文献类型：期刊文献

英文题名：Structural characterization of a glycosaminoglycan sulfate from Sepia esculenta ink, and its apoptosis induction in MDA-MB-231 cells via miR-18a-5p/ORAI3 pathway mediated intracellular calcium overload

作者：Wu, Jiayi[1];Yang, Xiaomei[2];Xiao, Wei[3];Lin, Zhen[1];Luo, Ping[1];Gu, Yipeng[2];Liu, Huazhong[1]

机构：[1]Guangdong Ocean Univ, Sch Chem & Environm, Dept Appl Chem, Zhanjiang 524088, Peoples R China;[2]Hezhou Univ Inst Food Sci & Technol, Guangxi Key Lab Hlth Care Food Sci & Technol, Hezhou 542899, Peoples R China;[3]Guangdong Ocean Univ, Sch Coastal Agr Sci, Zhanjiang 524088, Peoples R China

年份：2026

卷号：363

外文期刊名：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES

收录：SCI-EXPANDED(收录号：WOS:001759352000001)、、EI(收录号：20261720594726)、WOS

基金：This work was predominantly funded by the Guangdong Basic and Applied Basic Research Foundation (No. 2022A1515012091) , the Special Project in Key Fields of Guangdong Universities (No. 2022ZDZX2025) , the Guangxi Science and Technology Base and Talent Special Project (Guike AD23026036) , the General Project of Guangxi Natural Science Foundation (2025GXNSFAA069861) , and Guangdong Ocean University Innovation and Entrepreneurship training Program for College Students (CXXL2022186) .

语种：英文

外文关键词：SIP4; MDA-MB-231 cells; miR-18a-5p/ORAI3; Apoptosis

外文摘要：Based on our previous findings regarding anti-TNBC activity of SIP4, this study aims to further explore the antitumor mechanisms of the marine polysaccharide. Firstly, this study simplified the preparation methods of SIP4 based on our report, and identified the polysaccharide as a polymer of the repeating units of 5 sugars,-4GalpNAc1-2GlcAp1-4(GalpNAc1-4GlcpNAc1-3)Fucp1-that consists of trisaccharide backbone, a disaccharide branch and an unlocated sulfate ester group. SIP4 induced overexpression of ORAI3 and excessive calcium ion accumulation in MDA-MB-231 cells, and resulted in apoptosis. Exposure of miR-18a mimic promoted over-expression of ORAI3, augmentation of calcium ion content, and consequent apoptosis in MDA-MB-231 cells, although miR-18a inhibitor did not change the indicators. Moreover, combination of SIP4 and miR-18a significantly enhanced the promotion of ORAI3 expression, calcium concentration and apoptosis in the TNBC cells. But the blockage using inhibitor of miR-18a markedly decreased the enhancement by SIP4. Comprehensively, SIP4 mediated apoptosis in MDA-MB-231 cells via activating miR-18a/ORAI3 pathway to induce intracellular calcium overload is an important anti-TNBC mechanism.