ArticleAutophagy2024
Autophagy-dependent expression of osteopontin and its downstream Stat3 signaling contributes to lymphatic malformation progression to lymphangiosarcoma.
Article in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Lapatinib Promotes Apoptosis in Hepatoma Cells by Regulating SPP1 Expression.Anti-cancer agents in medicinal chemistry · 2026Article
- Targeting the Osteopontin-regulated PI3K/AKT signaling pathway: A molecular approach to overcome drug resistance and metastasis in gastrointestinal tumors.World journal of gastrointestinal oncology · 2025Review
- OPN silencing reduces hypoxic pulmonary hypertension via PI3K-AKT-induced protective autophagy.Scientific reports · 2024Article
- Immunoregulatory Roles of Osteopontin in Diseases.Nutrients · 2024Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Lymphatic malformation (LM) is a vascular anomaly from lymphatic endothelial cells (ECs), and a fraction of the patients could progress to the deadly malignant lymphangiosarcoma (LAS). Using genetic tools to delete an essential autophagy gene Rb1cc1/FIP200 or its mutation specifically blocking its autophagy function, we demonstrated that autophagy inhibition abrogated LM progression to LAS although not affecting LM formation in our recently developed mouse model of LAS. Analysis of the mouse models in vivo and vascular tumor cells in vitro showed that autophagy inhibition reduced vascular tumor cell proliferation in vitro and tumorigenicity in vivo without affecting mTORC1 signaling as an oncogenic driver directly. Transcriptional profiling of autophagy-deficient tumor cells and further mechanistic studies revealed a role for osteopontin (OPN) and its downstream Jak/Stat3 signaling in mediating regulation of vascular tumor cells by autophagy. Together, these results support potential new prophylactic strategies to targeting autophagy and/or its downstream OPN expression to prevent progression of the benign LM to the malignant and deadly LAS.
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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.