The lncRNA UCA1 promotes proliferation, migration, immune escape and inhibits apoptosis in gastric cancer by sponging anti-tumor miRNAs
Authors: Chao-Jie Wang
Chun-Chao Zhu
Gang Zhao
Jia Xu
Qiang Liu
Ming Wang
Wen-Yi Zhao
Zi-Zhen Zhang
Journal: Molecular Cancer (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Gastric cancer; PDL1; UCA1; lncRNA; miRNA.
Affiliations: Department of Gastrointestinal Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160 Pu Jian Road, Shanghai, 200127, China., Department of Gastrointestinal Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160 Pu Jian Road, Shanghai, 200127, China. .

Abstract:  Background: UCA1 is a long non-coding RNA which was found overexpressed in various human cancers including gastric cancer (GC). It is identified that UCA1 promotes GC cells proliferation, migration and invasion, however, the role of UCA1 during the processes of immune escape is still not unclear. Methods: We collected 40 paired GC and non-tumor tissue samples. The level of UCA1 in GC and control tissue samples were determined by in situ hybridization and qRT-PCR. Cell viability was determined by MTT assay. GC cells' migration capacities were examined by transwell assay. To understand the roles of UCA1 during immune escape, wildtype or UCA1 KO GC cells co-cultured with peripheral blood mononuclear cells or cytokine-induced killer cells in vitro. Mouse model was used to examine the function of UCA1 in vivo. Results: UCA1 promoted GC cells proliferation and migration, and inhibit apoptosis. UCA1 repressed miR-26a/b, miR-193a and miR-214 expression through direct interaction and then up-regulated the expression of PDL1. UCA1-KO GC cells could induce a higher IFNγ expression when co-cultured with peripheral blood mononuclear cells (PBMCs), and have a lower survival rate when co-cultured with cytokine-induced killer (CIK) cells in vitro. UCA1-KO GC cells formed smaller tumors, had higher miR-26a, -26b, -193a and - 214 level, reduced cell proliferation and increased apoptosis in xenograft mouse model. Conclusions: UCA1 overexpression protected PDL1 expression from the repression of miRNAs and contributed to the GC cells immune escape. UCA1 could serve as a potential novel therapeutic target for GC treatment. 

Retracted: No

PubPeer comments:
 ![file] , 
 Fig 2 G and H have multiple overlaps. Some of the overlaps have adjustment in scale. ![file] , 
 Dear Tulipa Fosteriana and Hoya Camphorifolia, I am the corresponding author of this manuscript. We are greatly appreciated for your critical review and pointing out the problems in our paper. After rechecking the original figures of our transwell experiment, we realized that we made an unexpected mistake. The figures showed in the manuscript actually were the draft figures of preliminary experiment. We feel regret for such an error that shouldnu2019t being made. In order to fix this problem, we have already contacted the editorial office for errata. We will provide original figures of this transwell experiment to the journal. We do appreciate your careful review, and we will give further response after we get the result from editorial office. ,