Lactobacillus Acidophilus Cytotoxicity Effect and Apoptosis in Human Bladder Carcinoma Cells: An In Vitro Study

Abstract

Introduction: Anticancer effects of Lactobacillus acidophilus, as a probiotic bacterium, have been indicated in several studies. There are common therapeutic options for bladder cancer treatment; however, their side effects and recurrence of disease are considerable. Therefore, complementary medication is essential and it must be safe and effective. In the present research, we assessed the anti-tumor activity of Lactobacillus acidophilus (LB) on the bladder cancer cell line by evaluating the apoptosis mechanism. Materials and Methods: EJ138 bladder cancer cell line was provided and the cytotoxicity level of LB was evaluated with various concentrations after 24, 48, and 72 h. To evaluate the apoptosis effect, the gene expression of Bax, BCL2, and TNF-α was assessed using real-time PCR. Results: The optimum concentration of the cytotoxicity level was 12.5μg/mL at 24, 48, and 72 h. Bax expression was upregulated in tumor cells treated with LB alone and the mixture of LB and BCG (LB/BCG) as compared to the control group after 24 and 48 h. Also, the mRNA level of TNF-α increased in treated cells with LB and LB/BCG compared to the control group. BCL2 expression did not show a significant difference between experimental groups versus the control group. Conclusion: Our findings showed that LB has a synergistic effect with BCG through increasing apoptotic gene expression and TNF-α cytokine. Besides, at 48 h treatment, the apoptosis effect is more than 24 h. Thus, it seems that the mode of action of LB is time-dependent.

The Urinary Microbiome: Role in Bladder Cancer and Treatment

“…Lactobacillus rhamnosus GG (LGG) and Lactobacillus casei Shirota were reported to kill BC cells through apoptosis and necrosis [ 173 ]. Additionally, Lactobacillus acidophilus was discovered to have a synergistic impact with BCG in the therapy of EJ138 bladder cancer cells via the upregulation of TNF-α cytokine and apoptotic Bax gene expression [ 176 ]. In addition, the immunomodulatory effects of LGG also promoted tumor regression by increasing the expression of lymphotactin (XCL1) to recruit T and NK cells [ 16 , 177 , 178 ].…”