scholarly journals Inhibition of Aurora-A kinase induces cell cycle arrest in epithelial ovarian cancer stem cells by affecting NFĸB pathway

Cell Cycle ◽  
2011 ◽  
Vol 10 (13) ◽  
pp. 2206-2214 ◽  
Author(s):  
Ilana Chefetz ◽  
Jennie C. Holmberg ◽  
Ayesha B. Alvero ◽  
Irene Visintin ◽  
Gil Mor
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Epithelial Ovarian Cancer ◽  
Cell Cycle Arrest ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Ovarian Cancer Stem Cells ◽  
Cycle Arrest

scholarly journals PAWI-2 overcomes tumor stemness and drug resistance via cell cycle arrest in integrin β3-KRAS-dependent pancreatic cancer stem cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jiongjia Cheng ◽  
John R. Cashman
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Cycle Arrest ◽  
Specific Inhibitor ◽  
Feedback Mechanism ◽  
Major Health Problem ◽  
Cycle Arrest ◽  
Drug Inhibition

Abstract Today, pancreatic cancer (PC) remains a major health problem in the US. The fact that cancer stem cells (CSCs) become enriched in humans following anti-cancer therapy implicates CSCs as key contributors to tumor dormancy, metastasis, and relapse in PC. A highly validated CSC model (FGβ3 cells) was used to test a novel compound (PAWI-2) to eradicate CSCs. Compared to parental bulk FG cells, PAWI-2 showed greater potency to inhibit cell viability and self-renewal capacity of FGβ3 cells. For FGβ3 cells, dysregulated integrin β3-KRAS signaling drives tumor progression. PAWI-2 inhibited β3-KRAS signaling independent of KRAS. This is clinically relevant. PAWI-2 targeted the downstream TBK1 phosphorylation cascade that was negatively regulated by optineurin phosphorylation via a feedback mechanism. This was confirmed by TBK1 genetic knockdown or co-treatment with TBK1-specific inhibitor (MRT67307). PAWI-2 also overcame erlotinib (an EGFR inhibitor) resistance in FGβ3 cells more potently than bortezomib. In the proposed working model, optineurin acts as a key regulator to link inhibition of KRAS signaling and cell cycle arrest (G2/M). The findings show PAWI-2 is a new approach to reverse tumor stemness that resensitizes CSC tumors to drug inhibition.

scholarly journals Sulforaphane induces cell cycle arrest by protecting RB-E2F-1 complex in epithelial ovarian cancer cells

2010 ◽  
Vol 9 (1) ◽  
pp. 47 ◽  
Author(s):  
Christopher S Bryant ◽  
Sanjeev Kumar ◽  
Sreedhar Chamala ◽  
Jay Shah ◽  
Jagannath Pal ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Cycle Arrest

scholarly journals Induced growth inhibition, cell cycle arrest and apoptosis in CD133+/CD44+ prostate cancer stem cells by flavopiridol

2014 ◽  
Vol 34 (5) ◽  
pp. 1249-1256 ◽  
Author(s):  
BURAK CEM SONER ◽  
HUSEYIN AKTUG ◽  
EDA ACIKGOZ ◽  
FAHRIYE DUZAGAC ◽  
UMMU GUVEN ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Growth Inhibition ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Prostate Cancer Stem Cells

scholarly journals Radiosensitization effect of hsa-miR-138-2-3p on human laryngeal cancer stem cells

PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3233 ◽  
Author(s):  
Ying Zhu ◽  
Li-Yun Shi ◽  
Yan-Min Lei ◽  
Yan-Hong Bao ◽  
Zhao-Yang Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Cell Proliferation ◽  
Cancer Stem Cells ◽  
Cell Cycle Arrest ◽  
Laryngeal Cancer ◽  
Signal Pathway ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
Radio Sensitivity

