LncRNA UCA1 facilitated cell growth and invasion through the miR-206/CLOCK axis in glioma
Authors: Zhi Huang
Yingnan Yuan
Shi Zhou
Xiaowen Wu
Xuya Zhao
Wenfeng Yu
Lei Xiang
Journal: Cancer Cell International (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CLOCK; Cell growth; Glioma; lncRNA UCA1; miR-206.
Affiliations: 1Department of interventional radiology, The Second Affiliated Hospital of Guizhou Medical University, Guiyang, 556000 Guizhou People's Republic of China., 2Department of Interventional Radiology, The Affiliated Cancer Hospital of Guizhou Medical University, Guiyang, 550005 Guizhou People's Republic of China., 3Key Laboratory of Endemic and Ethnic Diseases, Ministry of Education, Guizhou Medical University, No. 9 Beijing Road, Guiyang, 550002 Guizhou People's Republic of China., 4Department of Interventional Radiology, The Affiliated Hospital of Guizhou Medical University, No. 9 Beijing Road, Guiyang, 550002 Guizhou People's Republic of China.

Abstract:  Background: Glioma is a lethal malignant brain tumor, which affects the brain functions and is life-threatening. LncRNA UCA1 was identified as a pivotal regulator for tumorigenesis of glioma. MiR-206 was discovered to promote tumorigenesis and is critical in the regulation of cell proliferation in glioma. This study will discuss the expression of UCA1 regarding miR-206 and CLOCK, and their integrative effects in the proliferation and cell cycle of glioma cells. Methods: qRT-PCR was conducted to measure the mRNA expressions of IgG and Ago2 in cells co-transfected with UCA1, and miR-216 in U251. Bioinformation was analyzed for the prediction of association between UCA1 and miR-206. Transwell migrations assays and invasion assays were utilized to observe the cell invasive ability. Western blot and immunofluorescence imaging were used to examine the protein expressions. In vivo comparisons and observations were also performed to investigate the role of UCA1 in glioma growth. Results: LncRNA UCA1 was up-regulated in glioma cell lines and tissues. It elevated cell invasion via the inducing of epithelial-mesenchymal transition. We found that UCA1 can modulate miR-206 expression and serve as an endogenous sponge of miR-206. The EMT-inducer CLOCK was validated as a messenger RNA target of miR-206. At last, we demonstrated that UCA1 exerted the biology function through regulating miR-206 and CLOCK in vivo. Conclusions: Overall, the results demonstrated that UCA1/miR-206/CLOCK axis participated in the progressing of glioma and could act as a promising therapeutic target. 

Retracted: No

PubPeer comments:
  Fig. 5 Silencing of UCA1 repressed glioma growth in vivo. a In vivo tumors co-transfected with LV-sh-con and LV-sh-UCA1 . ![file] The ruler here (distinguished by blemishes including a scrape to the left of 1 ) appears in other tumor line-ups from four other teams at various institutions in various provinces. E.g. Fig 5a of [He et al (2020)] . ![] [Pang et al (2019)] , Fig 9A (and linked papers). ![] Is it possible that this part of the study was performed by an outside laboratory? , 
  Sixty groups of glioma tissues and adjacent normal tissues were harvested from the Affiliated Hospital of Guizhou Medical University. The normal tissue was obtained from patients with fresh autopsy material (donation from individuals who died in traffic accident and confirmed to be free of any prior pathologically detectable conditions).  This is contradictory. Were the normal brain-tissue obtained from the glioma patients, adjacent to the excised gliomas, or from victims of traffic accidents? , 
 - *[left]* Fig 5D from  Exosomal long non-coding RNA UCA1 functions as growth inhibitor in esophageal cancer ([Zhu et al 2020] ). - *[right}* **Fig 2a**. ![file] ,