scholarly journals Recurrence-Associated Long Non-coding RNA LNAPPCC Facilitates Colon Cancer Progression via Forming a Positive Feedback Loop with PCDH7

2020 ◽  
Vol 20 ◽  
pp. 545-557 ◽  
Author(s):  
Ting Li ◽  
Zhiqiang Li ◽  
Hongxing Wan ◽  
Xifeng Tang ◽  
Han Wang ◽  
...  
2020 ◽  
Vol 40 (8) ◽  
Author(s):  
Shicai Ye ◽  
Bilan Sun ◽  
Weiyun Wu ◽  
Caiyuan Yu ◽  
Ting Tian ◽  
...  

Abstract Colon cancer is one of the major causes of cancer-related deaths worldwide. Long non-coding RNA (lncRNA) LINC01123 has been suggested to act as an oncogene in non-small cell lung cancer and a prognostic signature in head and neck squamous cell carcinoma. However, its role in colon cancer remains obscure. From TCGA database, LINC01123 was observed to be up-regulated in colon adenocarcinoma (COAD). Subsequently, the up-regulated LINC01123 was also detected in colon cancer cells. Functionally, LINC01123 could enhance cell proliferation, migration, invasion and angiogenesis. Moreover, the chemoresistance of colon cancer cells was verified to be promoted by LINC01123. Afterward, LINC01123 was found to bind with Ago2 and miR-34c-5p. Besides, miR-34c-5p was confirmed to inhibit the cellular process and chemoresistance of colon cancer cells. Then, VEGFA was disclosed to coexist with LINC01123 and miR-34c-5p in RNA-induced silencing complex. And TCGA database suggested that its expression was correlated with different stages of COAD. Moreover, it was uncovered that VEGFA could bind with miR-34c-5p and its expression positively correlated with LINC01123 expression. Finally, LINC01123 was proofed to regulate colon cancer progression and cells chemoresistance via VEGFA. In conclusion, LINC01123/miR-34c-5p/VEGFA axis promotes colon cancer malignancy and cells chemoresistance.


2016 ◽  
Vol 22 ◽  
pp. 3281-3287 ◽  
Author(s):  
Hui-yuan Zhai ◽  
Ming-hua Sui ◽  
Xiao Yu ◽  
Zhen Qu ◽  
Jin-chen Hu ◽  
...  

2019 ◽  
Vol 167 (4) ◽  
pp. 379-388 ◽  
Author(s):  
Chenghong Wang ◽  
Fangping Chen ◽  
Zili Fan ◽  
Chenjiao Yao ◽  
Lijun Xiao

Abstract Acute myeloid leukaemia (AML) is a frequently diagnosed malignancy in adults. Long non-coding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) has been well known to play vital roles in multiple malignancies including AML. Unfortunately, the detailed mechanism of CCAT1 in AML progression remains obscure. In this study, we demonstrated that CCAT1 was up-regulated in AML samples while its target, miR-490-3p, was relatively down-regulated. CCAT1 markedly increased viability and metastasis of AML cells, while miR-490-3p had opposite effects. CCAT1 could specifically bind to miR-490-3p and reduce its expression and activity, and MAPK1 was a target gene of miR-490-3p. Overexpressed CCAT1 could induce MAPK1 expression and c-Myc reciprocally increased CCAT1 expression. Our data implied that miR-490-3p could be a novel therapeutic target for AML, and highlights the crucial role of CCAT1/miR-490-3p/MAPK1/c-Myc positive feedback loop in AML progression.


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