BackgroundTreatments that target cancer stem cells play an important role in the controlling and eliminating of tumor initiation as well as in development, progression, and chemotherapy/radiotherapy resistance. In our previous study, we cultured and harvested human laryngeal cancer stem cells (CSCs) and applied microRNA biochips to screen differentially expressed miRNAs that were related to radiation tolerance in irradiated human laryngeal CSCs. According to the predicted genes and pathways of differential miRNAs target, down-regulated expression of hsa-miR-138-2-3p under radiation was thought to play a key role in enhancing the radio-sensitivity in human laryngeal squamous cancer stem cells.MethodTo investigate the radiational enhancement of hsa-miR-138-2-3p, we transfected hsa-miR-138-2-3p mimics that were synthesized based on the sequences of hsa-miR-138-2-3pin vitrointo human laryngeal CSCs (Hep-2, M2e, and TU212 cell lines) to make hsa-miR-138-2-3p overexpressed, and the tumorous specialities of CSCs, like cell proliferation, invasion, apoptosis, cell cycle arrest, and DNA damage were evaluated by CCK-8 assay, clone formation assay, invasion assay, flow cytometry, and comet assay. Furthermore, we explored the signal transduction pathways that regulated the cancer stem cell initiation, development, invasion, apoptosis and cell cycle arrest, which were controlled by hsa-miR-138-2-3p.ResultOverexpressed hsa-miR-138-2-3p played a key role in many anti-cancer biological processes in human laryngeal CSCs: (1) it decreased laryngeal CSCs proliferation and invasion in response to radiotherapy; (2) it increased the proportion of early and late apoptosis in laryngeal CSCs after radiation, raised G1 phase arrest in laryngeal CSCs after radiation, and decreased the proportion of S stage cells of cell cycle that were related to radio-resistance in laryngeal CSCs; (3) it down-regulated the expression of β-catenin in Wnt signal pathway that was related to the tolerance of laryngeal CSCs to radiotherapy; (4) it down-regulated the expression of YAP1 in Hippo signal pathway that regulated cell proliferation, invasion and apoptosis; (5) it up-regulated the expression of p38 and JNK1 in MAPK signal pathway that was concerned to radio-sensitivity.ConclusionIn the present study, it was found that hsa-miR-138-2-3p regulated the Wnt/β-catenin pathways, the Hippo/YAP1 pathways, and the MAPK/p38/JNK1 pathways that were involved in cell proliferation, invasion, apoptosis, cell cycle arrest, radio-resistance and radio-sensitivity in laryngeal CSCs. These results will be useful for a better understanding of the cell biology of hsa-miR-138-2-3p in laryngeal CSCs, and for serving hsa-miR-138-2-3p as a promising biomarker and as a target for diagnosis and for novel anti-cancer therapies for laryngeal cancers.

Abstract 3405: Epithelial ovarian cancer stem cells are the source of metastatic progenitor cells

2011 ◽  
Author(s):  
Gang Yin ◽  
Vinny Craveiro ◽  
Jennie Holmberg ◽  
Han-Hsuan Fu ◽  
Michael K. Montagna ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Epithelial Ovarian Cancer ◽  
Progenitor Cells ◽  
Ovarian Cancer Stem Cells

Estrogen Mustard Induces Cell Cycle Arrest of Human Epithelial Ovarian Cancer Cell Lines

1994 ◽  
Vol 1 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Jaimie D. Nathan ◽  
David L. Keefe ◽  
Marc A. Weinstein ◽  
Zhaocong Chen ◽  
Frederick Naftolin
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Epithelial Ovarian Cancer Cell ◽  
Cycle Arrest ◽  
Ovarian Cancer Cell Lines

LRD-22, a novel dual dithiocarbamatic acid ester, inhibits Aurora-A kinase and induces apoptosis and cell cycle arrest in HepG2 cells

2015 ◽  
Vol 458 (1) ◽  
pp. 201-207 ◽  
Author(s):  
Huiling Wang ◽  
Ridong Li ◽  
Li Li ◽  
Zemei Ge ◽  
Rouli Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
Acid Ester ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Cycle Arrest

scholarly journals Defining the Anti-Cancer Activity of Tricarbonyl Rhenium Complexes: Induction of G2/M Cell Cycle Arrest and Blockade of Aurora-A Kinase Phosphorylation

2017 ◽  
Vol 23 (27) ◽  
pp. 6518-6521 ◽  
Author(s):  
Peter V. Simpson ◽  
Ilaria Casari ◽  
Silvano Paternoster ◽  
Brian W. Skelton ◽  
Marco Falasca ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Aurora A Kinase ◽  
Aurora A ◽  
M Cell ◽  
Rhenium Complexes ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
Kinase Phosphorylation ◽  
Cancer Activity
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