Results 141 to 150 of about 9,921 (221)

PLK1 inhibitors for the treatment of colorectal cancer

open access: yesAnnals of Medicine & Surgery
Polo-like kinase 1 (PLK1) is a key regulator in mitosis and a highly potent target for anti-cancer therapies. Several PLK1 inhibitors have been developed and evaluated for cancer treatment. However, none of them has yet been approved for clinical usage, mostly due to their low response rates in cancer patients.
Peng Ye   +7 more
openaire   +2 more sources

Tension-sensitive Plk1 phosphorylation on BubR1 regulates the stability of kinetochore microtubule interactions

open access: yes, 2007
Mitotic phosphorylation of the spindle checkpoint component BubR1 is highly conserved throughout evolution. Here, we demonstrate that BubR1 is phosphorylated on the Cdk1 site T620, which triggers the recruitment of Plk1 and phosphorylation of BubR1 by ...
Erich A. Nigg   +9 more
core  

Dynamic and multi-pharmacophore modeling for designing polo-box domain inhibitors.

open access: yesPLoS ONE, 2014
The polo-like kinase 1 (Plk1) is a critical regulator of cell division that is overexpressed in many types of tumors. Thus, a strategy in the treatment of cancer has been to target the kinase activity (ATPase domain) or substrate-binding domain (Polo-box
Sugunadevi Sakkiah   +4 more
doaj   +1 more source

Metabolism in Tumor: Mechanisms and Therapeutic Perspectives

open access: yesMedComm, Volume 7, Issue 9, September 2026.
Tumor metabolic reprogramming converges on three hubs—the SREBP1/2–FASN–SCD1 lipogenic axis, the HIF‐1α–GLUT1–LDHA glycolytic axis, and the LDLR–SCARB1–LXR cholesterol system—which integrate transcriptional, epigenetic (histone lactylation, m6A), and microenvironmental inputs to generate metabolic plasticity, immune evasion, and therapy resistance ...
Jia‐Chen Cheng   +6 more
wiley   +1 more source

Determining expression of wild type PLK1 and drug-resistant mutant C67V PLK1 in cervical cancer cells

open access: yes, 2015
Polo-like kinase 1 has been identified as a potential oncology target due to its importance in regulating cell cycle progression; when highly expressed, wild-type PLK1 can cause cervical cancer, non-small cell lung cancer, gastric carcinoma, breast ...
Kulkarni, Ronit
core   +1 more source

DHCR24 Alleviates DNA Damage in Senescent Vascular Endothelial Cells via ENKUR/Ca2+ Signaling

open access: yesAging Cell, Volume 25, Issue 9, September 2026.
In senescent vascular endothelial cells, DHCR24 deficiency triggers ENKUR‐dependent Ca2+ overload, which in turn induces endoplasmic reticulum stress and mitochondrial dysfunction, ultimately exacerbating oxidative stress and DNA damage. ABSTRACT DNA damage is considered one of the major contributors to aging.
Han Li   +11 more
wiley   +1 more source

Targeting Cell Cycle Vulnerabilities in Cancers: Emerging Strategies for Therapeutic Development

open access: yesCancer Science, Volume 117, Issue 9, Page 2335-2344, September 2026.
Dysregulated cell cycle control often involves alternative compensatory pathways in cancers to maintain its robustness but provide unique targetable vulnerabilities. We overview recent insights on cancer‐specific vulnerabilities across the cell cycle and discuss how these can be used to develop new therapeutic strategies.
Nana Kamakura   +3 more
wiley   +1 more source

Effect of FOXM1 and PLK1 siRNA knockdown on FOXM1 and PLK1 protein expression in PAH HPASMC.

open access: yes, 2019
HPASMC were transfected with control, FOXM1 and PLK1 siRNAs. Following transfection, the cells were cultured in medium containing 5% FBS for a 24 h. Proteins were harvested and probed for FOXM1 (A) or PLK1 (B) using western blots.
Lizhen Wang (340620)   +4 more
core   +1 more source

Proteomic analysis reveals a PLK1-dependent G2/M degradation program and a role for AKAP2 in coordinating the mitotic cytoskeleton

open access: yesCell Reports
Summary: Ubiquitination is an essential regulator of cell division. The kinase Polo-like kinase 1 (PLK1) promotes protein degradation at G2/M phase through the E3 ubiquitin ligase Skp1-Cul1-F box (SCF)βTrCP.
Ryan D. Mouery   +14 more
doaj   +1 more source

Targeting Egfr‐Mediated Cell Proliferation and Lipid Metabolism Separation Effectively Accelerate Liver Regeneration

open access: yesCell Proliferation, Volume 59, Issue 9, September 2026.
AREG coordinates cell proliferation and lipid metabolism reprogramming during liver regeneration and targeting lipid metabolism can promote liver regeneration. ABSTRACT Hepatocyte proliferation restores liver mass after partial hepatectomy (PHx), but the metabolic cost of this process remains unclear.
Yuelei Hu   +7 more
wiley   +1 more source

Home - About - Disclaimer - Privacy