scholarly journals Active Constituents fromLiriope platyphyllaRoot against Cancer GrowthIn Vitro

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Hui-Chun Wang ◽  
Chin-Chung Wu ◽  
Ti-Sheng Cheng ◽  
Ching-Ying Kuo ◽  
Yu-Chi Tsai ◽  
...  
Keyword(s):  
Anticancer Activity ◽  
Cell Cycle Checkpoint ◽  
Inhibition Of Proliferation ◽  
Akt Phosphorylation ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint ◽  
Liriope Platyphylla ◽  
Neural Disorders ◽  
Caspase Cascades ◽  
Mcf 7

Liriope spicatais a well-known herb in traditional Chinese medicine, and its root has been clinically demonstrated to be effective in the treatment of metabolic and neural disorders. The constituents isolated fromLiriopehave also recently been shown to possess anticancer activity, although the mechanism of which remains largely unknown. Here, we illustrate the anticancer activity of LPRP-9, one of the active fractions we fractionated from theLiriope platyphyllaroot part (LPRP) extract. Treatment with LPRP-9 significantly inhibited proliferation of cancer cell lines MCF-7 and Huh-7 and down-regulated the phosphorylation of AKT. LPRP-9 also activates the stress-activated MPAK, JNK, p38 pathways, the p53 cell-cycle checkpoint pathway, and a series of caspase cascades while downregulating expression of antiapoptotic factors Bcl-2, Bcl-XL, and survivin. Such activities strongly suggest a role for LPRP-9 in apoptosis and autophagy. We further purified and identified the compound (−)-Liriopein B from LPRP-9, which is capable of inhibiting AKT phosphorylation at low concentration. The overall result highlights the anticancer property of LPRP-9, suggests its mechanism for inhibition of proliferation and promotion of cell death for cancer cells via regulation of multitarget pathways, and denotes the importance of purifying components of fraction LPRP-9 to aid cancer therapy.

scholarly journals Centrosome Dynamics and Its Role in Inflammatory Response and Metastatic Process

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 629
Author(s):  
Massimo Pancione ◽  
Luigi Cerulo ◽  
Andrea Remo ◽  
Guido Giordano ◽  
Álvaro Gutierrez-Uzquiza ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rho Gtpases ◽  
Human Cancer ◽  
Genetic Disorders ◽  
Cell Cycle Checkpoint ◽  
Animal Cells ◽  
Normal Tissues ◽  
Checkpoint Pathway ◽  
New Findings ◽  
Cycle Checkpoint

Metastasis is a process by which cancer cells escape from the location of the primary tumor invading normal tissues at distant organs. Chromosomal instability (CIN) is a hallmark of human cancer, associated with metastasis and therapeutic resistance. The centrosome plays a major role in organizing the microtubule cytoskeleton in animal cells regulating cellular architecture and cell division. Loss of centrosome integrity activates the p38-p53-p21 pathway, which results in cell-cycle arrest or senescence and acts as a cell-cycle checkpoint pathway. Structural and numerical centrosome abnormalities can lead to aneuploidy and CIN. New findings derived from studies on cancer and rare genetic disorders suggest that centrosome dysfunction alters the cellular microenvironment through Rho GTPases, p38, and JNK (c-Jun N-terminal Kinase)-dependent signaling in a way that is favorable for pro-invasive secretory phenotypes and aneuploidy tolerance. We here review recent data on how centrosomes act as complex molecular platforms for Rho GTPases and p38 MAPK (Mitogen activated kinase) signaling at the crossroads of CIN, cytoskeleton remodeling, and immune evasion via both cell-autonomous and non-autonomous mechanisms.

scholarly journals An Intrinsic Cell Cycle Checkpoint Pathway Mediated by MEK and ERK in Drosophila

2006 ◽  
Vol 11 (4) ◽  
pp. 575-582 ◽  
Author(s):  
Vladic Mogila ◽  
Fan Xia ◽  
Willis X. Li
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint

scholarly journals The Maize Homologue of the Cell Cycle Checkpoint Protein MAD2 Reveals Kinetochore Substructure and Contrasting Mitotic and Meiotic Localization Patterns

1999 ◽  
Vol 145 (3) ◽  
pp. 425-435 ◽  
Author(s):  
Hong-Guo Yu ◽  
Michael G. Muszynski ◽  
R. Kelly Dawe
Keyword(s):  
Cell Cycle ◽  
Spindle Assembly ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Protein ◽  
Microtubule Attachment ◽  
Checkpoint Pathway ◽  
Outer Domain ◽  
Cycle Checkpoint ◽  
Mitosis And Meiosis ◽  
Meiosis I

