학술논문
Ciprofloxacin promotes polarization of [CD86.sup.+][CD206.sup.-] macrophages to suppress liver cancer
Document Type
Academic Journal
Author
Source
Oncology Reports. July 2020, Vol. 44 Issue 1, p91, 12 p.
Subject
Language
English
ISSN
1021-335X
Abstract
Introduction Liver cancer is one of the most common malignant tumors worldwide (1), and may be treated with several methods, such as surgery (2), radiotherapy (3) and chemotherapy (4). However, [...]
Gut microbiota can promote tumor development by producing toxic metabolites and inhibiting the function of immune cells. Previous studies have demonstrated that gut microbiota can reach the liver through the circulation and promote the occurrence of liver cancer. Ciprofloxacin, an effective broad-spectrum antimicrobial agent, can promote cell apoptosis and regulate the function of immune cells. As an important part of the tumor microenvironment, macrophages play an important role in tumor regulation. The present study demonstrated that the treatment of macrophages with ciprofloxacin was able to promote the production of interleukin-1[beta], tumor necrosis factor-[alpha] and the polarization of [CD86.sup.+][CD206.sup.-] macrophages, while inhibiting the polarization of [CD86.sup.-] [CD206.sup.+] macrophages. This transformation may help macrophages promote tumor cell apoptosis, inhibit tumor cell proliferation, reduce metastasis and downregulate the phosphoinositide 3-kinase/AKT signaling pathway in liver cancer cell lines. In vivo experiments demonstrated that macrophages treated with ciprofloxacin inhibited the growth of subcutaneous implanted tumors in nude mice. In conclusion, the findings of the present study indicated that ciprofloxacin may inhibit liver cancer by upregulating the expression of [CD86.sup.+][CD206.sup.-] macrophages. This study further revealed the biological mechanism underlying the potential value of ciprofloxacin in antitumor therapy and provided new targets for the treatment of liver cancer.
Gut microbiota can promote tumor development by producing toxic metabolites and inhibiting the function of immune cells. Previous studies have demonstrated that gut microbiota can reach the liver through the circulation and promote the occurrence of liver cancer. Ciprofloxacin, an effective broad-spectrum antimicrobial agent, can promote cell apoptosis and regulate the function of immune cells. As an important part of the tumor microenvironment, macrophages play an important role in tumor regulation. The present study demonstrated that the treatment of macrophages with ciprofloxacin was able to promote the production of interleukin-1[beta], tumor necrosis factor-[alpha] and the polarization of [CD86.sup.+][CD206.sup.-] macrophages, while inhibiting the polarization of [CD86.sup.-] [CD206.sup.+] macrophages. This transformation may help macrophages promote tumor cell apoptosis, inhibit tumor cell proliferation, reduce metastasis and downregulate the phosphoinositide 3-kinase/AKT signaling pathway in liver cancer cell lines. In vivo experiments demonstrated that macrophages treated with ciprofloxacin inhibited the growth of subcutaneous implanted tumors in nude mice. In conclusion, the findings of the present study indicated that ciprofloxacin may inhibit liver cancer by upregulating the expression of [CD86.sup.+][CD206.sup.-] macrophages. This study further revealed the biological mechanism underlying the potential value of ciprofloxacin in antitumor therapy and provided new targets for the treatment of liver cancer.