Abstract
Oral biofilms harbour gram-negative bacterial antigen lipopolysaccharide (LPS) involved in oral cancer progression and gram-positive bacterial surface-associated adhesive, lipoteichoic acid (LTA). Thus, we hypothesised that LPS and LTA together would increase the proliferation of cancer cells compared to stimulation by LPS alone. Oral cancer cell lines SCC4, SCC9, SCC25, Cal 27 and the normal oral cell line, OKF6, were studied. The bacterial antigen stimulation indices were determined using the MT Glo assay. Cell proliferation after bacterial antigen stimulation was validated by clonogenic assays. Phosphokinase array, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and Western blot were employed to study proliferative and apoptotic pathways in bacterial antigen-stimulated cells. Bacterial antigens significantly stimulated Cal 27 (p ≤ 0.001) alone. SCC4 and SCC9 showed negligible stimulation with either antigen, while SCC25 results were comparable to OKF6. The combined antigen stimulation of Cal 27 led to a decrease in phosphorylated p53 and β-catenin and higher PI3K compared to LPS only stimulated cells (p ≤ 0.001). Combined bacterial antigen stimulation results in increased proliferation of Cal 27 cells due to lowering of tumor suppressor proteins and increased tumor proliferation-related proteins.
Highlights
Oral cancer is the sixth most common cancer in the world, high risk in South Asia with male preponderance [1, 2]
We present here the effect of combined bacterial antigen on select oral cancer cell lines and explore the proliferation pathways that may be affected by these bacterial antigens
Based on the results of Cal 27 MT Glo and clonogenic assays, the LPS+lipoteichoic acid (LTA) combination has a significant effect than LPS stimulation, supporting bacterial biofilm as plaque may result in increased progression of oral cancer than anaerobic bacteria alone
Summary
Oral cancer is the sixth most common cancer in the world, high risk in South Asia with male preponderance [1, 2]. While P. gingivalis LPS downregulates p53 and upregulates NF-kB, MMP-9, and the JAK/STAT pathway, STAT3 (which controls the intrinsic mitochondrial apoptotic pathway) [4]. This results in inflammation, antiapoptosis, increased viability of oral cancer cells and increased oral cancer invasion [4]. Human hepatocyte growth factor (HuHGF) stimulates stromal fibroblast-induced invasion (epithelial-mesenchymal cells) in the progression of oral cancer [5]. Other than its induction of HuHGF, the role of LTA in the proliferation of oral cancer cells remains elusive [6]. We present here the effect of combined bacterial antigen on select oral cancer cell lines and explore the proliferation pathways that may be affected by these bacterial antigens
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