FARP1 Mediates cMET-Driven Motility in Androgen-Independent Prostate Cancer Cells

Clicks: 1
ID: 314769
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal

Ranked #293 of 301 articles by views in american journal of physiology endocrinology and metabolism

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 301 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Activation of Rac1, a member of the Rho family of small GTPases and a well-established downstream effector of receptor tyrosine kinases (RTKs), has been linked to prostate cancer progression and predicts poor progression in prostate cancer patients. Rac1 and its upstream activators, the Rac guanine nucleotide exchange factors (Rac-GEFs), act as key drivers for RTK-mediated formation of actin-rich protrusions, structures involved in cancer cell motility and invasion. Our previous study identified VAV2 as the main Rac-GEF effector of epidermal growth factor receptor (EGFR) in androgen-independent cellular models. An unbiased RNAi screen targeting Rac-GEFs as effectors of cMET, an RTK frequently overexpressed in castration-resistant prostate cancer (CRPC) and associated with invasion and metastasis, identified FARP1 as a pivotal contributor to Rac1-mediated migration and invasion. Notably, stimulation of cMET with its ligand HGF promotes the formation of actin-rich protrusions through a PI3K-FARP1-Rac1-dependent pathway and independently of VAV2. Furthermore, FARP1 relocalizes to actin-rich protrusions in PC3 cells in response to HGF stimulation. Our results shed light on the distinctive contribution of Rac-GEFs to prostate cancer cell motility via RTKs and identify FARP1 as a crucial cMET-invasive effector. The differential coupling of RTKs to Rac-GEFs underscores the complexities of signaling events leading to Rac1 activation. It provides insight into the RTK effectors that contribute to prostate cancer cell invasiveness.
Reference Key
openalex_W7162205133 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Paola Robayo, Marcelo G. Kazanietz, Martin J. Baker, Mariana Cooke
Journal american journal of physiology endocrinology and metabolism
Year 2026
DOI
10.1210/endocr/bqag062
URL
https://doi.org/10.1210/endocr/bqag062
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.