We have identified a maize homologue of yeast MAD2, an essential component in the spindle checkpoint pathway that ensures metaphase is complete before anaphase begins. Combined immunolocalization of MAD2 and a recently cloned maize CENPC homologue indicates that MAD2 localizes to an outer domain of the prometaphase kinetochore. MAD2 staining was primarily observed on mitotic kinetochores that lacked attached microtubules; i.e., at prometaphase or when the microtubules were depolymerized with oryzalin. In contrast, the loss of MAD2 staining in meiosis was not correlated with initial microtubule attachment but was correlated with a measure of tension: the distance between homologous or sister kinetochores (in meiosis I and II, respectively). Further, the tension-sensitive 3F3/2 phosphoepitope colocalized, and was lost concomitantly, with MAD2 staining at the meiotic kinetochore. The mechanism of spindle assembly (discussed here with respect to maize mitosis and meiosis) is likely to affect the relative contributions of attachment and tension. We support the idea that MAD2 is attachment-sensitive and that tension stabilizes microtubule attachments.

scholarly journals Interactions between p53 and MDM2 in a mammalian cell cycle checkpoint pathway.

1994 ◽  
Vol 91 (7) ◽  
pp. 2684-2688 ◽  
Author(s):  
C. Y. Chen ◽  
J. D. Oliner ◽  
Q. Zhan ◽  
A. J. Fornace ◽  
B. Vogelstein ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mammalian Cell ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Mammalian Cell Cycle ◽  
Cycle Checkpoint

A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

Cell ◽  
1992 ◽  
Vol 71 (4) ◽  
pp. 587-597 ◽  
Author(s):  
Michael B. Kastan ◽  
Qimin Zhan ◽  
Wafik S. El-Deiry ◽  
France Carrier ◽  
Tyler Jacks ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mammalian Cell ◽  
Ataxia Telangiectasia ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Mammalian Cell Cycle ◽  
Cycle Checkpoint

scholarly journals Dyskerin Ablation in Mouse Liver Inhibits rRNA Processing and Cell Division

2009 ◽  
Vol 30 (2) ◽  
pp. 413-422 ◽  
Author(s):  
Jingping Ge ◽  
David A. Rudnick ◽  
Jun He ◽  
Dan L. Crimmins ◽  
Jack H. Ladenson ◽  
...  
Keyword(s):  
Cellular Proliferation ◽  
Dyskeratosis Congenita ◽  
Cellular Level ◽  
Cell Cycle Checkpoint ◽  
Rna Modification ◽  
Rrna Processing ◽  
Pseudouridine Synthase ◽  
Ribonucleoprotein Complexes ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint

ABSTRACT Dyskerin is a component of small nucleolar ribonucleoprotein complexes and acts as a pseudouridine synthase to modify newly synthesized ribosomal, spliceosomal, and possibly other RNAs. It is encoded by the DKC1 gene, the gene mutated in X-linked dyskeratosis congenita, and is also part of the telomerase complex. The yeast ortholog, Cbf5, is an essential protein, but in mammals the effect of dyskerin ablation at the cellular level is not known. Here we show that mouse hepatocytes can survive after induction of a Dkc1 deletion. In the absence of dyskerin, rRNA processing is inhibited with the accumulation of large precursors, and fibrillarin does not accumulate in nucleoli. A low rate of apoptosis is induced in the hepatocytes, which show an induction of the p53-dependent cell cycle checkpoint pathway. Signs of liver damage including an increase in serum alanine aminotransferase activity and a disordered structure at the histological and macroscopic levels are observed. In response to carbon tetrachloride administration, when wild-type hepatocytes mount a rapid proliferative response, those without dyskerin do not divide. We conclude that hepatocytes can survive without dyskerin but that the role of dyskerin in RNA modification is essential for cellular proliferation.

scholarly journals Chromothripsis: A Cause of Genome Instability in Cancer

2021 ◽  
Vol 3 (4) ◽  
pp. 5-11
Author(s):  
Ishita Agrawal ◽  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Growth ◽  
Genome Instability ◽  
Cell Cycle Checkpoint ◽  
Genetic Changes ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint

Cancer is a term given to uncontrolled cell growth, which is the result of accumulation of genetic changes during cell division. It can occur due to both genetic and environmental reasons. One such genetic cause of cancer discovered recently is known as Chromothripsis. It is defined as the fragmentation and rearrangement of chromosomes. Researchers are still trying to find the true mechanism underlying Chromothripsis. Two models have been significantly described; first one is the ‘micronuclei hypothesis’, which occurs as a result of chromosome mis-segregation during Mitosis. Second model is based on the ‘telomere crisis’, which occurs due to faulty telomerase enzyme and cell cycle checkpoint pathway. In this letter, we have tried to give brief information about the mechanisms behind Chromothripsis and their role in causing genome instability leading to cancer.

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