scholarly journals CCDC57 Cooperates with Microtubules and Microcephaly Protein CEP63 and Regulates Centriole Duplication and Mitotic Progression

Cell Reports ◽  
2020 ◽  
Vol 31 (6) ◽  
pp. 107630 ◽  
Author(s):  
H. Kubra Gurkaslar ◽  
Efraim Culfa ◽  
Melis D. Arslanhan ◽  
Mariana Lince-Faria ◽  
Elif Nur Firat-Karalar
Keyword(s):  
Mitotic Progression ◽  
Centriole Duplication

scholarly journals Human Microcephaly Protein RTTN Is Required for Proper Mitotic Progression and Correct Spindle Position

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1441
Author(s):  
En-Ju Chou ◽  
Tang K. Tang
Keyword(s):  
Brain Size ◽  
Neurodevelopmental Disorder ◽  
Mitotic Progression ◽  
Centriole Duplication ◽  
Spindle Poles ◽  
Multipolar Spindles ◽  
Mitotic Abnormalities ◽  
Cortical Localization ◽  
Spindle Position ◽  
Autosomal Recessive Primary Microcephaly

Autosomal recessive primary microcephaly (MCPH) is a complex neurodevelopmental disorder characterized by a small brain size with mild to moderate intellectual disability. We previously demonstrated that human microcephaly RTTN played an important role in regulating centriole duplication during interphase, but the role of RTTN in mitosis is not fully understood. Here, we show that RTTN is required for normal mitotic progression and correct spindle position. The depletion of RTTN induces the dispersion of the pericentriolar protein γ-tubulin and multiple mitotic abnormalities, including monopolar, abnormal bipolar, and multipolar spindles. Importantly, the loss of RTTN altered NuMA/p150Glued congression to the spindle poles, perturbed NuMA cortical localization, and reduced the number and the length of astral microtubules. Together, our results provide a new insight into how RTTN functions in mitosis.

LY6K-AS lncRNA is a lung adenocarcinoma prognostic biomarker and regulator of mitotic progression

Oncogene ◽  
2021 ◽  
Vol 40 (13) ◽  
pp. 2463-2478
Author(s):  
Mohamad Moustafa Ali ◽  
Mirco Di Marco ◽  
Sagar Mahale ◽  
Daniel Jachimowicz ◽  
Subazini Thankaswamy Kosalai ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Prognostic Biomarker ◽  
Mitotic Progression

scholarly journals Inhibition of Ganglioside Synthesis Suppressed Liver Cancer Cell Proliferation through Targeting Kinetochore Metaphase Signaling

Metabolites ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 167
Author(s):  
Ting Su ◽  
Xian-Yang Qin ◽  
Naoshi Dohmae ◽  
Feifei Wei ◽  
Yutaka Furutani ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cell Proliferation ◽  
Mitotic Progression ◽  
Cycle Arrest ◽  
Persistent Inflammation ◽  
Promising Target ◽  
Mechanistic Analysis ◽  
Incidence And Mortality ◽  
Dependent Cell ◽  
Lifestyle Diseases

The incidence and mortality of liver cancer, mostly hepatocellular carcinoma (HCC), have increased during the last two decades, partly due to persistent inflammation in the lipid-rich microenvironment associated with lifestyle diseases, such as obesity. Gangliosides are sialic acid-containing glycosphingolipids known to be important in the organization of the membrane and membrane protein-mediated signal transduction. Ganglioside synthesis is increased in several types of cancers and has been proposed as a promising target for cancer therapy. Here, we provide evidence that ganglioside synthesis was increased in the livers of an animal model recapitulating the features of activation and expansion of liver progenitor-like cells and liver cancer (stem) cells. Chemical inhibition of ganglioside synthesis functionally suppressed proliferation and sphere growth of liver cancer cells, but had no impact on apoptotic and necrotic cell death. Proteome-based mechanistic analysis revealed that inhibition of ganglioside synthesis downregulated the expression of AURKA, AURKB, TTK, and NDC80 involved in the regulation of kinetochore metaphase signaling, which is essential for chromosome segregation and mitotic progression and probably under the control of activation of TP53-dependent cell cycle arrest. These data suggest that targeting ganglioside synthesis holds promise for the development of novel preventive/therapeutic strategies for HCC treatment.

scholarly journals Disruption of Mitotic Progression by Arsenic

2015 ◽  
Vol 166 (1) ◽  
pp. 34-40 ◽  
Author(s):  
J. Christopher States
Keyword(s):  
Mitotic Progression
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