Anti-tumor effect of chitin oligosaccharide plus cisplatin in vitro and in vivo.

Onco Targets Ther

Oncology Department, General Hospital of Northern Theater Command, Shenyang, Liaoning Province, People's Republic of China.

Published: September 2019

Background: Lung cancer is one of the most common malignant tumors in human beings, and cisplatin is a widely used chemotherapy drug, but its clinical application is limited because of its dose-dependent toxicity and drug resistance. Chitin is known to have various biological activities including anti-tumor, but the insoluble feature in common solvents greatly restricts its application. Chitin oligosaccharide is a small water-soluble molecule degraded from chitin without any toxic effect.

Methods: Chitin oligosaccharide was adopted to investigate the effects on lung adenocarcinoma A549 cells and tumor xenografts of nude mice. The experiments were divided into control group, chitin oligosaccharide group, cisplatin group and combination group. MTS assay, cell scratch test and migration assay were used to observe the proliferation and migration of A549 cells, and Western blot was used to detect the expression levels of caspase8, caspase3 and BAK. Ki67 and P53 expressions of tumor xenografts were detected to explore the effects of drugs on tumor prognosis.

Results: The results in vitro showed that chitin oligosaccharides could inhibit the proliferation and migration of A549 cells, and the effect was superior to chitin oligosaccharide or cisplatin when combined with cisplatin. Chitin oligosaccharide plus cisplatin up-regulated the expression level of caspase8 and caspase3, while had minor influence on the expression level of BAK. In vivo experiments showed that chitin oligosaccharide plus cisplatin could down-regulate the expression level of Ki67, while had minor influence on the expression level of P53.

Conclusion: The study demonstrated that chitin oligosaccharide plus cisplatin had positive synergistic effects, and it is possible to improve the prognosis of lung adenocarcinoma patients by up-regulating the expression level of caspase8, caspase3 and down-regulating the expression level of Ki67.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6754620PMC
http://dx.doi.org/10.2147/OTT.S220619DOI Listing

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