Purinergic Signalling, Journal Year: 2024, Volume and Issue: unknown
Published: Aug. 31, 2024
Language: Английский
Purinergic Signalling, Journal Year: 2024, Volume and Issue: unknown
Published: Aug. 31, 2024
Language: Английский
Cancers, Journal Year: 2023, Volume and Issue: 15(19), P. 4900 - 4900
Published: Oct. 9, 2023
Mannose-binding lectin 2 (MBL2), a member of the multimeric family, is crucial in immune regulation and tumor development. MBL2 gene polymorphisms are associated with risk prognosis various tumors, including hepatocellular carcinoma (HCC). Its functional role HCC remains largely unclear. In this study, we aimed to identify whether key regulator potential therapeutic target for HCC. A bioinformatics analysis revealed close relationships among downregulation, tumor-associated proliferation metastasis pathway, immunosuppressive microenvironments. Lower expression patients was linked an unfavorable prognosis. cell counting kit-8 assay, colony formation transwell migration wound healing assay further confirmed that overexpression could directly inhibit Moreover, regulated by miR-34c-3p, as dual-luciferase reporter thereby demonstrating progression cells. Thus, our study offers first comprehensive confirmation development through multi-omics experimental validation. Furthermore, miR-34c-3p found be upstream mechanism downregulation promising target, expanding treatment options
Language: Английский
Citations
2Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown
Published: Feb. 29, 2024
Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest and most metastatic cancers in human. PDACs respond poorly to therapies, partly due cancer stem cells (CSCs) that self-renew, survive chemotherapies, metastasise replenish tumour. Factors secreted by tumour mediate autocrine/paracrine crosstalk with surroundingcells contributing cell niche but are still insufficiently characterised. Here we used quantitative SILAC proteomics identify factors enriched CSC secretome compared non-CSCs. Among them were GDF15 VGF, involved cachexia pain stimuli. VGF promoted self-renewal growth through autocrine effects. TGFβ/Activin signalling lowered expression via SMAD2/3-SMAD4-SNON, switching ATF4-CREB-mediated induction upon stress. Co-culture PDAC-CSCs hESC-derived neural for mimicking cellular PDAC revealed paracrine GDF15/VGF nociceptor formation neurite outgrowth. In turn, Substance P from neurons supported self-renewal, EMT/migration clonal evolution was also impacted SMAD4 genetic status. Lastly, serum levels elevated patients suggesting their utility as biomarkers detection. Collectively, our data uncovered between CSCs nociceptors.
Language: Английский
Citations
0Science China Life Sciences, Journal Year: 2024, Volume and Issue: 67(8), P. 1563 - 1578
Published: April 9, 2024
Language: Английский
Citations
0Cellular Signalling, Journal Year: 2024, Volume and Issue: 120, P. 111231 - 111231
Published: May 18, 2024
Language: Английский
Citations
0Purinergic Signalling, Journal Year: 2024, Volume and Issue: unknown
Published: Aug. 31, 2024
Language: Английский
Citations
0