MiR-210 Links Hypoxia With Cell Proliferation Regulation in Human Laryngocarcinoma Cancer

2015 ◽  
Vol 116 (6) ◽  
pp. 1039-1049 ◽  
Author(s):  
Jianhong Zuo ◽  
Meiling Wen ◽  
Mingsheng Lei ◽  
Xiang Peng ◽  
Xuefeng Yang ◽  
...  
2010 ◽  
Vol 89 (3) ◽  
pp. 279-289 ◽  
Author(s):  
Caihua Zhu ◽  
Qin Chen ◽  
Zuoquan Xie ◽  
Jing Ai ◽  
Linjiang Tong ◽  
...  

Neuroreport ◽  
2006 ◽  
Vol 17 (9) ◽  
pp. 863-867 ◽  
Author(s):  
Hu Chen ◽  
Ghanshyam N. Pandey ◽  
Yogesh Dwivedi

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhengwei Yan ◽  
Minzhang Cheng ◽  
Guohui Hu ◽  
Yao Wang ◽  
Shaopeng Zeng ◽  
...  

AbstractHedgehog (Hh) signaling plays a critical role in embryogenesis and tissue homeostasis, and its deregulation has been associated with tumor growth. The tumor suppressor SuFu inhibits Hh signaling by preventing the nuclear translocation of Gli and suppressing cell proliferation. Regulation of SuFu activity and stability is key to controlling Hh signaling. Here, we unveil SuFu Negating Protein 1 (SNEP1) as a novel Hh target, that enhances the ubiquitination and proteasomal degradation of SuFu and thus promotes Hh signaling. We further show that the E3 ubiquitin ligase LNX1 plays a critical role in the SNEP1-mediated degradation of SuFu. Accordingly, SNEP1 promotes colorectal cancer (CRC) cell proliferation and tumor growth. High levels of SNEP1 are detected in CRC tissues and are well correlated with poor prognosis in CRC patients. Moreover, SNEP1 overexpression reduces sensitivity to anti-Hh inhibitor in CRC cells. Altogether, our findings demonstrate that SNEP1 acts as a novel feedback regulator of Hh signaling by destabilizing SuFu and promoting tumor growth and anti-Hh resistance.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zeenia Kaul ◽  
Caroline T. Y. Cheung ◽  
Priyanshu Bhargava ◽  
Anissa Notifa Sari ◽  
Yue Yu ◽  
...  

AbstractActivation of a telomere length maintenance mechanism (TMM), including telomerase and alternative lengthening of telomeres (ALT), is essential for replicative immortality of tumor cells, although its regulatory mechanisms are incompletely understood. We conducted a microRNA (miRNA) microarray analysis on isogenic telomerase positive (TEP) and ALT cancer cell lines. Amongst nine miRNAs that showed difference in their expression in TEP and ALT cancer cells in array analysis, miR-708 was selected for further analysis since it was consistently highly expressed in a large panel of ALT cells. miR-708 in TEP and ALT cancer cells was not correlated with C-circle levels, an established feature of ALT cells. Its overexpression induced suppression of cell migration, invasion, and angiogenesis in both TEP and ALT cells, although cell proliferation was inhibited only in TEP cells suggesting that ALT cells may have acquired the ability to escape inhibition of cell proliferation by sustained miR-708 overexpression. Further, cell proliferation regulation in TEP cells by miR708 appears to be through the CARF-p53 pathway. We demonstrate here that miR-708 (i) is the first miRNA shown to be differentially regulated in TEP and ALT cancer cells, (ii) possesses tumor suppressor function, and (iii) deregulates CARF and p21WAF1-mediated signaling to limit proliferation in TEP cells.


Molecules ◽  
2019 ◽  
Vol 24 (23) ◽  
pp. 4334
Author(s):  
Lucie Appy ◽  
Crystalle Chardet ◽  
Suzanne Peyrottes ◽  
Béatrice Roy

Dinucleoside 5′,5′-polyphosphates (DNPs) are endogenous substances that play important intra- and extracellular roles in various biological processes, such as cell proliferation, regulation of enzymes, neurotransmission, platelet disaggregation and modulation of vascular tone. Various methodologies have been developed over the past fifty years to access these compounds, involving enzymatic processes or chemical procedures based either on P(III) or P(V) chemistry. Both solution-phase and solid-support strategies have been developed and are reported here. Recently, green chemistry approaches have emerged, offering attracting alternatives. This review outlines the main synthetic pathways for the preparation of dinucleoside 5′,5′-polyphosphates, focusing on pharmacologically relevant compounds, and highlighting recent advances.


Author(s):  
C. W. Kischer

The morphology of the fibroblasts changes markedly as the healing period from burn wounds progresses, through development of the hypertrophic scar, to resolution of the scar by a self-limiting process of maturation or therapeutic resolution. In addition, hypertrophic scars contain an increased cell proliferation largely made up of fibroblasts. This tremendous population of fibroblasts seems congruous with the abundance of collagen and ground substance. The fine structure of these cells should reflect some aspects of the metabolic activity necessary for production of the scar, and might presage the stage of maturation.A comparison of the fine structure of the fibroblasts from normal skin, different scar types, and granulation tissue has been made by transmission (TEM) and scanning electron microscopy (SEM).


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