SNHG17 enhances the malignant characteristics of tongue squamous cell carcinoma by acting as a competing endogenous RNA on microRNA-876 and thereby increasing specificity protein 1 expression
Authors: Ming Fu
Baorong Zhang
Xiaoming Liu
Yue Jia
Journal: Cell Cycle (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SNHG17; Tongue squamous cell carcinoma; anticancer therapy; miR-876.
Affiliations: Institute of Oral Diseases, Oral Medicine Center, University of Chinese Academy of Sciences, Shenzhen Hospital, Shenzhen, Guangdong, P.R. China.

Abstract:  A long noncoding RNA called SNHG17 (small nucleolar RNA host gene 17) is aberrantly expressed and plays essential roles in multiple human cancer types. Nevertheless, its expression pattern and specific functions in tongue squamous cell carcinoma (TSCC) have not been well studied until now. Hence, in this study, we aimed to measure SNHG17 expression in TSCC and to examine the actions of SNHG17 on the malignant characteristics of TSCC cells. The regulatory mechanism that mediates the oncogenic effects of SNHG17 on TSCC cells was investigated too. In this study, SNHG17 was found to be upregulated in TSCC, and this overexpression closely correlated with adverse clinical parameters and shorter overall survival among the patients with TSCC. The SNHG17 knockdown significantly decreased TSCC cell proliferation, migration, and invasion in vitro and tumor growth in vivo. Mechanism investigation revealed that SNHG17 acts as a competing endogenous RNA on microRNA-876 (miR-876) in TSCC cells. In addition, specificity protein 1 (SP1) was validated as a direct target gene of miR-876 in TSCC cells. SP1 expression restoration in TSCC cells reversed miR-876 overexpression-induced anticancer effects. MiR-876 downregulation strongly attenuated the actions of the SNHG17 knockdown in TSCC cells. SNHG17 plays an oncogenic part in TSCC cells both in vitro and in vivo via sponging of miR-876 and thereby upregulating SP1, which could be regarded as a promising target for TSCC therapy. 

Retracted: No

PubPeer comments:
 Fig 8b.  Representative images of tumor xenografts derived from the mice inoculated with either si-SNHG17u2013transfected or si-NCu2013transfected Tca8113 cells . Rotated through 90 deg.  The ruler used to provide scale appears to be the same (with the stain at one corner) as in *[left]* Fig 7A from [Zhang et al (2019)] .  Photograph of tumor xenografts obtained from nude mouse injected with miR-802 mimics- or miR-NC-transfected H460 cells . Rotated through 90 deg to facilitate comparison. *[upper right]* **Fig 8A from [Wang, Xiao Zhao (2019)] **.  miR-675 mimics or miR-NC were transfected into TPC-1 cells and then injected to nude mice. A representative image of tumor xenografts is shown . *[lower right]* Fig 7B from [Tan et al (2019)] .  Representative images of tumor xeno-grafts derived from H460 cells transfected with agomir-625 or agomir-NC .  Presumably all the tumors were photographed at the same laboratory. Is it possible that this part of the study was outsourced to a contractor? , 
 - *[above]* Fig 2d. - *[below]* Fig 6B from  MicroRNA-652 suppresses malignant phenotypes in glioblastoma multiforme via FOXK1-mediated AKT mTOR signaling pathway ([Yang et al 2019] ) **[retracted]**.  , 
 - *[above]* Fig 6D. - *[below]* Fig 4C from  MicroRNA-675 directly targets MAPK1 to suppress the oncogenicity of papillary thyroid cancer and is sponged by long non-coding RNA RMRP ([Wang et al 2019] ) **[retracted]**.  , 
 - *[above]* Fig 7f. - *[below]* Fig 4C D from  Long noncoding RNA TTN-AS1 enhances the malignant characteristics of osteosarcoma by acting as a competing endogenous RNA on microRNA-376a thereby upregulating dickkopf-1 ([Li et al 2019] ).  Two panels overlap. ,