scholarly journals Editorial Expression of Concern: WWOX gene restoration prevents lung cancer growth in vitro and in vivo

2017 ◽  
Vol 114 (16) ◽  
pp. E3365-E3365
Keyword(s):  
2005 ◽  
Vol 102 (43) ◽  
pp. 15611-15616 ◽  
Author(s):  
M. Fabbri ◽  
D. Iliopoulos ◽  
F. Trapasso ◽  
R. I. Aqeilan ◽  
A. Cimmino ◽  
...  
Keyword(s):  

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Xin Diao ◽  
Danfen Yang ◽  
Yu Chen ◽  
Wentian Liu

AbstractBaicalin is the main bioactive component extracted from the traditional Chinese medicine Baical Skullcap Root, and its anti-tumor activity has been studied in previous studies. PDZ-binding kinase/T-LAK cell-originated protein kinase (PBK/TOPK), a serine/threonine protein kinase, is highly expressed in many cancer cells and stimulates the tumorigenic properties, and so, it is a pivotal target for agent to cure cancers. We reported for the first time that baicalin suppressed PBK/TOPK activities by directly binding with PBK/TOPK in vitro and in vivo. Ex vivo studies showed that baicalin suppressed PBK/TOPK activity in JB6 Cl41 cells and H441 lung cancer cells. Moreover, knockdown of PBK/TOPK in H441 cells decreased their sensitivity to baicalin. In vivo study indicated that injection of baicalin in H441 tumor-bearing mice effectively suppressed cancer growth. The PBK/TOPK downstream signaling molecules Histone H3 and ERK2 in tumor tissues were also decreased after baicalin treatment. Taken together, baicalin can inhibit proliferation of lung cancer cells as a PBK/TOPK inhibitor both in vitro and in vivo.


1996 ◽  
Vol 63 (S24) ◽  
pp. 269-275 ◽  
Author(s):  
Farah Zia ◽  
Steve Jacobs ◽  
Frederick Kull ◽  
Frank Cuttitta ◽  
James L. Mulshine ◽  
...  

2015 ◽  
Vol 33 (6) ◽  
pp. 3053-3060 ◽  
Author(s):  
XINGYU LIN ◽  
ZHIGUANG YANG ◽  
PENG ZHANG ◽  
GUOGUANG SHAO

2015 ◽  
Vol 396 (8) ◽  
pp. 929-936 ◽  
Author(s):  
Weihua Xu ◽  
Kanqiu Jiang ◽  
Mingjing Shen ◽  
Yongyue Qian ◽  
Yong Peng

Abstract Lung cancer has been the most prolific cancer in China – as in the rest of the world – with a high death rate and low 5-year survival rate. Previous evidence showed that JMJD2A is over-expressed in human non-small cell lung cancer (NSCLC) tissues compared to adjacent normal tissues, and that high level of JMJD2A predicts poor overall and disease-free survival. However, the mechanism by which JMJD2A is regulated in human NSCLC is not fully understood. In the present study, we identified that the SIRT2 as an anti-oncogenic protein in NSCLC was down-regulated. JMJD2A as a target of SIRT2 was negatively correlated with SIRT2 level in NSCLC. SIRT2 bound to the promoter region of JMJD2A and negatively regulated JMJD2A expression. In addition, we found that SIRT2 inhibited NSCLC cells proliferation, colony formation and tumor growth in vitro and in vivo in a JMJD2A-dependent manner. In summary, our findings implicate that SIRT2 suppresses non-small cell lung cancer growth through targeting JMJD2A and SIRT2 activator may serve as candidate drug for NSCLC therapy.


Marine Drugs ◽  
2017 ◽  
Vol 15 (7) ◽  
pp. 210 ◽  
Author(s):  
Ting-Wen Chung ◽  
Jui-Hsin Su ◽  
Chi-Chen Lin ◽  
Yi-Rong Li ◽  
Ya-Hsuan Chao ◽  
...  

2017 ◽  
Vol 43 (6) ◽  
pp. 2505-2515 ◽  
Author(s):  
Zhao Wang ◽  
Zhimin Liu ◽  
Xiaojie Fang ◽  
Han Yang

Background/Aims: Numerous studies have demonstrated that aberrant microRNA (miRNA) expression is involved in human disease including cancer. To date, the potential miRNAs regulating lung cancer growth and progression are not fully identified yet. Methods: In this study, the expression of miR-142-5p was measured in non-small cell lung cancer tissue and cell lines by qRT-PCR. The functional assays including the cell viability, colony formation, cell migration and invasion were performed in miR-142-5p mimic or inhibitor transfected cell lines (in vitro) and the cell tumorigenesis in nude mice (in vivo). The fluorescence ratios of cell viability were recorded using a multi-plate reader (Synergy 2, BioTek, Winooski, VT, USA) and the colonies were counted using an ELIspot Bioreader 5000 (BIO-SYS, Karben, GE). Results: MiR-142-5p was significantly downregulated in non-small cell lung cancer tissue and cell lines compared to normal human lung tissues. Overexpression of miR-142-5p resulted in decreased expression of PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha) at both mRNA and protein levels. We found that miR-142-5p overexpression markedly suppressed cell proliferation in vitro and in vivo. Conversely, inhibition of miR-142-5p promoted lung cancer growth. Mechanistic studies showed that PIK3CA was a potential target of miR-142-5p and it mediated reduction of PIK3CA resulting in suppression of PI3K/Akt pathway. Conclusions: Our results demonstrate that miR-142-5p functions as a growth suppressive miRNA and plays an important role in inhibiting the tumorigenesis through targeting PIK3CA in non-small cell lung cancer.


2014 ◽  
Vol 7 ◽  
pp. 287-297 ◽  
Author(s):  
Kwang-Il Park ◽  
Hyeon-Soo Park ◽  
Mun-Ki Kim ◽  
Gyeong-Eun Hong ◽  
Arulkumar Nagappan ◽  
...  

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