Sheng Meiling, Wang Qunzhi, Lou Yabo, Xiao Yuanchao, Wu Xiaoming
Department of Respiratory and Critical Care Medicine, Jinhua Hospital Affiliated to Wenzhou Medical University, Jinhua, China.
Interventional Department, Jinhua Hospital Affiliated to Wenzhou Medical University, Jinhua, China.
Physiol Genomics. 2025 Jan 1;57(1):1-7. doi: 10.1152/physiolgenomics.00119.2024. Epub 2024 Oct 22.
The elusive function of myosin light chain 9 (MYL9) in cancer is an area ripe for further investigation. Bioinformatics was used to compare the expression levels of MYL9 in non-small-cell lung cancer (NSCLC) and normal tissues. Gene set enrichment analysis was used to investigate the pathways associated with MYL9. The BioGRID database was used to screen for potential targets of MYL9. The expression of MYL9 and myosin 19 (MYO19) mRNA was quantified using quantitative reverse transcriptase PCR. Cell migration was assessed using a scratch wound healing assay. The protein levels of MYL9, MYO19, and epithelial-mesenchymal transition (EMT) biomarkers were examined using Western blot (WB). Epithelial cell adhesion molecule (EpCAM) expression in different cell groups was profiled using flow cytometry analysis. Coimmunoprecipitation assays were performed to determine the binding affinity between MYL9 and MYO19. In addition, the direct protein interaction between MYL9 and MYO19 was explored using a glutathione-S-transferase (GST) pull-down assay. In NSCLC patients, MYL9 was significantly downregulated both in vivo and in cell cultures and had a high enrichment score in the EMT pathway. Scratch assays pointed to its inhibitory effect on cancer cell migration. WB showed that MYL9 could suppress EMT marker protein expression in NSCLC cells. Flow cytometry found that MYL9 greatly reduced the distribution of EpCAM on the cell surface. MYO19 was pinpointed as a potential target of MYL9, as confirmed by coimmunoprecipitation and GST pull-down assays. Rescue experiments confirmed that MYO19 could enhance cell migration, promote the expression of EMT markers, and increase EpCAM levels on the cell surface, but these effects were reserved by MYL9 overexpression. MYL9 impedes the migration and EMT in NSCLC cells by binding to MYO19. Myosin light chain 9 (MYL9) is downregulated in non-small-cell lung cancer (NSCLC). MYL9 suppresses epithelial-mesenchymal transition (EMT) in NSCLC cells. MYL9 binds to myosin 19 (MYO19). MYL9/MYO19 signaling inhibits EMT in NSCLC.
肌球蛋白轻链9（MYL9）在癌症中难以捉摸的功能是一个亟待进一步研究的领域。运用生物信息学比较非小细胞肺癌（NSCLC）和正常组织中MYL9的表达水平。采用基因集富集分析来研究与MYL9相关的信号通路。利用BioGRID数据库筛选MYL9的潜在靶点。通过定量逆转录PCR定量MYL9和肌球蛋白19（MYO19）mRNA的表达。使用划痕伤口愈合试验评估细胞迁移。通过蛋白质免疫印迹法（WB）检测MYL9、MYO19和上皮-间质转化（EMT）生物标志物的蛋白质水平。使用流式细胞术分析不同细胞组中上皮细胞粘附分子（EpCAM）的表达。进行免疫共沉淀试验以确定MYL9与MYO19之间的结合亲和力。此外，使用谷胱甘肽-S-转移酶（GST）下拉试验探索MYL9与MYO19之间的直接蛋白质相互作用。在NSCLC患者中，MYL9在体内和细胞培养物中均显著下调，并且在EMT信号通路中具有高富集分数。划痕试验表明其对癌细胞迁移具有抑制作用。WB显示MYL9可抑制NSCLC细胞中EMT标志物蛋白的表达。流式细胞术发现MYL9极大地减少了EpCAM在细胞表面的分布。免疫共沉淀和GST下拉试验证实，MYO19被确定为MYL9的潜在靶点。挽救实验证实，MYO19可增强细胞迁移、促进EMT标志物的表达并增加细胞表面EpCAM水平，但这些作用被MYL9过表达所抑制。MYL9通过与MYO19结合来阻碍NSCLC细胞的迁移和EMT。肌球蛋白轻链9（MYL9）在非小细胞肺癌（NSCLC）中表达下调。MYL9抑制NSCLC细胞中的上皮-间质转化（EMT）。MYL9与肌球蛋白19（MYO19）结合。MYL9/MYO19信号传导抑制NSCLC中的EMT。
