High expression of long non-coding RNA ATB indicates a poor prognosis and regulates cell proliferation and metastasis in non-small cell lung cancer

2016 ◽  
Vol 19 (5) ◽  
pp. 599-605 ◽  
Author(s):  
L. Ke ◽  
S.-B. Xu ◽  
J. Wang ◽  
X.-L. Jiang ◽  
M.-Q. Xu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Poor Prognosis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Proliferation And Metastasis ◽  
Long Non Coding Rna ◽  
Cell Proliferation And Metastasis

Long non-coding RNA MVIH indicates a poor prognosis for non-small cell lung cancer and promotes cell proliferation and invasion

Tumor Biology ◽  
2014 ◽  
Vol 35 (8) ◽  
pp. 7587-7594 ◽  
Author(s):  
Feng-qi Nie ◽  
Quan Zhu ◽  
Tong-peng Xu ◽  
Yan-fen Zou ◽  
Min Xie ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Poor Prognosis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Proliferation And Invasion

c-Myc-regulated long non-coding RNA H19 indicates a poor prognosis and affects cell proliferation in non-small-cell lung cancer

Tumor Biology ◽  
2015 ◽  
Vol 37 (3) ◽  
pp. 4007-4015 ◽  
Author(s):  
Erbao Zhang ◽  
Wei Li ◽  
Dandan Yin ◽  
Wei De ◽  
Liangjun Zhu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Poor Prognosis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA LUCAT1 is associated with poor prognosis in human non-small cell lung cancer and regulates cell proliferation via epigenetically repressing p21 and p57 expression

Oncotarget ◽  
2017 ◽  
Vol 8 (17) ◽  
pp. 28297-28311 ◽  
Author(s):  
Yue Sun ◽  
Shi-Dai Jin ◽  
Quan Zhu ◽  
Liang Han ◽  
Jing Feng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Poor Prognosis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Erratum to: c-Myc-regulated long non-coding RNA H19 indicates a poor prognosis and affects cell proliferation in non-small-cell lung cancer

Tumor Biology ◽  
2015 ◽  
Vol 37 (4) ◽  
pp. 5653-5653 ◽  
Author(s):  
Erbao Zhang ◽  
Wei Li ◽  
Dandan Yin ◽  
Wei De ◽  
Liangjun Zhu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Poor Prognosis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Yafeng Fan ◽  
Hongxia Li ◽  
Zhongping Yu ◽  
Wen Dong ◽  
Xiaoyan Cui ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cancer Cell ◽  
Small Cell ◽  
Cancer Cell Proliferation ◽  
Lung Cancer Cell ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Long non-coding RNA (lncRNA) FYVE, RhoGEF and PH domain containing 5 antisense RNA 1 (FGD5-AS1) has been reported as an oncogene in colorectal cancer, promoting its tumorgenesis. The present paper focused on searching the potential function of FGD5-AS1 in non-small cell lung carcinoma (NSCLC). There are connections between the expression of lncRNA FGD5-AS1 and human NSCLC tumor growth and progression. Also, the relationships between FGD5-AS1, hsa-miR-107 and mRNA fibroblast growth factor receptor like 1 (FGFRL1) are going to test their interaction in NSCLC cell lines, which may cause a series of biological behaviors of NSCLC cells. qRT-PCR analysis was conducted to test the expression of RNAs in different situation. CCK-8 experiment and clone formation assay were performed to assess proliferation of NSCLC cells. Also, connection between FGD5-AS1 and hsa-miR-107 were investigated by luciferase reporter assay and RNA pull-down assay. Rescue experiments were performed to verify the modulating relationship between FGD5-AS1, hsa-miR-107 and FGFRL1. High-level expression of FGD5-AS1 was found in NSCLC. FGD5-AS1 may promote the proliferation of NSCLC cells. Also, the combination between hsa-miR-107, FGD5-AS1 and NSCLC have been proved, which means they can play an interaction function in NSCLC cells. Thence, we concluded that lncRNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1.

scholarly journals Long non-coding RNA CCAT1 promotes non-small cell lung cancer progression by regulating the miR-216a-5p/RAP2B axis

2020 ◽  
pp. 153537022096101
Author(s):  
Lingling Pang ◽  
Qianqian Zhang ◽  
Yanmin Wu ◽  
Qingru Yang ◽  
Jinghao Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Cell Progression ◽  
Long Non Coding Rna

The long non-coding RNA colon cancer-associated transcript 1 (CCAT1) has been investigated to involve in the progression of non-small cell lung cancer (NSCLC). Thus, this study aims to explore the detailed molecular mechanisms of CCAT1 in NSCLC. The expression of CCAT1, miR-216a-5p, RAP2B, Bax, Bcl-2, and cleaved caspase 3 was detected by qRT-PCR or Western blot. Cell proliferation, apoptosis, migration, and invasion were analyzed using cell counting kit-8, flow cytometry or Transwell assays, respectively. The interaction between miR-216a-5p and CCAT1 or RAP2B was analyzed by luciferase reporter, RNA immunoprecipitation, and pull-down assays. The expression of CCAT1 was elevated in NSCLC, and CCAT1 deletion could inhibit NSCLC cell proliferation, migration, and invasion but induce apoptosis in vitro as well as imped tumor growth in vivo. MiR-216a-5p was confirmed to be a target of CCAT1, and silencing miR-216a-5p could reverse CCAT1 depletion-mediated inhibitory effects on cell tumorigenesis in NSCLC. Besides that, miR-216a-5p was decreased in NSCLC, and miR-216a-5p restoration inhibited cell tumorigenesis by regulating RAP2B, which was verified to be a target of miR-216a-5p. Additionally, co-expression analysis suggested that CCAT1 indirectly regulated RAP2B level by targeting miR-216a-5p in NSCLC cells. Taken together, CCAT1 deletion could inhibit cell progression in NSCLC through miR-216a-5p/RAP2B axis, indicating a novel pathway underlying NSCLC cell progression and providing new potential targets for NSCLC treatment. Impact statement We investigated that CCAT1 expression was elevated in NSCLC and CCAT1 deletion was identified to inhibit cell carcinogenic phenotypes in NSCLC cells via miR-216a-5p/RAP2B axis, which reveals a novel pathway underlying progression in NSCLC cells and providing potential targets for NSCLC treatment.

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