scholarly journals Epigallocatechin-3-gallate inhibits cell growth, induces apoptosis and causes S phase arrest in hepatocellular carcinoma by suppressing the AKT pathway

2014 ◽  
Vol 44 (3) ◽  
pp. 791-796 ◽  
Author(s):  
XIAOYUN SHEN ◽  
YONG ZHANG ◽  
YAN FENG ◽  
LITU ZHANG ◽  
JILIN LI ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
S Phase ◽  
Akt Pathway ◽  
Phase Arrest ◽  
S Phase Arrest

scholarly journals Inhibition of tumor cell growth by adenine is mediated by apoptosis induction and cell cycle S phase arrest

Oncotarget ◽  
2017 ◽  
Vol 8 (55) ◽  
pp. 94286-94296 ◽  
Author(s):  
Ming Han ◽  
Xin Cheng ◽  
Zhiqin Gao ◽  
Rongrong Zhao ◽  
Shizhuang Zhang
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Tumor Cell ◽  
S Phase ◽  
Tumor Cell Growth ◽  
Apoptosis Induction ◽  
Phase Arrest ◽  
S Phase Arrest

scholarly journals Minocycline and cisplatin exert synergistic growth suppression on hepatocellular carcinoma by inducing S phase arrest and apoptosis

2014 ◽  
Vol 32 (2) ◽  
pp. 835-844 ◽  
Author(s):  
FU-YAO LIU ◽  
AN-HUI WU ◽  
SHAO-JUN ZHOU ◽  
YUE-LING DENG ◽  
ZUN-YI ZHANG ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Growth Suppression ◽  
S Phase ◽  
Phase Arrest ◽  
S Phase Arrest

scholarly journals Selenocystine inhibits JEG-3 cell growth in vitro and in vivo by triggering oxidative damage-mediated S-phase arrest and apoptosis

2018 ◽  
Vol 14 (7) ◽  
pp. 1540 ◽  
Author(s):  
Zhigang Wei ◽  
Ming Zhao ◽  
Yajun Hou ◽  
Xiaoting Fu ◽  
Dawei Li ◽  
...  
Keyword(s):  
Cell Growth ◽  
Oxidative Damage ◽  
S Phase ◽  
Phase Arrest ◽  
S Phase Arrest

scholarly journals Eugenol alleviated breast precancerous lesions through HER2/PI3K-AKT pathway-induced cell apoptosis and S-phase arrest

Oncotarget ◽  
2017 ◽  
Vol 8 (34) ◽  
pp. 56296-56310 ◽  
Author(s):  
Min Ma ◽  
Yi Ma ◽  
Gui-Juan Zhang ◽  
Rui Liao ◽  
Xue-Feng Jiang ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Precancerous Lesions ◽  
S Phase ◽  
Akt Pathway ◽  
Phase Arrest ◽  
S Phase Arrest

scholarly journals RSK Inhibition Suppresses AML Proliferation through Activation of DNA Damage Pathways and S Phase Arrest

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2894-2894 ◽  
Author(s):  
Ritika Dutta ◽  
Maria Castellanos ◽  
Bruce Tiu ◽  
Hee-Don Chae ◽  
Kara L. Davis ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dna Damage ◽  
Cell Growth ◽  
Cell Lines ◽  
Conflicts Of Interest ◽  
S Phase ◽  
Hematopoietic Stem ◽  
Phase Arrest ◽  
S Phase Arrest

