MicroRNA-152 inhibits tumor cell growth by directly targeting RTKN in hepatocellular carcinoma
Authors: Dequan Yu
Jun Liang
Yanjun Zhang
Yuhong Qi
Qiuju Shao
Jiejing Zhou
Journal: Oncology Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: Hepatocellular carcinoma; Rhotekin; Oncogene; Proliferation; Apoptosis
Affiliations: Department of Radiotherapy, Tangdu Hospital, The 4th Military Medical University, Xi'an, Shaanxi 710038, P.R. China.

Abstract:  Hepatocellular carcinoma (HCC) is the most common form of adult liver cancer and accounts for approximately 90% of all cases of primary liver cancer annually. Rhotekin (RTKN), which functions as a cancer promoter, can be frequently detected in many human cancers, including gastric cancer, colorectal carcinoma and bladder carcinoma. The aim of this study was to investigate the role of RTKN in HCC. Using HCC cells and tissues from patients with liver cancer, we demonstrated that RTKN was significantly increased in HCC. To examine the effect of RTKN on HCC, RTKN overexpressed or silenced HepG2 and Hep3B cells were constructed. Cell proliferation and apoptosis were measured by RT-PCR and flow cytometry. The results showed that RTKN can function as an oncogene and promote the proliferation, while inhibiting apoptosis, of HepG2 and Hep3B cells. Furthermore, we identified that RTKN is a direct gene target of miR-152. miR-152 can reverse the growth promoting effect of RTKN on HCC cells through G2/M phase arrest and nuclear factor-κB (NF-κB) signal inhibition. In conclusion, our research identified that miRNA-152 can inhibit tumor cell growth by targeting RTKN in HCC. 

Retracted: No

PubPeer comments:
 Fig. S2 from this article shows unexpected similarities with figure 1B published by the same research team in Neuromuscular disorders (Wein et al 2010, PMID: 19854055). Individual dots that appear to be duplicated between FACS panels are indicated by colored circles or arrows. Any comments from the authors are welcome. ![file] ![file] , 
 Fig. S2 from this article shows unexpected similarities with figure 1A published by the same research team in Neuromuscular disorders (Wein et al 2010, PMID: 19854055). Individual dots that appear to be duplicated between FACS panels are indicated by colored circles or arrows. ![file] ![file] , 
 The photo presented as figure S2 is the same as the figure 1A published in Neuromuscular disorders (Wein et al 2010, PMID: 19854055). ![file] , 
 Regarding the similarities observed in the supplementary data of our publication in STM, it is very clear that the two panels in green and red in figure S2 correspond to the same conditions as in the 2010 Wein et al publication. The green panel is our healthy control and the red panel is the negative control found in the bottom panel of Figure 1A. This was clearly indicated in the supplementary data of the STM paper, and the same is true for the figure showing the positive control for monocyte immunostaining. Thus, this is not a mistake since this figure was voluntarily added for the reasons indicated and clearly stated in the article. As mentioned in the comment regarding the article by Wein et al. 2010 regarding the degradation of Dysferlin after 24-36 hours, we have the same comment. However, if you read carefully the article, you can note that this supplementary data that was used essentially to demonstrate mini-dysferlin expression, was in reality useless since, during the revision process we had access to the muscle biopsy from our patient with mini-dysferlin. The corresponding western blot is fully integrated as the main figure 3 (3A) in the article, showing the expression of mini-dysferlin at the expected size. Thus, mini-dysferlin expression from monocytes was only maintained in the supplemental data to reinforce our conclusions but was not necessary. ,