Placenta specific 8 gene induces epithelial-mesenchymal transition of nasopharyngeal carcinoma cells via the TGF-β/Smad pathway
Authors: Ze-Zhang Tao
Rui Yang
Jian-Fei Sheng
Yong-Gang Kong
Shi-Ming Chen
Yang Jiang
Ji-Bo Han
You Zou
Mao-Ling Huang
Journal: Experimental Cell Research (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: EMT; Gene knockout; Nasopharyngeal carcinoma; Placenta specific 8; TGF-β/smad pathway.
Affiliations: Department of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, 238 Jie-Fang Road, Wuhan, Hubei 430060, PR China., Department of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, 238 Jie-Fang Road, Wuhan, Hubei 430060, PR China; Research Institute of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, 238 Jie-Fang Road, Wuhan, Hubei 430060, PR China. Electronic address: .

Abstract:  The present study aimed to investigate the effects and mechanisms of PLAC8 on the epithelial-mesenchymal transition (EMT) of Nasopharyngeal carcinoma (NPC). The expression of PLAC8 in NPC and nasopharyngitis (NPG) tissues from 150 patients was determined using immunohistochemistry. The levels of PLAC8 in five NPC cell lines and nasopharyngeal permanent epithelial cell line were measured using western blotting. We then knocked out or overexpressed PLAC8 in CNE2 cells. Cell proliferation, wound healing, migration, and invasion assays were used to analyze the effects of PLAC8 on the proliferation, migration, and invasion in vivo and vitro. The results showed that the expression of PLAC8 was much higher in NPC tissues than in NPG tissues. The expression of PLAC8 was higher in all the cell lines than in the nasopharyngeal permanent epithelial cells. PLAC8 knockout resulted in significant decreases in cell proliferation, migration, and invasion; associated with lower protein levels of N-cadherin; and increased levels of E-cadherin. Overexpression of PLAC8 had the opposite effect. Furthermore, knockout of PLAC8 inactivated TGF-β/SMAD signaling pathway and suppressed the growth of NPC xenografts. PLAC8 may promote the carcinogenesis and EMT of NPC via the TGF-β/Smad pathway, which suggests that PLAC8 may be a potential biomarker for NPC. 

Retracted: No

PubPeer comments:
 Some bands in figure 5A and 5B appear to be similar ![file] , 
 No bands in figure 5A and 5B are similar. As shown in the original images of the figure 5A and 5B, 1,4,7 was the maker, 2,5 was koPLAC8, and 3,6 was the control. In the overexpressed-PLAC8 experiment, 9 and 10 was oePLAC8; 8 was the control. In this published paperuff0cthe original bands 2 and 3 were selected as the result of Vimentin expression changes following knockdown of the PLAC 8 gene. The 8 and 9 of the original bands were selected as the result of changes in Vimentin expression after PLAC 8 upregulation. In order to keep with the display order of other results in Figure 5, bands 2 and 3 in the original figure were rotated by 180 degrees, that is, the results of the control group were shown first, and then the results of the koPlac8 group were shown. , 
 #2 No bands in figure 5A and 5B are similar. As shown in the original images of the figure 5A and 5B, 1,4,7 was the maker, 2,5 was koPLAC8, and 3,6 was the control. In the overexpressed-PLAC8 experiment, 9 was oePLAC8; 8 was the control. In this published paperuff0cthe original bands 2 and 3 were selected as the result of Vimentin expression changes following knockdown of the PLAC 8 gene. The 8 and 9 of the original bands were selected as the result of changes in Vimentin expression after PLAC 8 upregulation. In order to keep with the display order of other results in Figure 5, bands 2 and 3 in the original figure were rotated by 180 degrees, that is, the results of the control group were shown first, and then the results of the koPlac8 group were shown. ![file] ,