Molecular mechanisms of quinalizarin induces apoptosis and G0 / G1 cell cycle of human esophageal cancer HCE ‐4 cells depends on MAPK , STAT3, and NF‐κB signaling pathways

2020 ◽  
Vol 36 (2) ◽  
pp. 276-286
Author(s):  
Yan‐Qing Zang ◽  
Yu‐Qing Zhai ◽  
Yan‐Yu Feng ◽  
Xue‐Ying Ju ◽  
Feng Zuo
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Human Esophageal Cancer

Specific ligands of the peripheral benzodiazepine receptor induce apoptosis and cell cycle arrest in human esophageal cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A444
Author(s):  
Andreas Sutter ◽  
Kerstin Maaser ◽  
Bettina Barthel ◽  
Bernd Von Lampe ◽  
Ernst-Otto Riecken ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Benzodiazepine Receptor ◽  
Peripheral Benzodiazepine Receptor ◽  
Cycle Arrest ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells

scholarly journals Lithium inhibits proliferation of human esophageal cancer cell line Eca-109 by inducing a G2/M cell cycle arrest

2008 ◽  
Vol 14 (25) ◽  
pp. 3982 ◽  
Author(s):  
Jin-Sheng Wang ◽  
Cui-Lian Wang ◽  
Ji-Fang Wen ◽  
Yong-Jin Wang ◽  
Yong-Bin Hu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cell Cycle Arrest ◽  
Cell Line ◽  
Cancer Cell Line ◽  
M Cell ◽  
Cycle Arrest ◽  
Esophageal Cancer Cell ◽  
Esophageal Cancer Cell Line ◽  
Human Esophageal Cancer

Polarization of cell growth in yeast. I. Establishment and maintenance of polarity states

2000 ◽  
Vol 113 (3) ◽  
pp. 365-375 ◽  
Author(s):  
D. Pruyne ◽  
A. Bretscher
Keyword(s):  
Cell Cycle ◽  
Yeast Cell ◽  
Signaling Pathways ◽  
Cell Polarity ◽  
Molecular Mechanisms ◽  
Fundamental Property ◽  
Yeast Cells ◽  
Cell Cortex ◽  
Yeast Saccharomyces Cerevisiae ◽  
Dependent Protein

The ability to polarize is a fundamental property of cells. The yeast Saccharomyces cerevisiae has proven to be a fertile ground for dissecting the molecular mechanisms that regulate cell polarity during growth. Here we discuss the signaling pathways that regulate polarity. In the second installment of this two-part commentary, which appears in the next issue of Journal of Cell Science, we discuss how the actin cytoskeleton responds to these signals and guides the polarity of essentially all events in the yeast cell cycle. During the cell cycle, yeast cells assume alternative states of polarized growth, which range from tightly focused apical growth to non-focused isotropic growth. RhoGTPases, and in particular Cdc42p, are essential to guiding this polarity. The distribution of Cdc42p at the cell cortex establishes cell polarity. Cyclin-dependent protein kinase, Ras, and heterotrimeric G proteins all modulate yeast cell polarity in part by altering the distribution of Cdc42p. In turn, Cdc42p generates feedback signals to these molecules in order to establish stable polarity states and coordinate cytoskeletal organization with the cell cycle. Given that many of these signaling pathways are present in both fungi and animals, they are probably ancient and conserved mechanisms for regulating polarity.

scholarly journals RBL1/p107 Expression Levels Are Modulated by Multiple Signaling Pathways

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 5025
Author(s):  
Elisa Ventura ◽  
Carmelina Antonella Iannuzzi ◽  
Francesca Pentimalli ◽  
Antonio Giordano ◽  
Andrea Morrione
Keyword(s):  
Cell Cycle ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Oncogenic Signaling ◽  
Expression Levels ◽  
Close Family Member ◽  
Calcium Calmodulin Dependent ◽  
Cycle Arrest ◽  
Significant Difference ◽  
Multiple Signaling

The members of the retinoblastoma (RB) protein family, RB1/p105, retinoblastoma-like (RBL)1/p107 and RBL2/p130 are critical modulators of the cell cycle and their dysregulation has been associated with tumor initiation and progression. The activity of RB proteins is regulated by numerous pathways including oncogenic signaling, but the molecular mechanisms of these functional interactions are not fully defined. We previously demonstrated that RBL2/p130 is a direct target of AKT and it is a key mediator of the apoptotic process induced by AKT inhibition. Here we demonstrated that RBL1/p107 levels are only minorly modulated by the AKT signaling pathway. In contrast, we discovered that RBL1/p107 levels are regulated by multiple pathways linked directly or indirectly to Ca2+-dependent signaling. Inhibition of the multifunctional calcium/calmodulin-dependent kinases (CaMKs) significantly reduced RBL1/p107 expression levels and phosphorylation, increased RBL1/p107 nuclear localization and led to cell cycle arrest in G0/G1. Targeting the Ca2+-dependent endopeptidase calpain stabilized RBL1/p107 levels and counteracted the reduction of RBL1/p107 levels associated with CaMKs inhibition. Thus, these novel observations suggest a complex regulation of RBL1/p107 expression involving different components of signaling pathways controlled by Ca2+ levels, including CaMKs and calpain, pointing out a significant difference with the mechanisms modulating the close family member RBL2/p130.

scholarly journals Tumor‐derived exosomes influence the cell cycle and cell migration of human esophageal cancer cell lines

2020 ◽  
Vol 111 (12) ◽  
pp. 4348-4358
Author(s):  
Yasunori Matsumoto ◽  
Masayuki Kano ◽  
Kentaro Murakami ◽  
Takeshi Toyozumi ◽  
Hiroshi Suito ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cell Migration ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Esophageal Cancer Cell ◽  
Human Esophageal Cancer

scholarly journals Therapeutic and Radiosensitizing Effects of Armillaridin on Human Esophageal Cancer Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Chih-Wen Chi ◽  
Chien-Chih Chen ◽  
Yu-Jen Chen
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Transmembrane Potential ◽  
Mitochondrial Transmembrane Potential ◽  
Cell Counts ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells

Background. Armillaridin (AM) is isolated fromArmillaria mellea. We examined the anticancer activity and radiosensitizing effect on human esophageal cancer cells.Methods. Human squamous cell carcinoma (CE81T/VGH and TE-2) and adenocarcinoma (BE-3 and SKGT-4) cell lines were cultured. The MTT assay was used for cell viability. The cell cycle was analyzed using propidium iodide staining. Mitochondrial transmembrane potential was measured by DiOC6(3) staining. The colony formation assay was performed for estimation of the radiation surviving fraction. Human CE81T/VGH xenografts were established for evaluation of therapeutic activityin vivo.Results. AM inhibited the viability of four human esophageal cancer cell lines with an estimated concentration of 50% inhibition (IC50) which was 3.4–6.9 μM. AM induced a hypoploid cell population and morphological alterations typical of apoptosis in cells. This apoptosis induction was accompanied by a reduction of mitochondrial transmembrane potential. AM accumulated cell cycle at G2/M phase and enhanced the radiosensitivity in CE81T/VGH cells.In vivo, AM inhibited the growth of CE81T/VGH xenografts without significant impact on body weight and white blood cell counts.Conclusion. Armillaridin could inhibit growth and enhance radiosensitivity of human esophageal cancer cells. There might be potential to integrate AM with radiotherapy for esophageal cancer treatment.

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