Corresponding Author: Xiaolan You

Medical College, Yangzhou University, 88 South Daxue Road. Hanjiang District, Yangzhou, Jiangsu 225001 (China)


In the article “Galectin-1 Promotes Metastasis in Gastric Cancer Through a Sphingosine-1- Phosphate Receptor 1-Dependent Mechanism” [Cell Physiol Biochem 2018;51:11-30; DOI: 10.1159/000495157] by You et al., the following incorrect representative images were included in the article due to authors' selection of the wrong folder when uploading the figures.

Figure 4D - Bright SGC-7901+OE-Gal-1 and the corresponding Figure 4D - GFP SGC-7901+OEGal- 1 has been replaced with the correct representative image.
Figure 4H- KD-Gal1 has been replaced with the correct representative image.
Figure 5G the incorrect image was included for 5G-MGC-803 and 5G-NC,Figure 5G-MGC-803 is now correctly be labelled as 5G-NC and Figure 5G-NC is now correctly be labelled as 5G-MGC-803.
Figure 5I- MGC-803 has been replaced with the correct representative image.
The corrected Figures 4 and Figure 5 are shown here.

Fig. 4. Gal-1 and S1PR1 associates with invasiveness of gastric cancer cells. Western blot analysis of a Gal-1 and S1PR1 protein expression and RT-PCR analysis of b Gal-1 and c S1PR1 gene expression in AGS, SGC-7901, BGC-823, MGC-803, and HGC-27 gastric cancer cell lines. d. Transduction efficiency confirmed by GFP. Original magnification was 100×. e. Western blot confirmation of stable knockdown of Gal-1 and decreased expression of S1PR1 in MGC-803 cell line when Gal-1 is knocked down. f. Stable overexpression of Gal-1 increases expression of S1PR1 in SGC-7901 cells. Invasiveness of SGC-7901 was enhanced when g Gal-1 was over-expressed and h invasiveness of MGC-803 was weakened when Gal-1 was knocked down. The number of invaded cells was quantified by counting in six randomly-selected fields at × 200 magnification. OE-Gal-1:over-expression of Gal-1; NC: negative control (empty vector), KD-Gal: knockdown of Gal-1 expression. NS: not significant.

Fig. 5. Gal-1 promotes invasion in gastric cancer through a mechanism dependent on enhanced expression of S1PR1. Lentiviral transduction efficiency was confirmed by a GFP fluorescence and RT-PCR analysis for GFP in b MGC-803 cells and c SGC-7901 cells. Original magnification was 100×. S1PR1 knockdown or over-expression was confirmed with western blot in d MGC-803 cells and e SGC-7091 cells. f. Simultaneous knockdown of Gal-1 and over-expression of S1PR1 in MGC803 cells confirmed by western blot. Invasiveness of g MGC-803 cells was reduced with S1PR1 knockdown, while invasiveness of h SGC-7901 cells was enhanced with over-expression of S1PR1. i. Simultaneous knockdown of Gal-1 and over-expression of S1PR1 in MGC-803 cells rescued reduction in invasiveness from Gal-1 knockdown; magnification: ×200.