In the past 20 years, natural active polysaccharides as a renewable biological resource have attracted extensive attention. In a new study in published in Glycoscience & Therapy , a team of researchers from China investigated the molecular mechanism underlying the anti-cervical cancer activity of Lentinus edodes-derived β-glucan (LNT) and, for the first time, identified DMBT1 as a key target.
"It was found that LNT specifically bound to DMBT1 on the membrane of HeLa cells through hydrogen bonds, hydrophobic interactions, and van der Waals forces, and significantly upregulated its expression in a concentration-dependent manner," shares corresponding author Xiaojun Xu. "This interaction inhibited cancer cell proliferation and induced apoptosis."
Using a DMBT1 knockdown cell model, the tumor-suppressive role of DMBT1 was further validated: the inhibitory effect of LNT was significantly diminished in DMBT1-knockdown cells, accompanied by a marked reduction in its regulatory capacity over the downstream PI3K/Akt signaling pathway.
"This finding not only elucidates a novel mechanism by which LNT exerted its anticancer activity through the DMBT1–PI3K/Akt axis, but also provides a theoretical basis for targeted therapy of cervical cancer," says Xu.
Moreover, both in vitro and in vivo experiments confirm that the efficacy of LNT was closely correlated with DMBT1 expression levels, suggesting that DMBT1 may serve as a prognostic marker or a novel target for drug development in cervical cancer.
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Contact the author: Shuqian Hu, Xuan Li, Xiaojuan Xu. Department of Plastic Surgery at Zhongnan Hospital, College of Chemistry and Molecular Sciences, Hubei Engineering Center of Natural Polymer-Based Medical Materials, Wuhan University, Wuhan 430072, China; Shandong Laboratory of Yantai Drug Discovery, Bohai Rim Advanced Research Institute for Drug Discovery, Yantai, Shandong 264117, China. E-mail address: xuxj@whu.edu.cn (X. Xu)
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Glycoscience & Therapy
Experimental study
Cells
Lentinus edodes-derived β-glucan inhibits human cervical cancer progression through a potential target of DMBT1 on HeLa cell
All authors declare no competing interests.