MicroRNA-520b targets interlukin-2 to regulate the growth, metastasis and drug sensitivity of liver cancer cells
Authors: Xiaoyan Ding
Wei Sun
Wendong Li
Jinglong Chen
Ying Teng
Journal: American journal of translational research (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Liver cancer; cell cycle arrest; microRNA; proliferation.
Affiliations: Department of Cancer Center, Beijing Ditan Hospital Capital Medical University No 8, Jingshundong Street, Chaoyang District, Beijing 100015, China.

Abstract:  Liver cancer is ranked as the 5th major type of cancer and is responsible for significant number of human deaths across the world. Recent investigations have shown microRNAs (miRs) to be involved in diverse cellular processes. Additionally, they have been shown to exhibit therapeutic implications in treatment of different diseases including cancer. This study investigated the role and therapeutic implications of miR-520b in liver cancer. The results of the present study revealed significant downregulation of miR-520b in liver cancer cell lines. Overexpression of miR-520b suppresses the growth of the SNU-182 and HepG2 cells by triggering apoptosis. This was also accompanied by upsurge of Bax and Caspase-3 and depletion of Bcl-2 in SNU-182 and HepG2 cells. Additionally, miR-520b caused a significant decrease in the migratory and invasive potential of the SNU-182 and HepG2 cells and enhanced their chemosensitivity to Gemcitabine. Bioinformatic analysis and the dual luciferase showed that miR-520b targets IL2 in HepG2 cells. Suppression of IL2 inhibits the growth of the HepG2 cells while as IL2 overexpression could avoid the tumor suppressive effects of miR-520b in HepG2 cells. Taken together, miR-520b may prove to be essential therapeutic target in liver cancer treatment and warrants further research endeavours. 

Retracted: No

PubPeer comments:
 This concern may be considered pedantic, especially as this only concerns the introduction, but inaccuracies in the scientific literature have a way of propagating outward. The authors may wish to double-check one of the statistics quoted in their introduction, u201cAccording to a recent study, LEDVT prevalence is approximately 1 out of 1000 adults every year [4]... [4] Ho, V.B., van Geertruyden, P.H., Yucel, E.K. et al. (2011) Acr appropriateness criteria((r)) on suspected lower extremity deep vein thrombosis. J. Am. Coll. Radiol. 8, 383u2013387, https: doi.org 10.1016 j.jacr.2011.02.016u201d Reading the Ho 2011 citation leads a reader to the *underlying* study from which the statistic was obtained, Fowkes 2003, and reveals that this statistic is calculated from studies as old as 38 years and not more recently than 18 years (in 2018) - which I suggest shouldnu2019t be described here as u201crecent.u201d Careful readers may also note that u201c5 10,000 of the general populationu201d is the statistic provided in the Ho 2011 paper, not u201c1 out of 1,000 adultsu201d stated here, although perhaps this number appears somewhere in Fowkes 2003. I believe the correct statistic in this paper should read u201c0.5 out of 1,000 of the general population,u201d although the authors might consider whether more recent data is available. Note: The [1] citation in Ho 2011 is to Eur J Vasc Endovasc Surg 25, 1-5 (2003) doi:10.1053 ejvs.2002.1778. A reading of that paper explains their analysis encompassed 9 studies published between 1976 and 2000, from ~18-38 years ago, at the time this paper was written. , 
 I share my colleague s reluctance to descend into pedantry, but I feel compelled to point out that two panels overlap in Fig 2A ( Immunocytochemical staining of CD31 and CD34 in endothelial cells in vitro ).  , 
 I also have concerns about Fig 6A ( Cell cycle in each group after transfection detected by flow cytometry ), which appears to be hand-drawn, with lines that overhang alarmingly and do not add up in a way that makes any sense.  , 
 Further concerns about Figs 4C, 8E. These Western Blots are stylised in appearance, with no backgrounds, and no development of the shape of the bands as the proteins progress along the gels.  The p-NF-kappaB bands differ in shape and profile from their unphosphorylated counterparts than I would expect if the gels had been stripped and reblotted. Were they from different gels? ,