<p>Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway</p>
Authors: Wu Zhong Zhang
Jun Bo Zhao
Dong Ming Yan
Yong Lu Ren
Jun Feng Xue
Journal: Cancer Management and Research (2020)
Discipline: CLINICAL MEDICINE
Keywords: cell proliferation; glioma; lncRNA FGD5-AS1; migration; wnt/β-catenin pathway.
Affiliations: Department of Neurosurgery, Jiaozuo People's Hospital, Jiaozuo 454000, Henan Province, People's Republic of China., Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, People's Republic of China.

Abstract:  Purpose: To investigate the specific function of long noncoding RNA FGD5 antisense RNA 1 (lncRNA FGD5-AS1) in glioma. Materials and methods: The level of FGD5-AS1 was detected in clinical samples and cell lines by qRT-PCR. Small interfering RNA (siRNA) of FGD5-AS1 or scramble siRNA was transfected into U87 cell lines to examine the role of FGD5-AS1 on glioma development. The proliferation of glioma cells was tested by Cell Counting Kit-8 (CCK-8), the migration and invasion of glioma cells were tested by transwell assay without matrigel or with matrigel. Western blot was used to detect the protein expression, and XAV-939 was used to inhibit wnt/β-catenin pathway. The effect of FGD5-AS1 on tumorigenesis of glioma was confirmed by xenograft nude mice model. Results: FGD5-AS1 was significantly increased in glioma tissues and cells. Loss of FGD5-AS1 inhibited the proliferation, migration and invasion of U87 cells. Furthermore, overexpression of FGD5-AS1 increased the mRNA and protein levels of β-catenin and cyclin D1. Blocking of wnt/β-catenin using XAV-939 reversed the promotion role of FGD3-AS1 on glioma cells' migration and invasion. The in vivo tumor growth assay showed that FGD3-AS1 accelerated glioma tumorigenesis with activating wnt/β-catenin pathway. Conclusion: Our research emphasized FGD5-AS1 acting as an oncogene by regulating wnt/β-catenin signaling pathway, thus providing some novel experimental basis for clinical treatment of glioma. 

Retracted: No

PubPeer comments:
 As noted on other threads, what appear to be the same tumors (and transformations of them) appear in three papers by unrelated groups of researchers: - Fig 4F from [Liu et al (2019)] . - Fig 7C from [Shi et al (2020)] . - Fig 5C from [Wen et al (2021)] . ![] ![] Here I am interested in the **ruler**, which migrated around the institutions along with the tumors. Note its distinctive markings: on the 10 , a stain at the tip of the leftward stroke of the 1 , and a stain in the middle of the righthand curve of the 0 . On the 20 , a stain along the tops of both digits. The ruler continued its travels and we find it in Fig 6A of [Ji Shang (2020)] ,  Effects of RPL38 knockdown on the size of MKN-45 xenograft tumors in nude mice. ![file] Fig 7A of [Liu et al (2020)] .  Tumors in nude mice after tumorigenesis . ![file] Figs 3C, 5E, 7F of [Wang et al (2020)] .  Tumor volume and tumor weight in mice . ![file] In **Fig 4B of [Zhao et al (2020)] **,  Tumor weight was determined in the isolated tumors from the nude mice , the resolution is lower but the 20 seems to display the same stain. ![file] The same low-resolution caveat applies to Fig 8B of [Xu et al (2020)] ,  Tumor weight was increased after miR-483-3p overexpression . ![file] It would make sense if the xenograft experiments were all the work of a single laboratory, but none of the papers mention outsourcing any research to an outside agency. ,