ArticleMolecular biology of the cell2015
Cross-talk between androgen receptor/filamin A and TrkA regulates neurite outgrowth in PC12 cells.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 45 citations in OpenAlex.
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- TrkB Agonist Treatment Decreases Hippocampal Testosterone Contents in a Sex-Dependent Manner Following Neonatal Hypoxia and Ischemia.Biomolecules · 2026Article
- Nerve growth factor: what can surgeons and oncologists learn from a neurological and psychological biomarker?Molecular medicine (Cambridge, Mass.) · 2025Review
- Androgens as the "old age stick" in skeletal muscle.Cell communication and signaling : CCS · 2025Review
- Role of the androgen receptor in melanoma aggressiveness.Cell death & disease · 2025Article
- Unleashing the power of peptides in prostate cancer immunotherapy: mechanism, facts and perspectives.Frontiers in pharmacology · 2025Review
- Mutant androgen receptor induces neurite loss and senescence independently of ARE binding in a neuronal model of SBMA.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Filamin A cooperates with the androgen receptor in preventing skeletal muscle senescence.Cell death discovery · 2023Article
- The nerve growth factor-delivered signals in prostate cancer and its associated microenvironment: when the dialogue replaces the monologue.Cell & bioscience · 2023Review
- Article
- Inhibition of Vps34 and p110δ PI3K Impairs Migration, Invasion and Three-Dimensional Spheroid Growth in Breast Cancer Cells.International journal of molecular sciences · 2022Article
- New Insights and Emerging Therapeutic Approaches in Prostate Cancer.Frontiers in endocrinology · 2022Review
- Article
- The androgen receptor/filamin A complex as a target in prostate cancer microenvironment.Cell death & disease · 2021Article
- Targeting the Nerve Growth Factor Signaling Impairs the Proliferative and Migratory Phenotype of Triple-Negative Breast Cancer Cells.Frontiers in cell and developmental biology · 2021Article
- The MYH9 Cytoskeletal Protein Is a Novel Corepressor of Androgen Receptors.Frontiers in oncology · 2021Article
- Hits Discovery on the Androgen Receptor: In Silico Approaches to Identify Agonist Compounds.Cells · 2019Article
- From psychology to physicality: how nerve growth factor transduces early life stress into gastrointestinal motility disorders later in life.Cell cycle (Georgetown, Tex.) · 2019Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Steroids and growth factors control neuronal development through their receptors under physiological and pathological conditions. We show that PC12 cells harbor endogenous androgen receptor (AR), whose inhibition or silencing strongly interferes with neuritogenesis stimulated by the nonaromatizable synthetic androgen R1881 or NGF. This implies a role for AR not only in androgen signaling, but also in NGF signaling. In turn, a pharmacological TrkA inhibitor interferes with NGF- or androgen-induced neuritogenesis. In addition, androgen or NGF triggers AR association with TrkA, TrkA interaction with PI3-K δ, and downstream activation of PI3-K δ and Rac in PC12 cells. Once associated with AR, filamin A (FlnA) contributes to androgen or NGF neuritogenesis, likely through its interaction with signaling effectors, such as Rac. This study thus identifies a previously unrecognized reciprocal cross-talk between AR and TrkA, which is controlled by β1 integrin. The contribution of FlnA/AR complex and PI3-K δ to neuronal differentiation by androgens and NGF is also novel. This is the first description of AR function in PC12 cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.