Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A Positive Feedback Loop between Inactive VHL-Triggered Histone Lactylation and PDGFRβ Signaling Drives Clear Cell Renal Cell Carcinoma Progression

1 Jan 2022

Abstract excerpt

Inactive von Hippel-Lindau (VHL) is linked to metabolic reprogramming and plays pivotal roles in the pathogenesis of clear cell renal cell carcinoma (ccRCC). Here, we identify a previously unknown oncogenic role for inactive VHL in actively triggering histone lactylation to promote ccRCC progression. In patients with ccRCC, inactive VHL positively correlates with the presence of histone lactylation, and high...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer, Hypoxia, and Metabolism
Share to Epigenetics and DNA Methylation
Share to Renal cell carcinoma treatment

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 35637958
DOI: 10.7150/ijbs.73398

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 24 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A Positive Feedback Loop between Inactive VHL-Triggered Histone Lactylation and PDGFRβ Signaling Drives Clear Cell Renal Cell Carcinoma ProgressionPMID 35637958Read ↗

Histone lactylation-related genes correlate with the molecular patterns and functions of cancer-associated fibroblasts and have significant clinical implications in clear cell renal cell carcinomaSemantic proximity Read ↗

VHL mutation-mediated SALL4 overexpression promotes tumorigenesis and vascularization of clear cell renal cell carcinoma via Akt/GSK-3β signaling.Semantic proximity Read ↗

VHL loss reprograms the immune landscape to promote an inflammatory myeloid microenvironment in renal tumorigenesisSemantic proximity Read ↗

Lysyl oxidase drives ccRCC progression by coordinating HIF-2α transcription program with tumor microenvironmentSemantic proximity Read ↗

Lysine methyltransferase 5C increases the proliferation and metastatic abilities of clear cell renal cell carcinoma via aerobic glycolysisSemantic proximity Read ↗

Sequential pathogenesis of metastatic VHL mutant clear cell renal cell carcinoma: putting it together with a translational perspective.Semantic proximity Read ↗

VHL missense mutation delineate aggressive clear cell renal cell carcinoma subtype with favorable immunotherapeutic responseSemantic proximity Read ↗

HIF-1α/LAPTM5/STAT1 axis promotes the malignant progression of clear cell renal cell carcinomaSemantic proximity Read ↗

A clearer view of the molecular complexity of clear cell renal cell carcinoma.Semantic proximity Read ↗

Lactylation modifications in urological diseases: molecular mechanisms and biological implicationsSemantic proximity Read ↗

The von Hippel-Lindau tumor suppressor protein regulates gene expression and tumor growth through histone demethylase JARID1C.Semantic proximity Read ↗

Deubiquitinase UCHL1 stabilizes KDM4B to augment VEGF signaling and confer bevacizumab resistance in clear cell renal cell carcinomaSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.