Long non-coding RNA LINC01133 inhibits epithelial–mesenchymal transition and metastasis in colorectal cancer by interacting with SRSF6

2016 ◽  
Vol 380 (2) ◽  
pp. 476-484 ◽  
Author(s):  
Jianlu Kong ◽  
Wenjie Sun ◽  
Chen Li ◽  
Ledong Wan ◽  
Shuo Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA (lncRNA) and epithelial-mesenchymal transition (EMT) in colorectal cancer: a systematic review

2020 ◽  
Vol 21 (9) ◽  
pp. 769-781
Author(s):  
Stephen J. O’Brien ◽  
Campbell Bishop ◽  
Jacob Hallion ◽  
Casey Fiechter ◽  
Katharina Scheurlen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Systematic Review ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals The long non-coding RNA HOXA11-AS promotes epithelial mesenchymal transition by sponging miR-149-3p in Colorectal Cancer

2020 ◽  
Vol 11 (20) ◽  
pp. 6050-6058
Author(s):  
Dong Chen ◽  
Min Zhang ◽  
Jian Ruan ◽  
Xiaolin Li ◽  
Saisai Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long Non-Coding RNA: A Potential Strategy for the Diagnosis and Treatment of Colorectal Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Shanshan Chen ◽  
Yi Fang ◽  
Lingyu Sun ◽  
Ruonan He ◽  
Beihui He ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Diagnosis And Treatment ◽  
Molecular Signaling ◽  
Mesenchymal Transition ◽  
Immunological Responses ◽  
Non Coding Rna ◽  
Pathological Mechanism ◽  
Potential Strategy ◽  
Long Non Coding Rna

Colorectal cancer (CRC), being one of the most commonly diagnosed cancers worldwide, endangers human health. Because the pathological mechanism of CRC is not fully understood, there are many challenges in the prevention, diagnosis, and treatment of this disease. Long non-coding RNAs (lncRNAs) have recently drawn great attention for their potential roles in the different stages of CRC formation, invasion, and progression, including regulation of molecular signaling pathways, apoptosis, autophagy, angiogenesis, tumor metabolism, immunological responses, cell cycle, and epithelial-mesenchymal transition (EMT). This review aims to discuss the potential mechanisms of several oncogenic lncRNAs, as well as several suppressor lncRNAs, in CRC occurrence and development to aid in the discovery of new methods for CRC diagnosis, treatment, and prognosis assessment.

scholarly journals Correction to: The long non-coding RNA TUG1 indicates a poor prognosis for colorectal cancer and promotes metastasis by affecting epithelial-mesenchymal transition

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Junfeng Sun ◽  
Chaohui Ding ◽  
Zhen Yang ◽  
Tao Liu ◽  
Xiefu Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

An amendment to this paper has been published and can be accessed via the original article.

scholarly journals Long non-coding RNA FOXD2-AS1 promotes cell proliferation, metastasis and EMT in glioma by sponging miR-506-5p

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 921-931
Author(s):  
Juan Zhao ◽  
Xue-Bin Zeng ◽  
Hong-Yan Zhang ◽  
Jie-Wei Xiang ◽  
Yu-Song Liu
Keyword(s):  
Cell Proliferation ◽  
Epithelial Mesenchymal Transition ◽  
Human Cancer ◽  
Glioma Cells ◽  
Suppressor Gene ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

AbstractLong non-coding RNA forkhead box D2 adjacent opposite strand RNA 1 (FOXD2-AS1) has emerged as a potential oncogene in several tumors. However, its biological function and potential regulatory mechanism in glioma have not been fully investigated to date. In the present study, RT-qPCR was conducted to detect the levels of FOXD2-AS1 and microRNA (miR)-506-5p, and western blot assays were performed to measure the expression of CDK2, cyclinE1, P21, matrix metalloproteinase (MMP)7, MMP9, N-cadherin, E-cadherin and vimentin in glioma cells. A luciferase reporter assay was performed to verify the direct targeting of miR-506-5p by FOXD2-AS1. Subsequently, cell viability was analyzed using the CCK-8 assay. Cell migration and invasion were analyzed using Transwell and wound healing assays, respectively. The results demonstrated that FOXD2-AS1 was significantly overexpressed in glioma cells, particularly in U251 cells. Knockdown of FOXD2-AS1 in glioma cells significantly inhibited cell proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) and regulated the expression of CDK2, cyclinE1, P21, MMP7 and MMP9. Next, a possible mechanism for these results was explored, and it was observed that FOXD2-AS1 binds to and negatively regulates miR-506-5p, which is known to be a tumor-suppressor gene in certain human cancer types. Furthermore, overexpression of miR-506-5p significantly inhibited cell proliferation, migration, invasion and EMT, and these effects could be reversed by transfecting FOXD2-AS1 into the cells. In conclusion, our data suggested that FOXD2-AS1 contributed to glioma proliferation, metastasis and EMT via competitively binding to miR-506-5p. FOXD2-AS1 may be a promising target for therapy in patients with glioma.

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