Changes in Cell Cycle Phase Distribution during Growth of Heterotransplanted Squamous Cell Carcinoma

2015 ◽  
pp. 186-189
Author(s):  
Johan Wennerberg ◽  
Claes Trop�
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Phase Distribution ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Cell Cycle Phase Distribution

scholarly journals mTOR Inhibitor PP242 Increases Antitumor Activity of Sulforaphane by Blocking Akt/mTOR Pathway in Esophageal Squamous Cell Carcinoma

2021 ◽  
Author(s):  
Zhaoming Lu ◽  
Yalin Zhang ◽  
Yujia Xu ◽  
Huiyun Wei ◽  
Wen Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Molecular Mechanism ◽  
Squamous Cell ◽  
Cell Cycle Phase ◽  
Mtor Pathway ◽  
Cycle Phase ◽  
Anti Tumor Activity

Abstract This study aims to explore the anti-tumor activity of Sulforaphane (SFN) alone and combined with Akt/mTOR pathway inhibitors as well as the potential molecular mechanism in esophageal squamous cell carcinoma (ESCC). MTT assay, clone formation experiment, wound healing assays, flow cytometry, Western blot and xenograft experiment were used to test the effects and molecular mechanism of SFN alone or combined with Akt/mTOR inhibitors on proliferation, migration, cell cycle phase, apoptosis of ESCC cells and tumor growth, respectively. The results showed that SFN significantly inhibited the viability and induced apoptosis of ECa109 and EC9706 cells in a dose-dependent manner by increasing the expression of the apoptotic proteins Cleaved-caspase 9. SFN combined with PP242, but not MK2206 and RAD001, had synergetic inhibition effects on the proliferation of ESCC cells. Moreover, the combination of SFN and PP242 had better inhibiting efficiency on clone formation, migratory, cell cycle phase and the growth of xenografts of ESCC cells, as well as the more powerful apoptosis-inducing effects on ESCC cells. Results of protein expression showed that PP242 abrogated the promotion effects of SFN on p-p70S6K (Thr389) and p-Akt (Ser473). These foundings demonstrated PP242 enhances the anti-tumor activity of SFN by blocking the activation of Akt/mTOR pathway by SFN in ESCC.

scholarly journals Oxymatrine DownregulatesHPV16E7Expression and Inhibits Cell Proliferation in Laryngeal Squamous Cell Carcinoma Hep-2 Cells In Vitro

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Xin-Jiang Ying ◽  
Bin Jin ◽  
Xin-Wei Chen ◽  
Jin Xie ◽  
Hong-Ming Xu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Carcinoma ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Phase Distribution ◽  
G1 Phase ◽  
Cycle Phase

Objective. To investigate the possible mechanisms of oxymatrine’s role in anti laryngeal squamous cell carcinoma.Methods. We examined the effects of oxymatrine on the proliferation, cell cycle phase distribution, apoptosis, and the protein and mRNA expression levels ofHPV16E7gene in laryngeal carcinoma Hep-2 cells in vitro. TheHPV16E7siRNA inhibition was also done to confirm the effect of downregulatingHPV16E7on the proliferation in Hep-2 cells.Results. Oxymatrine significantly inhibited the growth and proliferation of Hep-2 cells in a dose-dependence and time-dependence manner. Oxymatrine blocked Hep-2 cells in G0/G1 phase, resulting in an obvious accumulation of G0/G1 phase cells while decreasing S phase cells. Oxymatrine induced apoptosis of Hep-2 cells, whose apoptotic rate amounted to about 42% after treatment with 7 mg/mL oxymatrine for 72 h. Oxymatrine also downregulated the expression ofHPV16E7gene, as determined by the western blotting and reverse transcription-polymerase chain reaction analysis. Knockdown ofHPV16E7effectively inhibited the proliferation of Hep-2 cells.Conclusions. Oxymatrine inhibits the proliferation and induces apoptosis of laryngeal carcinoma Hep-2 cells, which might be mediated by a significant cell cycle arrest in G0/G1 phase and downregulation ofHPV16E7gene. Oxymatrine is considered to be a likely preventive and curative candidate for laryngeal cancer.

scholarly journals The G2-phase enriched lncRNA SNHG26 is necessary for proper cell cycle progression and proliferation

2021 ◽  
Author(s):  
Helle Samdal ◽  
Siv A. Hegre ◽  
Konika Chawla ◽  
Nina-Beate Liabakk ◽  
Per A. Aas ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rna Polymerase Ii ◽  
Cell Cycle Progression ◽  
Phase Distribution ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Cycle Progression ◽  
Chip Sequencing ◽  
Cell Cycle Phase Distribution ◽  
Regulation Of Cell Cycle

AbstractLong noncoding RNAs (lncRNAs) are involved in the regulation of cell cycle, although only a few have been functionally characterized. By combining RNA sequencing and ChIP sequencing of cell cycle synchronized HaCaT cells we have previously identified lncRNAs highly enriched for cell cycle functions. Based on a cyclic expression profile and an overall high correlation to histone 3 lysine 4 trimethylation (H3K4me3) and RNA polymerase II (Pol II) signals, the lncRNA SNHG26 was identified as a top candidate. In the present study we report that downregulation of SNHG26 affects mitochondrial stress, proliferation, cell cycle phase distribution, and gene expression in cis- and in trans, and that this effect is reversed by upregulation of SNHG26. We also find that the effect on cell cycle phase distribution is cell type specific and stable over time. Results indicate an oncogenic role of SNHG26, possibly by affecting cell cycle progression through the regulation of downstream MYC-responsive genes.

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