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Abstract
The bacterial antigen, lipopolysaccharide (LPS) and disruptions in calcium channels are independently known to influence oral cancer progression. Previously, we found that bacterial antigens, LPS and lipoteichoic acid (LTA) act as confounders during the action of capsaicin on Cal 27 oral cancer proliferation. As calcium channel drugs may affect oral cancer cell proliferation, we investigated the effect of ML218 HCl, a T-type voltage-gated calcium channel blocker, on the proliferation of Cal 27 oral cancer cells. We hypothesized that ML218 HCl could effectively reduce LPS-induced oral cancer cell proliferation. LPS and LTA antigens were added to Cal 27 oral cancer cells either prior to and/or concurrently with ML218 HCl treatment, and the efficacy of the treatment was evaluated by measuring Cal 27 proliferation, cell death and apoptosis. ML218 HCl inhibited oral cancer cell proliferation, increased apoptosis and cell death, but their efficacy was significantly reduced in the presence of bacterial antigens. ML218 HCl proved more effective than capsaicin in reducing bacterial antigen-induced Cal 27 oral cancer cell proliferation. Our results also suggest an interplay of proliferation factors during the bacterial antigens and calcium channel drug interaction in Cal 27. Bacterial antigen reduction of drug efficacy should be considered for developing newer pharmacological agents or testing the efficacy of the existing oral cancer chemotherapeutic agents. Finally, voltage gated calcium channel drugs should be considered for future oral cancer research.
Highlights
IntroductionLipopolysaccharide (LPS), resulted in increased proliferation of the oral cancer cell
Cancer of the oral cavity is one of the most prevalent cancers worldwide, resulting in high morbidity and mortality rates [1].We recently reported that the combination of bacterial antigens, lipoteichoic acid (LTA)and lipopolysaccharide (LPS), resulted in increased proliferation of the oral cancer cellCal 27, but not SCC4, SCC9 and SCC25, compared to stimulation with LPS alone [2]
The effect of combined antigens was greater than LPS alone. These results suggest that the presence of the bacterial antigen lowered the inhibition percentage of calcium channel drugs, and combined LPS+LTA acted synergistically to lower the effect of calcium channel drugs on
Summary
Lipopolysaccharide (LPS), resulted in increased proliferation of the oral cancer cell. Cal 27, but not SCC4, SCC9 and SCC25, compared to stimulation with LPS alone [2]. We developed an in vitro assay to measure the efficacy of drug treatment on Cal 27 in the presence of bacterial antigens, and examined the effect of capsaicin, which is known to induce apoptosis in several cancers [3]. The bacterial antigens LPS and LTA decreased the anti-cancer efficacy of capsaicin, both for antigenic stimulation given prior to and concurrently with this drug [3]. Calcium channels are linked directly or indirectly to all the ‘hallmarks of cancer’ [4]. Changes in the activity of calcium channels lead to alterations in the calcium flux across plasma membrane and intracellular organelles in cancer cells, relative
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