LINC00152 promotes the growth and invasion of oral squamous cell carcinoma by regulating miR-139-5p
Authors: Zhihong Li
Jun Ning
Lei Wang
Minghe Li
Jing Wang
Cong Zhao
Journal: OncoTargets and Therapy (2018)
Discipline: CLINICAL MEDICINE
Keywords: LINC00152; lncRNA; miR-139-5p; oral squamous cell carcinoma.
Affiliations: Department of Oral and Maxillofacial Surgery, School of Stomatology Hospital of Jilin University, Changchun, China., Key Laboratory of Tooth Development and Bone Remodeling, School of Stomatology Jilin University, Changchun, China., Department of Gynaecology II, The First Hospital of Jilin University, Changchun, China., Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun, China, ., Department of Endodontics, School of Stomatology Hospital of Jilin University, Changchun, China., Department of Periodontology, School of Stomatology Hospital of Jilin University, Changchun, China.

Abstract:  Background: LINC00152 plays a crucial role in tumorigenesis and progression of multiple types of cancer. However, the biological significance of LINC00152 and its potential role in oral squamous cell carcinoma (OSCC) remain to be determined. In the present study, we investigated the role of LINC00152 and the underlying mechanism of its oncogenic activity in OSCC. Materials and methods: The expression of LINC00152 in OSCC tissues and cell lines was detected using qRT-PCR. Cell proliferation, colony formation, migration, and invasion were measured using a cell counting kit, colony formation assay, wound healing, and transwell invasion assays, respectively. The target gene of LINC00152 was confirmed using a dual-luciferase reporter assay and qRT-PCR. A nude mouse model was established to analyze the function of LINC00152 in vivo. Results: LINC00152 expression was significantly upregulated in OSCC tissues and cell lines compared with that in normal counterparts. Upregulated LINC00152 served as an independent prognostic predictor in patients with OSCC. Moreover, knockdown of LINC00152 inhibited cell proliferation, colony formation, migration, and invasion, and suppressed the epithelial to mesenchymal transition in vitro, as well as impairing tumor growth in vivo. A mechanistic investigation indicated that LINC00152 could directly bind to miR-139-5p in OSCC. LINC00152 expression was inversely correlated with miR-139 expression in OSCC tissues. Conclusion: Taken together, these results suggested that LINC00152 may function as oncogene in OSCC and could be a potential therapeutic target in patients with OSCC. 

Retracted: Yes

PubPeer comments:
 Fig 3C.  Western blotting analysis of the levels of epithelial to mesenchymal transition-related proteins (N-cadherin, Vimentin, and E-cadherin) in SCC-9 cells transfected with sh-LINC00152 or sh-NC . ![file] Other appearances of the loading control include Fig 4C from [Wen et al (2015)] . ![] 5B from [Dong et al (2016)] ![] Those threads link many other manifestations. , 
 Fig 3B.  Cell invasion was determined in SCC-9 cells transfected with sh-LINC00152 or sh-NC using a transwell invasion assay . ![file] Fig 2E from [Fei et al (2018)] . Cell invasion  determined in U2OS cells, transfected with pFER1L4 plasmid pCDNA3.1. ![file] Could the authors of either paper explain what happened here? , 
 *[below]* Fig 5B.  Images of tumor tissues in the sh-LINC00152 and sh-NC groups . *[above]* Fig 5B from [Qu et al (2018)] .  Photographs of tumors derived from U2OS cells 30 days after injection . ![file] Could the authors of either paper comment on the appearance of the same tumors in both? (albeit differently identified, in a different arrangement, and at a different scale). , 
 There are two problems about the cell lines used in this paper which state:  Four OSCC cell lines: Tca8113, OSCC-15, SCC-9, and SCC-25; and the human normal oral keratinocytes (hNOKs) cell line, were obtained from the Institute of Biochemistry and Cell Biology of the Chinese Academy of Sciences (Shanghai, China). 1) There is, to our knowledge no OSCC-15 cell line, probably the authors have used SCC-15. 2) More problematic: Tca8113 is not an OSCC cell line, it is a HeLa contaminated cell line. As only 1 out of the 4 cell lines is not from OSCC, the use of a contaminated cell line does not completely invalidate the conclusions of the paper, but it does invalidate the analysis of figure 1B: ![file] The overexpression of LINC00152 is thus not specific to OSCC as it is also statistically significant for Tca8113=HeLa See the relevant [Cellosaurus entry] , 
 Retracted [26 July 2021] . -------------------------------- The Editor-in-chief and Publisher of OncoTargets and Therapy wish to retract the published article. Concerns were raised regarding the alleged duplication of images within the article with images from other publications. Specifically: - The western blot bands for GAPDH in Figure 3C appear to have been duplicated with the western blot bands for u03b2-actin in Figure 4C from Wen et al, 2015 and the western blot bands for GAPDH in Figure 5B from Dong et al, 2016 . - The cell invasion image from Figure 3B panel sh-LINC00152 appears to have been duplicated with the cell invasion image in Figure 2E panel pFER1L4 from Fei et al, 2018 . - The tumor images shown in Figure 5B appear to have been duplicated with tumor images in Figure 5B from Qu et al, 2018 . The authors responded to our queries but were unable to provide an explanation for the alleged image duplication. The authors agreed with the decision to retract the article. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u201cRetractedu201d. ,