Aberrant expression of B7-H3 in gastric adenocarcinoma promotes cancer cell metastasis
Authors: Wei Dai
Xin Zhao
Jianping Qiu
Genhai Shen
Quangen Gao
Journal: Oncology Reports (2014)
Discipline: CLINICAL MEDICINE
Keywords: B7-H3; T cell responses; cancer; gastric tissues; RNAi
Affiliations: Department of General Surgery, The First People's Hospital of Wujiang, Wujiang, Jiangsu 215200, P.R. China., Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.

Abstract:  B7-H3 belongs to the B7 superfamily, a group of molecules that costimulate or downmodulate T cell responses. Although it has been shown that B7-H3 can inhibit T cell responses, several studies, most of them performed in murine systems, found B7-H3 to act in a co-stimulatory manner. In addition, B7-H3 is also expressed in various human cancers and is correlated with the poor outcome of cancer patients. The functional role of B7-H3 in cancer is still controversially discussed. In the present study, we compared B7-H3 expression in normal gastric tissues and gastric cancer tissue specimens and determined the effects of low B7-H3 expression on the human gastric cancer cell line SGC-7901 by using RNAi. B7-H3 expression in gastric specimens was determined by tissue qPCR and immunohistochemisty. A SGC-7901 cell line with low B7-H3 expression was established by lentiviral-mediated RNA interference to investigate the effect of B7-H3 on cancer cell migration and invasion in vitro. By establishing an orthotopic transplantation gastric cancer mouse model, the effect of B7-H3 on cell migration and invasion was studied in vivo. B7-H3 expression was significantly higher in the gastric cancer group than that in the normal gaster group. B7-H3 knockdown by RNA interference decreased cell migration and Transwell invasion up to 50% in vitro. In the orthotopic transplantation gastric cancer mouse model, the effect of inhibiting metastasis by knockdown of B7-H3 was assessed in terms of the average postmortem abdominal visceral metastatic tumor weight. The results revealed that inhibition of B7-H3 expression reduced gastric cancer metastasis in vivo. In conclusion, B7-H3 is aberrantly expressed in gastric cancer. In addition to modulating tumor immunity, B7-H3 may have a novel role in regulating SGC-7901 cell metastasis. 

Retracted: No

PubPeer comments:
 Two of the assays in Figure 5 have regions that are unexpectedly similar, although not identical. Arrows show some common features for easier identification. Shown with enhanced sharpness. ***  , 
 Three images in Figure 5 (red, green, blue boxes) also seem to appear in another paper, Figure 6 of International Journal of Molecular Medicine (2013), doi: 10.3892 ijmm.2012.1212, posted here: https: pubpeer.com publications D094C50FCC34E4AE9762059CF7E035 Penultimate author on this paper seems to be first author on the other. ***  *** This study was supported by grants from the National Natural Science Foundation of China (no. 81302146) and Natural Science Foundation of Jiangsu Provincial University (no. 13KJB320018), China. , 
 Retracted [3 October 2022] . Following the publication of the above paper, an interested reader drew to the authors attention that the scratchu2011wound assay data featured in Fig. 5A on p. 2090 appeared to contain some overlapping data comparing between the panels, such that these data, which were intended to show the results from differently performed experiments, may have been derived from the same original source. After having reu2011examined their original data, the authors conceded that the figure had been assembled incorrectly (specifically, four of the images selected out of the nine data panels included in this figure part had been chosen erroneously). Furthermore, the first author on the paper (Wei Dai) also acknowledged that several of the named authors had not given their prior consent to be included as such as authors on the paper, and therefore a request was made that the paper be retracted from the publication. In view of these admissions, the Editor of Oncology Reports has accepted the authors request that the paper be retracted from the journal. The Editor apologizes to the readership for any inconvenience caused. ,