scholarly journals Flavonoids identified from Korean Citrus aurantium L. inhibit Non-Small Cell Lung Cancer growth in vivo and in vitro

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


Phytomedicine ◽  
2021 ◽  
pp. 153834
Author(s):  
Yueyi Kan ◽  
Min Song ◽  
Xihe Cui ◽  
Qing Yang ◽  
Yuanlong Zang ◽  
...  

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Jianjiao Ni ◽  
Xiaofei Zhang ◽  
Juan Li ◽  
Zhiqin Zheng ◽  
Junhua Zhang ◽  
...  

AbstractBone is a frequent metastatic site of non-small cell lung cancer (NSCLC), and bone metastasis (BoM) presents significant challenges for patient survival and quality of life. Osteolytic BoM is characterised by aberrant differentiation and malfunction of osteoclasts through modulation of the TGF-β/pTHrP/RANKL signalling pathway, but its upstream regulatory mechanism is unclear. In this study, we found that lncRNA-SOX2OT was highly accumulated in exosomes derived from the peripheral blood of NSCLC patients with BoM and that patients with higher expression of exosomal lncRNA-SOX2OT had significantly shorter overall survival. Additionally, exosomal lncRNA-SOX2OT derived from NSCLC cells promoted cell invasion and migration in vitro, as well as BoM in vivo. Mechanistically, we discovered that NSCLC cell-derived exosomal lncRNA-SOX2OT modulated osteoclast differentiation and stimulated BoM by targeting the miRNA-194-5p/RAC1 signalling axis and TGF-β/pTHrP/RANKL signalling pathway in osteoclasts. In conclusion, exosomal lncRNA-SOX2OT plays a crucial role in promoting BoM and may serve as a promising prognostic biomarker and treatment target in metastatic NSCLC.


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