MiR-140-5p suppresses retinoblastoma cell growth via inhibiting c-Met/AKT/mTOR pathway
Authors: Xiaowei Peng
Yan Deng
Xiaolong Yin
Yujun Liao
Journal: Bioscience Reports (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MiR-140-5p; c-Met/AKT/mTOR signaling pathway; retinoblastoma; tumorigenesis.
Affiliations: Department of Pediatric Ophthalmology, The Second Affiliated Hospital of Nanchang University, Nanchang 330000, China., Department of Pediatric Ophthalmology, The Second Affiliated Hospital of Nanchang University, Nanchang 330000, China .

Abstract:  MiR-140-5p is low expression and acts as a tumor suppressor in various types of human cancers. However, the potential role of miR-140-5p in retinoblastoma (RB) remains unknown. In the present study, we performed the miRNA microarray analysis to investigate whether miRNAs expression are associated with RB tumorigenesis in RB tissues. We found that a large set of miRNAs were ectopic expressions and miR-140-5p is most significantly down-regulated in human RB tissues compared with normal retinas. In addition, low miR-140-5p expression is associated with clinicopathological features (differentiation, invasion, T classification, N classification, cTNM stage, and largest tumor base) and poor survival in RB patients. Furthermore, our results showed that overexpression of miR-140-5p suppresses proliferation and induces apoptosis and cell cycle arrest in RB cell. Meanwhile, we confirmed that c-Met is the functional target of miR-140-5p in RB cell, and miR-140-5p expression is negatively correlated with c-Met in RB tissues. We also found that inhibition of c-Met also suppresses proliferation and induces apoptosis and cell cycle arrest in RB cell. Interestingly, c-Met can rescue the suppressive effects of miR-140-5p on RB cell growth and cell cycle arrest. More importantly, our findings indicated that miR-140-5p may inhibit cell growth via blocking c-Met/AKT/mTOR signaling pathway. Collectively, these results suggested that miR-140-5p might be a potential biomarker and target in the diagnosis and treatment of RB. 

Retracted: No

PubPeer comments:
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 #2 The similarity between the two right-hand panels is more extensive than you have suggested. ![file] , 
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 Fig 1:  (a) IHC analysis of ST6Gal-I expression in adjacent noncancerous tissues (ANT) and different grades of HCC tissues (n=80). I have no idea why the 3rd row of 1(a) is a different colour from the 1st and 2nd rows. Is it a different stain? The text is not helpful, with references to  matched representative pairs which makes no sense:  ST6Gal-I was stained by immunohistochemistry (IHC) in representative pairs of cancerous and matched non-tumor liver sections from HCC patients (Figure 1a). Perhaps the labels  200x and  400x are to be understood as magnification, but then we encounter the problem that overlapping sections of two panels from the T-I column do **not** differ by a scale factor of 2. ![file] , 
 2020 retraction. https: www.nature.com articles s41389-020-0211-6 The authors have retracted this article [1] because there are errors in some images. In Fig. 2g, a colony picture for Mock group was incorrect. In Fig. 2k, the invasion pictures for Mock and overexpression ST6Gal-1 cells were incorrect. In Fig. 3g, the colony picture for shNC was incorrect. In Fig. 4f, the authors mistakenly provided WB band for GAPDH. In Fig. 4g, the IHC pictures for 10w in Negative Control and DENA-induced Groups were incorrect, and in Fig. 7f, a IHC picture for GSK-3u03b2 in DENA-induced Group (10w) was presented incorrectly. Due to these errors the findings are no longer reliable. The following authors have agreed to this retraction - Zhao Y, Chen X, Wang L, Zhang J, Wang S, Wei A. The following authors have not responded to any correspondence from the publisher about this retraction - Zhang H, Zhang H, Yu X, Yuan Q. [1] Zhao Y, Wei A, Zhang H, Chen X, Wang L, Zhang H, Yu X, Yuan Q, Zhang J, Wang S. u03b12, 6-Sialylation mediates hepatocellular carcinoma growth in vitro and in vivo by targeting the Wnt u03b2-catenin pathway. Oncogenesis 6, e343. https: doi.org 10.1038 oncsis.2017.40 ,