Abstract
BackgroundColorectal cancer (CRC) is a major clinical challenge, and the gut microbiome plays important roles in the occurrence and metastasis of CRC. Lactobacillus and their metabolites are thought to be able to suppress the growth of CRC cells. However, the antimetastatic mechanism of Lactobacillus or their metabolites toward CRC cells is not clear. Therefore, the aim of this study was to assess the inhibitory mechanism of cell-free supernatants (CFSs) of L. rhamnosus GG, L. casei M3, and L. plantarum YYC-3 on metastasis of CRC cells.ResultsYYC-3 CFS showed the highest inhibitory effect on CRC cell growth, invasion and migration, and inhibited MMP2, MMP9, and VEGFA gene and protein expression, and protein secretion. Furthermore, it suppressed the activities of MMPs by gelatin zymography. Moreover, the effective compounds in these CFSs were analyzed by Q Exactive Focus liquid chromatography–mass spectrometry.ConclusionsOur results showed that metabolite secretions of YYC-3 may inhibited cell metastasis by downregulating the VEGF/MMPs signaling pathway. These data suggest that treatment of CRC cells with metabolites from L. plantarum YYC-3 may reduce colon cancer metastasis.
Highlights
Colorectal cancer (CRC) is a major clinical challenge, and the gut microbiome plays important roles in the occurrence and metastasis of CRC
The growth of the HT-29 cells were inhibited in a dose-dependent manner after treatment with cell-free supernatants (CFSs) of GG, M3, and YYC-3, the IC50 values of these were 358.21, 349.88, and 259.91 μL/mL, respectively
We demonstrated the inhibitory effect of CFSs by L. casei and L. rhamnosus GG on colon cancer cell invasion and migration using Caco-2 and HT-29 cells
Summary
Colorectal cancer (CRC) is a major clinical challenge, and the gut microbiome plays important roles in the occurrence and metastasis of CRC. Lactobacillus and their metabolites are thought to be able to suppress the growth of CRC cells. The anti-cancer mechanisms attributed to these LABs include promoting apoptosis of the cancer cells through intrinsic and extrinsic apoptotic pathways, anti-proliferative regulation of the cell cycle in cancer cell lines, sequestering of reactive oxygen species by antioxidative enzymes to prevent carcinogenesis, production of bacterial enzymes, effecting the metabolites and epigenetics of the host, and regulating different signalling pathways in colon cancer cells [17, 18]
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