Abstract The 90 kDa Ribosomal S6 Kinase (RSK), downstream of the ERK signaling pathway, has recently been implicated in a wide variety of cancers, ranging from lung cancer to medulloblastoma, as a driver of cancer cell proliferation and survival. However, its role in Acute Myeloid Leukemia (AML) remains unknown. Thus, the goal of this study was to characterize RSK-dependent signaling pathways in AML, with the overall hypothesis that disruption of this pathway represents a potential strategy for the treatment of AML. The RSK family consists of four gene isoforms, RSK1-4 (RPS6KA1 (RSK1), RPS6KA2 (RSK3), RPS6KA3 (RSK2), RPS6KA4 (RSK4). Knockdown (KD) of RSK1 by shRNA in HL-60 and KG-1 cell lines resulted in reduced AML cell growth in vitro. NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG) mice were injected with 2x106 HL-60 or KG-1 RSK1KD cells and vector control transduced cells in order to investigate the effects of RSK1 KD on AML cell growth and survival in vivo. Mice injected with RSK1 KD cells exhibited prolonged survival by 17 and 21 days respectively for HL-60 and KG-1 cell induced disease (p=0.0023 and 0.0018 respectively). These data indicate that RSK1 knockdown inhibits leukemia progression, and RSK1 is required for maximal proliferation of AML cells in vivo. Pharmacological inhibition of total RSK (RSK1-4) by the small molecule inhibitor BI-D1870 reduced AML cell growth and induced cell death in both AML cell lines and patient samples after treatment for 48 hours. The IC50 for growth inhibition was 1.8 uM for MOLM-13, 1.6 uM for MV-4-11, and 1.9 uM for HL-60 cells. In methylcellulose colony assays, normal hematopoietic stem and progenitor cell proliferation was not affected by RSK inhibition up to a concentration of 15 uM, establishing an approximately 10-fold therapeutic index. To elucidate the mechanism by which RSK inhibition suppresses AML proliferation, we performed cell cycle analysis with HL-60 cells. RSK inhibition by BI-D1870 resulted in delayed S-phase progression and accumulation of cells in late S-phase with increased pH2AX, cPARP, and CDK2/Cyclin A expression, as measured by flow cytometry. These data indicate that inhibition of RSK leads to activation of DNA damage pathways and arrest in S-phase, resulting in apoptosis. Inhibition of CDK activity rescued S-phase arrest, demonstrating that activation and dysregulation of CDK are crucial mediators of RSK inhibitor-induced S-phase arrest. In summary, this is the first study to demonstrate that RSK plays an important role in maintaining AML cell survival and proliferation and to position RSK as a promising target for treatment of AML. Disclosures No relevant conflicts of interest to declare.

scholarly journals Retracted: Down-regulation of Jagged-1 induces cell growth inhibition and S phase arrest in prostate cancer cells

2006 ◽  
Vol 119 (9) ◽  
pp. 2071-2077 ◽  
Author(s):  
Yuxiang Zhang ◽  
Zhiwei Wang ◽  
Fakhara Ahmed ◽  
Sanjeev Banerjee ◽  
Yiwei Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
S Phase ◽  
Cell Growth Inhibition ◽  
Prostate Cancer Cells ◽  
Down Regulation ◽  
Phase Arrest ◽  
S Phase Arrest

scholarly journals Antitumor Effect of Pyrogallol via miR-134 Mediated S Phase Arrest and Inhibition of PI3K/AKT/Skp2/cMyc Signaling in Hepatocellular Carcinoma

2019 ◽  
Vol 20 (16) ◽  
pp. 3985 ◽  
Author(s):  
Hyojin Ahn ◽  
Eunji Im ◽  
Dae Young Lee ◽  
Hyo-Jung Lee ◽  
Ji Hoon Jung ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Protein Expression ◽  
Cyclin E ◽  
S Phase ◽  
Carcinoma Cells ◽  
Antitumor Effects ◽  
Colon Cancers ◽  
Phase Arrest ◽  
Huh7 Cells ◽  
S Phase Arrest

Though Pyrogallol, one of the natural polyphenols, was known to have anti-inflammatory and antitumor effects in breast and colon cancers, the underlying antitumor mechanisms of Pyrogallol, still remain unclear so far. Here, the antitumor mechanisms of Pyrogallol were elucidated in Hep3B and Huh7 hepatocellular carcinoma cells (HCCs). Pyrogallol showed significant cytotoxicity and reduced the number of colonies in Hep3B and Huh7 cells. Interestingly, Pyrogallol induced S-phase arrest and attenuated the protein expression of CyclinD1, Cyclin E, Cyclin A, c-Myc, S-phase kinase-associated protein 2 (Skp2), p-AKT, PI3K, increased the protein expression of p27, and also reduced the fluorescent expression of Cyclin E in Hep3B and Huh7 cells. Furthermore, Pyrogallol disturbed the interaction between Skp2, p27, and c-Myc in Huh7 cells. Notably, Pyrogallol upregulated miRNA levels of miR-134, and conversely, miR-134 inhibition rescued the decreased expression levels of c-Myc, Cyclin E, and Cyclin D1 and increased the expression of p27 by Pyrogallol in Huh7 cells. Taken together, our findings provide insight that Pyrogallol exerts antitumor effects in HCCs via miR-134 activation-mediated S-phase arrest and inhibition of PI3K/AKT/Skp2/cMyc signaling as a potent anticancer candidate.

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