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

PRMT5 competitively binds to CDK4 to promote G1-S transition upon glucose induction in hepatocellular carcinoma.

Oncotarget - 1 Nov 2016

Yang Hao, Zhao Xiaoping, Zhao Li, Liu Liu, Li Jiajin, Jia Wenzhi, Liu Jianjun, Huang Gang

Abstract excerpt

Although cancer cells are known to be "addicted" to glucose, the effect of glucose in proliferation of these cells remains elusive. Here, we report that upon glucose induction, protein arginine methyltransferase 5 (PRMT5) exerts a profound effect on the G1-S cell cycle progression via directly interacting with cyclin dependent kinase 4 (CDK4) in hepatocellular carcinoma (HCC). Upregulation of both PRMT5 and CDK4...

Read the complete abstract on PubMed

Topics

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

Share to Cyclin-Dependent Kinase 4
Share to Cyclin-Dependent Kinase Inhibitor p16

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclin-Dependent Kinase Inhibitor p18

Share to E2F Transcription Factors

Share to G1 Phase Cell Cycle Checkpoints

Share to Mice, SCID

Share to Protein-Arginine N-Methyltransferases

Share to Retinoblastoma Binding Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 27708221
DOI: 10.18632/oncotarget.12351
PMCID: PMC5342150

Genes

CDK4
PRMT5

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

PRMT5 competitively binds to CDK4 to promote G1-S transition upon glucose induction in hepatocellular carcinoma.PMID 27708221Read ↗

PRMT5 is required for cell-cycle progression and p53 tumor suppressor function.Semantic proximity Read ↗

The Emerging Roles of the Metabolic Regulator G6PD in Human CancersSemantic proximity Read ↗

METTL5 stabilizes c‐Myc by facilitating USP5 translation to reprogram glucose metabolism and promote hepatocellular carcinoma progressionSemantic proximity Read ↗

Glucose-6-phosphate Dehydrogenase (G6PD): the Role in Tumor Progression and ImmunotherapySemantic proximity Read ↗

GLUT5-overexpression-related tumorigenic implicationsSemantic proximity Read ↗

Glucose-6-phosphate Dehydrogenase: a Biomarker and Potential Therapeutic Target for CancerSemantic proximity Read ↗

Glucose-regulated proteins in cancer: molecular mechanisms and therapeutic potentialSemantic proximity Read ↗

The protein arginine methyltransferase 5 promotes malignant phenotype of hepatocellular carcinoma cells and is associated with adverse patient outcomes after curative hepatectomy.Semantic proximity Read ↗

SNHG15 inhibits the tricarboxylic acid cycle and promotes HCC progression by facilitating the phosphorylation of PDK1 and PDHE1αSemantic proximity Read ↗

LYRM2 Promotes the Growth and Metastasis of Hepatocellular Carcinoma via Enhancing HIF ‐1α‐Dependent Glucose Metabolic ReprogrammingSemantic proximity Read ↗

Protein arginine methyltransferase 5 (PRMT5) is an actionable therapeutic target in CDK4/6 inhibitor-resistant ER+/RB-deficient breast cancerSemantic proximity Read ↗

CDK 2 positively regulates aerobic glycolysis by suppressing SIRT 5 in gastric cancerSemantic proximity Read ↗

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