Surfactin from Bacillus subtilis attenuates ambient air particulate matter-promoted human oral cancer cells metastatic potential
Journal
Journal of Cancer
Journal Volume
11
Journal Issue
20
Pages
6038
Date Issued
2020
Author(s)
Vo, Thi Thuy Tien
Lee, Chiang-Wen
Wu, Ching-Zong
Liu, Ju-Fang
Lin, Wei-Ning
Hsu, Lee-Fen
Tsai, Ming-Horng
Lee, I-Ta
Abstract
Recently, many studies have indicated that ambient air particulate matter (PM) can increase the risk of oral cancer. The most common malignant tumor in the oral cavity is oral squamous cell carcinoma (OSCC). Usually, cancer cell migration/invasion is the most important cause of cancer mortality. Matrix metalloproteinase-2 (MMP-2) and MMP-9 have been shown to play important roles in regulating metastasis and the tumor microenvironment. Here, we studied the anti-cancer effects of surfactin, a cyclic lipopeptide generated by Bacillus subtilis, on cancer cell migration and invasion. Surfactin suppressed PM-promoted cell migration and invasion and colony formation of SCC4 and SCC25 human oral squamous cell carcinoma cell lines. We observed that PM induced MMP-2 and MMP-9 expression, which was inhibited by surfactin. Transfection with p65, p50, c-Jun, c-Fos, p85, p110, Akt, mammalian target of rapamycin (mTOR), or interleukin-6 (IL-6) siRNA markedly inhibited PM-induced MMP-2 and MMP-9 expression. Moreover, surfactin could reduce Akt, mTOR, p65, and c-Jun activation and IL-6 secretion induced by PM. Finally, we proved that transfection with Akt, p65, or c-Jun siRNA significantly inhibited PM-induced IL-6 release. Taken together, these results suggest that surfactin functions as a suppressor of PM-induced MMP2/9-dependent oral cancer cell migration and invasion by inhibiting the activation of phosphoinositide 3-kinase (PI3K)/Akt/mTOR and PI3K/Akt/nuclear factor-κB (NF-κB) and activator protein-1 (AP-1)/IL-6 signaling pathways.
Subjects
Invasion; Matrix metalloproteinase; Oral cancer; Particulate matter; Surfactin
SDGs
Other Subjects
gelatinase A; gelatinase B; immunoglobulin enhancer binding protein; interleukin 6; mammalian target of rapamycin; messenger RNA; phosphatidylinositol 3 kinase; protein c fos; protein c jun; protein kinase B; protein p110; protein p50; protein p85; small interfering RNA; surfactin; synaptotagmin I; transcription factor AP 1; Akt/mTOR signaling; ambient air; antineoplastic activity; Article; Bacillus subtilis; cell invasion; cell migration; cell viability; colony formation; colony forming unit; cytokine release; down regulation; enzyme activity; human; human cell; metastasis potential; mouth cancer; mRNA expression level; nonhuman; oral squamous cell carcinoma cell line; particulate matter; protein expression level; SCC-4 cell line; SCC25 cell line; signal transduction; transient transfection; tumor microenvironment; upregulation
Publisher
IVYSPRING INT PUBL