data related to inhibitors of the PI3K/AKT/mTOR pathway, as these data will likely guide the further clinical development of such agents and describes predictive biomarkers explored in clinical trials and preclinical mechanisms of resistance.
The PTEN–PI3K pathway: of feedbacks and cross-talks
The current status of the PTEN– PI3K signaling pathway is reviewed with special emphasis on the most recent data on targets and regulation of thePTEN–PI3K axis, which provides novel provocative therapeutic implications based on the targeted modulation of PI3k-cross-talking signals.
Targeting the PI3K/Akt/mTOR pathway in castration-resistant prostate cancer.
The role of the PI3K/Akt/mTOR pathway in prostate cancer and the potential use of pathway inhibitors as single agents or in combination in the evolving treatment landscape of castration-resistant prostate cancer are reviewed.
Targeting PI3K/Akt/mTOR signaling pathway in the treatment of prostate cancer radioresistance.
PI3K-AKT-mTOR signaling in prostate cancer progression and androgen deprivation therapy resistance
The relevance of the PI3K-AKT-mTOR pathway in PCa progression and castration resistance is explored in order to inform the clinical development of specific pathway inhibitors in advanced PCa.
AR Signaling and the PI3K Pathway in Prostate Cancer
The role of the PI3K pathway in prostate cancer and, in particular, its association with androgen receptor signaling in the pathogenesis and evolution of prostate cancer is outlined, as well as a review of the clinical utility ofPI3K targeting.