CXCR3, belonging to CXC chemokine receptors, has been identified to be overexpressed in various kinds of tumors. There are three mRNA variants of CXCR3 (CXCR3A, CXCR3B and CXCR3alt) in human cells. The functions of major CXCR3 isoforms (CXCR3A, CXCR3B) have been reported in some tumors including prostate and breast cancer. However, the effects of CXCR3A and CXCR3B on gastric cancer cell progression remain unknown. The present investigation found that CXCR3A mRNA level was upregulated but CXCR3B mRNA level was downregulated in gastric cancer cells and tissues. In vitro growth analysis showed that CXCR3A acted as a positive mediator in regulating cell growth, whereas CXCR3B exerted the opposite effect. In vitro invasion and migration assays showed that CXCL10 promoted gastric cancer cell invasion and migration via CXCR3A, but not CXCR3B. Moreover, knockdown of CXCR3A inhibited cell growth and metastasis in vivo. Additionally, CXCR3A knockdown attenuated matrix metalloproteinase (MMP)‑13 and IL‑6 expression, and reduced ERK1/2 activation. Together, these data suggest that CXCR3A contributes to the growth, invasion and metastasis of gastric cancer cells in vitro and in vivo, and thus may be a key mediator of gastric cancer progression.

(-)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, could affect carcinogenesis and development of many cancers. However, the effects and underlying mechanisms of EGCG on gastric cancer remain unclear. We found that EGCG significantly inhibited proliferation and increased apoptosis of SGC-7901 cells in vitro. The decreased expressions of p-β-catenin(Ser552), p-GSK3β(S9) and β-catenin target genes were detected in SGC-7901 cells after treated by EGCG. XAV939 and β-catenin plasmid were further used to demonstrate the inhibition of EGCG on canonical Wnt/β-catenin signalling. Moreover, EGCG significantly inhibited gastric tumour growth in vivo by inhibiting Wnt/β-catenin signalling. Taken together, our findings establish that EGCG suppressed gastric cancer cell proliferation and demonstrate that this inhibitory effect is related to canonical Wnt/β-catenin signalling. This study raises a new insight into gastric cancer prevention and therapy, and provides evidence that green tea could be used as a nutraceutical beverage.

Background and purpose: Homo sapiens FOXF1 adjacent noncoding developmental regulatory RNA (FENDRR) is a novel long noncoding RNA (lncRNA) exerting important effects on transcriptional and post-transcriptional regulation. The purpose of this study was to investigate the potential role of FENDRR in colon cancer. Methods: Multiple cellular and molecular biology experiments were performed in the present study, such as CCK-8, Western blot, immunohistochemistry, confocal immunofluorescent and animal studies. Results: We determined that attenuation of FENDRR was a frequent event in colon cancer tissues and colon cancer cell lines, in contrast to their normal counterparts. Low levels of FENDRR were associated with the clinical stages and poor prognosis. Moreover, ectopic expression of FENDRR repressed colon cancer cell viability, invasion and epithelial–mesenchymal transition. Furthermore, through a series of in vitro and in vivo assays, we reported the discovery of FENDRR modulating the expression of SOX4 protein, and hence in the progression of colon cancer. Conclusion: Based on these data, we demonstrated that FENDRR may function as a tumor-suppressor gene by repressing SOX4 and as a potential therapeutic target for colon cancer.

Our study desired to investigate how miR-34c-3p regulates colon cancer cell proliferation and what is the relationship between miR-34c-3p and EIF3D. HCEpiC (normal human colonic epithelial cells), SW620, HT-29, SW480, and HCT-116 (human colon cancer cells lines) were used in our study. SW620 cells were chosen and divided into blank, miR-34c-3p mimics, miR-34c-3p NC, miR-34c-3p inhibitors, Lv-EIF3D, Lv-NC, and miR-34c-3p mimics+Lv-EIF3D groups. qRT-PCR was used for the detection of miR-34c-3p and EIF3D mRNA expressions. Dual-luciferase reporter assay was performed to investigate the effect of miR-34c-3p on EIF3D. Western blot was performed to detect EIF3D, cyclin D1, and c-Myc expressions. Clone formation and MTT assay were used to measure cell proliferation ability. colon cancer cells had lower miR-34c-3p expression, but higher EIF3D expression compared with HCEpiC. EIF3D mRNA expression was regulated negatively by miR-34c-3p. In the miR-34c-3p mimics group, colon cancer cell proliferation was significantly decreased, whereas c-Myc and cyclin D1 expressions were downregulated. Colon cancer cell proliferation in miR-34c-3p inhibitors and Lv-EIF3D groups was enhanced, and c-Myc and cyclin D1 expressions were decreased. The results suggested that by targeting EIF3D, miR-34c-3p inhibited colon cancer cell proliferation.

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