Association of CXCR1 and 2 expressions with gastric cancer metastasis in ex vivo and tumor cell invasion in vitro

Upregulation of miR-34a by diallyl disulfide suppresses invasion and induces apoptosis in SGC-7901 cells through inhibition of the PI3K/Akt signaling pathway

“…SGC-7901 cells were maintained in RPMI 1640 medium (Gibco; Thermo Fisher Scientific, Inc., Waltham, MA, USA) supplemented with 10% fetal bovine serum (Thermo Fisher Scientific, Inc.), 100 U/ml penicillin (Sigma-Aldrich, St. Louis, MO, USA) and 100 µg/ml streptomycin (Sigma-Aldrich) at 37˚C in a humidified incubator at an atmosphere of 5% CO 2 (4). A volume of 400 µM DADS (Sigma-Aldrich) was used to investigate the effects on SGC-7901 cells, and cells were incubated at 37˚C in a humidified atmosphere with 5% CO 2 for 24 h.…”

“…A Matrigel invasion assay was used to assay the capability of cell invasion. Briefly, 1x10 4 cells/well were plated with serum-free medium in the upper chamber (Corning, Inc., NY, USA), which was filter-coated with Matrigel (Sigma-Aldrich). The lower chamber was filled with 10% fetal bovine serum.…”

“…In China, GC remains the second leading cause of cancer-related mortality (4). At present, ~80% of patients diagnosed with GC are at an advanced stage with limited surgical options (5).…”

Interleukin-8 in gastrointestinal inflammation and malignancy: induction and clinical consequences

“…267 These positive correlations between CXCL8 and tissue invasion and metastasis are further supported by in vitro experiments, whereby knockdown of CXCR1 and CXCR2 proteins inhibited the migratory capability of gastric epithelial cells. 146 Similarly, overexpression of CXCL8 in in vitro colonic epithelial cell lines enhanced cellular proliferation, migration, and invasive potential of these cells. 268 Studies in prostate cancer found that CXCL8 enhances tumor cell migration and invasion via activation of Src and FAK.…”

“…146 Although both MMP-9 and CXCL8 are co-expressed in several GI disease states, it remains unknown whether proteolytic processing of CXCL8 by MMP-9 contributes to disease pathogenesis. However, in vivo studies have demonstrated that manipulation of MMP-9 alters susceptibility to experimental colitis, as inhibition of MMP-9 activity in mice is associated with decreased PMN accumulation and decreased expression of the CXCL8-related chemokine CXCL5.…”