scholarly journals A fluorescence in situ hybridization-based assay for improved detection of lung cancer cells in bronchial washing specimens

Cancer ◽  
2002 ◽  
Vol 96 (5) ◽  
pp. 306-315 ◽  
Author(s):  
Irina A. Sokolova ◽  
Lukas Bubendorf ◽  
Anna O'Hare ◽  
Mona S. Legator ◽  
Kris K.B. Jacobson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
In Situ Hybridization ◽  
Fluorescence In Situ Hybridization ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Bronchial Washing

Quantitative Detection of Lung Cancer Cells by Fluorescence In Situ Hybridization

CHEST Journal ◽  
2005 ◽  
Vol 128 (2) ◽  
pp. 906-911 ◽  
Author(s):  
Haruhiko Nakamura ◽  
Idiris Aute ◽  
Norihito Kawasaki ◽  
Masahiko Taguchi ◽  
Tatsuo Ohira ◽  
...  
Keyword(s):  
Lung Cancer ◽  
In Situ Hybridization ◽  
Fluorescence In Situ Hybridization ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Quantitative Detection

Detection of Lung Cancer Cells in Bronchial Washings Using Fluorescence in Situ Hybridization

2005 ◽  
Vol 56 (6) ◽  
pp. 470-475 ◽  
Author(s):  
Idiris Aute ◽  
Haruhiko Nakamura ◽  
Maidiniyeti Niyazi ◽  
Masahiko Taguchi ◽  
Norihito Kawasaki ◽  
...  
Keyword(s):  
Lung Cancer ◽  
In Situ Hybridization ◽  
Fluorescence In Situ Hybridization ◽  
Cancer Cells ◽  
Lung Cancer Cells

scholarly journals Silencing of LINC01279 is activated apoptosis and autophagy in lung cancer by regulating FAK/ERK via SIN3A

2021 ◽  
Author(s):  
Wenmei Su ◽  
Jiancong Wu ◽  
Xiaobi Huang ◽  
Xiaofang Li ◽  
Honglian Zhou ◽  
...  
Keyword(s):  
Lung Cancer ◽  
In Situ Hybridization ◽  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Noncoding Rna ◽  
Lung Cancer Cells ◽  
Loss Of Function

Abstract Background: In human lung adenocarcinoma (LUAD) tissues, Long noncoding RNA LINC01279 is significantly upregulated. However, the functions of LINC01279 in LUAD is yet to be clarified.Methods: In situ hybridization was employed to investigate the difference between expression of LINC01279 in LUAD and in normal tissues. The result of in situ hybridization is verified by qRT-PCR. Cytoplasmic and nuclear experiments showed that LINC01279 was mainly located in the cytoplasm of lung cancer cells. The loss of function experiment showed that LINC01279 could inhibit the proliferation, colony formation, invasion and migration of lung cancer cells. The interaction between SIN3A and LINC01279 was confirmed by RIP test. At the same time, through western bolt, we found that LINC01279 plays a key role in the regulation of apoptosis and autophagy in lung adenocarcinoma.Results: Our study confirmed that LINC01279 was upregulated in LUAD tissues, the knocking-down of which significantly inhibited the growth of LUAD cancer cells both in vitro and in vivo. Mechanistic investigations revealed that LINC01279 could directly interact with SIN3A and modulate the FAK and ERK protein expression in the cytoplasm. Moreover, the proteins of PARP and LC3B, P62, Beclin-1, respectively related with apoptosis and autophagy, were changed after LINC01279 siRNA. Conclusions: Taken together, our research found that LINC01279 which is significantly up-regulated in LUAD tissues and cell lines, and promotes the changes of FAK and ERK proteins in downstream pathways by combining with SIN3A, promotes the proliferation of LUAD cells, and inhibits apoptosis and autophagy. The results of this work illustrated how LINC01279 is part of a regulatory network that contributes to the oncogenesis of LUAD and proposed LINC01279 could be a potential target for LUAD diagnosis and treatment.

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