4.5 Article

Chloroquine inhibits MGC803 gastric cancer cell migration via the Toll-like receptor 9/nuclear factor kappa B signaling pathway

Journal

MOLECULAR MEDICINE REPORTS
Volume 11, Issue 2, Pages 1366-1371

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2014.2839

Keywords

chloroquine; gastric cancer; cell migration; Toll-like receptor 9; nuclear factor-kappa B p65

Funding

  1. Ningxia Natural Science Foundation [NZ0991, NZ11100, NZ14057]
  2. National Natural Science Foundation of China [31060140, 31260243, 31460257]
  3. Program for New Century Excellent Talents in University, State Education Ministry (Beijing, China)

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Stimulation of Toll-like receptor 9 (TLR9) has been associated with invasion in various types of cancer cell in vitro. The present study aimed to evaluate the expression of TLR9 in MGC803 gastric cancer cells and investigate the effect of a non-specific TLR9 inhibitor, chloroquine (CQ), on MGC803 cell migration via the TLR9/nuclear factor kappa B (NF kappa B) signaling pathway. The expression of TLR9 was investigated using reverse transcription polymerase chain reaction (RT-PCR), flow cytometry and western blot analysis. The effects of CQ on MGC803 cell proliferation were measured by MTT colorimetric assay. The mRNA expression levels of cyclooxygenase-2 (COX-2), matrix,metalloproteinase (MMP)-2, MMP-7 and NF kappa B p65 were evaluated by RT-PCR in MGC803 cells stimulated by various concentrations of CQ. The migration of gastric cancer cells treated with CQ at 12,24 and 36 h was measured by wound healing assay. The results indicated that MGC803 cells expressed TLR9 and that CQ had anti-proliferative effects on MGC803 cells and inhibited mRNA expression of COX-2, MMP-2, MMP-7 and NF kappa B p65 (P<0.05). Furthermore, CQ inhibited the bioactivity of NF kappa B p65 and prevented the migration of MGC803 cells in a dose-dependent manner (P<0.05). In conclusion, the results indicated that the TLR9/NF kappa B signaling pathway was involved in gastric cancer cell migration and that CQ had anti-tumor activity.

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