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. 2021 Jun;25(12):5372-5380.
doi: 10.1111/jcmm.16548. Epub 2021 May 14.

V体育官网入口 - Sulfasalazine, a potent suppressor of gastric cancer proliferation and metastasis by inhibition of xCT: Conventional drug in new use

Jinfu Zhuang  1 , Xing Liu  1 , Yuanfeng Yang  1 , Yiyi Zhang  1 , Guoxian Guan  1
Affiliations

Sulfasalazine, a potent suppressor of gastric cancer proliferation and metastasis by inhibition of xCT: Conventional drug in new use

Jinfu Zhuang et al. J Cell Mol Med. 2021 Jun.

Abstract

The aim of this study was to explore the role of sulfasalazine on proliferation and metastasis in gastric cancer by inhibition of xCT. The relationships between clinical characteristics and xCT expression were analysed. An immunohistochemical staining assay and Western blot were performed among gastric cancers and normal gastric tissues. qPCR and Western blot were also used to evaluate the mRNA and protein expression in the normal gastric cell and eight gastric cancer cells, respectively. CCK-8 and colony formation assays were used to evaluate the effect of sulfasalazine on the proliferation and colony formation ability of three gastric cancers. The effect of sulfasalazine on the migration and invasion abilities of three cancer cells was assessed by the Transwell assay. xCT protein is up-regulated in gastric cancer specimens and cells VSports手机版. Three gastric cancer cells with high, medium and low expression of xCT were selected for the following analyses. CCK-8 assays revealed that sulfasalazine could attenuate the proliferation of HGC-27 and AGS. Also, the colony formation assay revealed that sulfasalazine might attenuate the colony formation ability in HGC-27 and AGS cells. Plus, the Transwell assays demonstrated that sulfasalazine might attenuate the migration and invasion abilities in HGC-27 and AGS cells. In conclusion, higher expression of xCT is associated with advanced tumour stage and poor overall survival of gastric cancer. Sulfasalazine can attenuate the proliferation, colony formation, metastasis and invasion of gastric cancer in vitro. Further study is required to validate our findings. .

Keywords: gastric cancer; growth; metastasis; sulfasalazine; xCT. V体育安卓版.

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Conflict of interest statement

The authors declared that they have no conflicts of interest in this work.

Figures

FIGURE 1
FIGURE 1
mRNA and protein expression of xCT in gastric cancer clinical samples and gastric cancer cell lines. A, The upper panel demonstrates the HE staining of normal and tumour tissues at 100× and 200× magnification. The lower panel demonstrates the immunochemical staining of the expression of xCT in gastric cancer tissues and normal gastric cancer tissues at 100× and 200× magnification. B, qPCR demonstrated the relative expression of xCT in eight paired gastric cancer and normal gastric tissues. C, The protein expression of xCT in eight gastric cancer specimens and paired corresponding normal gastric tissues. D, The protein expression of xCT in eight gastric cancer cell lines and normal gastric cells. E, The mRNA expression of xCT in tumour and normal gastric tissues based on data from the TCGA database. F, Survival analysis demonstrated that higher expression of xCT is associated with poor overall survival (P < .05)
FIGURE 2
FIGURE 2
The effect of sulfasalazine on the proliferation, colony formation, metastasis and invasion of gastric cancer. A, CCK‐8 assays revealed the effect of sulfasalazine on HGC‐27, AGS and MGC‐803 cell proliferation. B, Cell colony formation assays were utilized to evaluate the effect of sulfasalazine on HGC‐27, AGS and MGC‐803 cell proliferation. C, Transwell assays were performed to evaluate sulfasalazine's effect on the migration and invasion abilities of HGC‐27, AGS and MGC‐803 cells (P < .05)
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