Peer review process
Revised: This Reviewed Preprint has been revised by the authors in response to the previous round of peer review; the eLife assessment and the public reviews have been updated where necessary by the editors and peer reviewers.
Read more about eLife’s peer review process.Editors
- Reviewing EditorRachel EvansKing's College London, London, United Kingdom
- Senior EditorRichard WhiteUniversity of Oxford, Oxford, United Kingdom
Reviewer #1 (Public review):
Summary:
The manuscript entitled "Phosphodiesterase 1A Physically Interacts with YTHDF2 and Reinforces the Progression of Non-Small Cell Lung Cancer" explores the role of PDE1A in promoting NSCLC progression by binding to the m6A reader YTHDF2 and regulating the mRNA stability of several novel target genes, consequently activating the STAT3 pathway and leading to metastasis and drug resistance.
Strengths:
The study addresses a novel mechanism involving PDE1A and YTHDF2 interaction in NSCLC, contributing to our understanding of cancer progression.
Reviewer #2 (Public review):
Summary:
This revised manuscript investigates the role and the mechanism by which PDE1 impacts NSCLC progression, providing solid data to demonstrate that PDE1 binds to m6A reader YTHDF2, in turn, regulating STAT3 signaling pathway through its interaction, promoting metastasis and angiogenesis. The study provides a valuable information to lung cancer field.
Strength:
The study uncovers a novel PDE1A/YTHDF2/SOCS2/STAT3 pathway in NSCLC progression and the findings provide a potential treatment strategy for NSCLC patients with metastasis.
Weakness:
Given that physical interaction of PDE1A and YTHDF2 plays a critical role in PDE1A-mediated NSCLC metastasis, the in vivo data to show that YTHDF2 mimics the effect of PDE1A in metastasis will strength the manuscript although this point was mentioned in the revised manuscript.