miR-26a and its target CKS2 modulate cell growth and tumorigenesis of papillary thyroid carcinoma
Authors: Zhongwei Lv
Wenqing Liang
Mingli Lv
Maoquan Li
Haidong Cai
Quanchi Chen
Da Fu
Lanbao Ding
Meng Ye
Xiaoping Zhang
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: miR-26a; papillary thyroid carcinoma; CKS2; cell growth; cell-cycle distribution
Affiliations: Department of Nuclear Medicine, Shanghai 10th People's Hospital, School of Medicine, Tongji University, Shanghai, China.

Abstract:  Background: While many studies have shown that levels of miR-26a are lower in papillary thyroid carcinoma (PTC), the role and mechanism of miR-26a in PTC are unclear. Method: We used database searches to select potential mRNA targets of miR-26a. Anti-miR-26a, miR-26a mimic, siRNA for CKS2 and their effects on cell growth, cell-cycle distribution and colony formation were evaluated. We also evaluate the over-expressed miR-26a in TPC-1 cells in severe combined immune-deficient mice. We used luciferase reporter assays, real-time PCR and western blot analysis to measure the expression and activity of miR-26a, CKS2, and related factors such as cyclin B1, cyclin A, cdk1, bcl-xl and Akt. Finally, we measured the relationship between the levels of miR-26a and CKS2 in PTC and normal thyroid tissues. Results: Relative to normal thyroid tissues, miR-26a is consistently down-regulated in TPC specimens, and CKS2 was identified as a potential target. Up-regulated miR-26a expression or down-regulated CKS2 expression in TPC-1 and CGTH W3 cells lines caused G2 phase-arrest. Decreased miR-26a expression or increased CKS2 expression could have inverse function on PTC cell lines. CyclinB1, cyclinA, bcl-xl and AKt are indirectly regulated by miR-26a in a CKS2-dependent manner. Finally, CKS2 is overexpressed in PTC specimens relative to normal thyroid tissue, and a significant inverse correlation exists between miR-26a and CKS2 expression in clinical PTC specimens. Conclusion: Our data indicate that miR-26a functions as a growth-suppressive miRNA in PTC, and that its suppressive effects are mediated mainly by repressing CKS2 expression. 

Retracted: Yes

PubPeer comments:
 2021 retraction. https: journals.plos.org plosone article?id=10.1371 journal.pone.0250313 Following the publication of this article [1], concerns were raised regarding results presented in Figs 2, 3, 4 and 5. Specifically, Similarities have been detected within and between the following FACS panels presenting different experimental conditions: u25cb. The Fig 2G miR-26a-TCP-1 cell panel, the Fig 2G EV-TPC-1 cell panel, the Fig 4D miR-26a mimic panel, and the Fig 4D CKS2 siRNA panel. u25cb. The Fig 4D miR-26a control panel and the Fig 4D CKS2 siRNA control panel. u25cb. The Fig 5D CKS2 panel and the Fig 5D anti-miR-26a panel. u25cb. The Fig 5D EV panel and the Fig 5D anti-miR control panel. Although these panels are not identical, they appear to be more similar than would be expected from independent samples. A vertical irregularity suggestive of gel splicing has been detected between the second and the third lane of the GAPDH panel of Fig 3C. The underlying data to support the published results are no longer available. In light of the concerns affecting multiple figure panels that question the integrity of these data, the PLOS ONE Editors retract this article. XZ agreed with the retraction and apologizes for the issues with the published article. MiL, MaL, QC, MY, WL, LD, HC, DF, and ZL either did not respond or could not be reached directly. Reference 1.Lv M, Zhang X, Li M, Chen Q, Ye M, Liang W, et al. (2013) miR-26a and its Target CKS2 Modulate Cell Growth and Tumorigenesis of Papillary Thyroid Carcinoma. PLoS ONE 8(7): e67591. https: doi.org 10.1371 journal.pone.0067591 pmid:23861775 ,