scholarly journals Metformin Eliminates CD133high/CD44high Prostate Cancer Stem Cells Via Cell Cycle Arrest and Apoptosis

2022 ◽  
Author(s):  
Eda Acikgoz
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Prostate Cancer Stem Cells

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 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 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.

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

Cell cycle arrest and apoptogenic properties of opium alkaloids noscapine and papaverine on breast cancer stem cells

2015 ◽  
Vol 25 (5) ◽  
pp. 388-395 ◽  
Author(s):  
Saharolsadat Sajadian ◽  
Melody Vatankhah ◽  
Maryam Majdzadeh ◽  
Shide Montaser Kouhsari ◽  
Mohammad Hossein Ghahremani ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Cycle Arrest ◽  
Breast Cancer Stem Cells ◽  
Opium Alkaloids ◽  
Cycle Arrest

scholarly journals Co-delivery of Salinomycin and Curcumin for Cancer Stem Cell Treatment by Inhibition of Cell Proliferation, Cell Cycle Arrest, and Epithelial–Mesenchymal Transition

2021 ◽  
Vol 8 ◽  
Author(s):  
Yongmei Zhao ◽  
Kaikai Wang ◽  
Yuanlin Zheng ◽  
Xiaobao Zeng ◽  
Yi Chieh Lim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Cycle Arrest ◽  
Epithelial Mesenchymal Transition ◽  
Disease Recurrence ◽  
Cell Surface Glycoprotein ◽  
Efficient Treatment ◽  
Mesenchymal Transition ◽  
Cycle Arrest

Malignant cancer is a devastating disease often associated with a poor clinical prognosis. For decades, modern drug discoveries have attempted to identify potential modulators that can impede tumor growth. Cancer stem cells however are more resistant to therapeutic intervention, which often leads to treatment failure and subsequent disease recurrence. Here in this study, we have developed a specific multi-target drug delivery nanoparticle system against breast cancer stem cells (BCSCs). Therapeutic agents curcumin and salinomycin have complementary functions of limiting therapeutic resistance and eliciting cellular death, respectively. By conjugation of CD44 cell-surface glycoprotein with poly(lactic-co-glycolic acid) (PLGA) nanoparticles that are loaded with curcumin and salinomycin, we investigated the cellular uptake of BCSCs, drug release, and therapeutic efficacy against BCSCs. We determined CD44-targeting co-delivery nanoparticles are highly efficacious against BCSCs by inducing G1 cell cycle arrest and limiting epithelial–mesenchymal transition. This curcumin and salinomycin co-delivery system can be an efficient treatment approach to target malignant cancer without the repercussion of disease recurrence.

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