4.2 Article

A New Lectin from Auricularia auricula Inhibited the Proliferation of Lung Cancer Cells and Improved Pulmonary Flora

Journal

BIOMED RESEARCH INTERNATIONAL
Volume 2021, Issue -, Pages -

Publisher

HINDAWI LTD
DOI: 10.1155/2021/5597135

Keywords

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Funding

  1. Science and Technology Project of Tibet Autonomous Region [XZ201801 GA 15]
  2. Tibet Autonomous Region Nature Fund Project [2016ZR NQ 01]

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Lectins, widely distributed in nature, are often involved in anti-tumor activities. This study successfully isolated and purified a 25 kDa lectin, AAL, from Auricularia auricula, showing anti-cancer activity by potentially regulating gene expression to inhibit tumor proliferation. The study also demonstrated that lectin treatment improved bacterial diversity characteristics by enhancing the colonization ability of normal microflora.
Lectins are widely distributed in the natural world and are usually involved in antitumor activities. Auricularia auricula (A. auricula) is a medicinal and edible homologous fungus. A. auricula contains many active ingredients, such as polysaccharides, melanin, flavonoids, adenosine, sterols, alkaloids, and terpenes. In this study, we expected to isolate and purify lectin from A. auricula, determine the glycoside bond type and sugar-specific protein of A. auricula lectin (AAL), and finally, determine its antitumor activities. We used ammonium sulfate fractionation, ion exchange chromatography, and affinity chromatography to separate and purify lectin from A. auricula. The result was a 25 kDa AAL with a relative molecular mass of 18913.22. Protein identification results suggested that this lectin contained four peptide chains by comparing with the UniProt database. The FT-IR and beta-elimination reaction demonstrated that the connection between the oligosaccharide and polypeptide of AAL was an N-glucoside bond. Analyses of its physical and chemical properties showed that AAL was a temperature-sensitive and acidic/alkaline-dependent glycoprotein. Additionally, the anticancer experiment manifested that AAL inhibited the proliferation of A549, and the IC50 value was 28.19 +/- 1.92 mu g/mL. RNA sequencing dataset analyses detected that AAL may regulate the expression of JUN, TLR4, and MYD88 to suppress tumor proliferation. Through the pulmonary flora analysis, the bacterial structure of each phylum in the lectin treatment group was more reasonable, and the colonization ability of the normal microflora was improved, indicating that lectin treatment could significantly improve the bacterial diversity characteristics.

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