ArticleCancer cell international2024
MSI2 regulates NLK-mediated EMT and PI3K/AKT/mTOR pathway to promote pancreatic cancer progression.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Characterization of ADGRG6 as a potential molecular oncotarget of pancreatic cancer.Cell death & disease · 2026Article
- Saikosaponin D overcomes gemcitabine resistance in pancreatic cancer via AKT/mTOR pathway inhibition and synergistic induction of apoptosis and autophagy.Oncology reports · 2026Article
- Differential hypothalamic expression of Musashi protein 2 in Mongolian sheep with single and double ovulation.Frontiers in veterinary science · 2026Article
- MSI2 in the dentate gyrus and ovary regulates the reproductive endocrine homeostasis of female mice.Communications biology · 2025Article
- Regulation of metabolic adaptation and leukemia progression by MUSASHI2-DEPTOR-KIF11 axis.Leukemia · 2025Article
- MSI2 exerts antitumor effects by regulating T-cell function in kidney renal clear cell carcinoma.Translational andrology and urology · 2025Article
- Genomic and Demographic Characteristics of Angiosarcoma as Described in the AACR Project GENIE Registry.Cancers · 2025Article
- Prognostic Role of Musashi-2 Immunohistochemical Expression and CD163+ Tumor- Associated Macrophages in Colorectal Cancer Progression.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Regulation of pancreatic cancer cells by suppressing KIN17 through the PI3K/AKT/mTOR signaling pathway.Oncology reports · 2025Article
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6 authors.
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Abstract
backgroundThe incidence of pancreatic cancer is increasing by years, and the 5-year survival rate is very low. Our team have revealed that Musashi2 (MSI2) could promote aggressive behaviors in pancreatic cancer by downregulating Numb and p53. MSI2 also facilitates EMT in pancreatic cancer induced by EGF through the ZEB1-ERK/MAPK signaling pathway. This study aims to further explore the molecular mechanisms of MSI2-regulated downstream pathways in pancreatic cancer.
methodsIn vitro and in vivo experiments were conducted to investigate the role and mechanism of MSI2 in promoting malignant behaviors of pancreatic cancer through regulation of NLK.
resultsGenes closely related to MSI2 were screened from the GEPIA and TCGA databases. We found that NLK showed the most significant changes in mRNA levels with consistent changes following MSI2 interference and overexpression. The high correlation between MSI2 and NLK was also observed at the protein level. Multivariate analysis revealed that both MSI2 and NLK were independent adverse indicators of survival in pancreatic cancer patients, as well as join together. In vitro, silencing or overexpressing NLK altered cell invasion and migration, by regulating EMT and the PI3K-AKT-mTOR pathway. Silencing MSI2 reduced protein expression in the EMT and PI3K-AKT-mTOR pathways, leading to decreased cell invasion and migration abilities, while these effects could be reversed by overexpression of NLK. In vivo, MSI2 silencing inhibited liver metastasis, which could be reversed by overexpressing NLK. Mechanistically, MSI2 directly binds to the translation regulatory region of NLK mRNA at positions 79-87 nt, enhancing its transcriptional activity and exerting post-transcriptional regulatory roles. The analysis of molecular docking showed the close relationship between MSI2 and NLK in pancreatic cancer patients.
conclusionsOur findings elucidate the regulatory mechanisms of the MSI2-NLK axis in modulating aggressive behaviors of pancreatic cancer cells, which providing new evidence for therapeutic strategies in pancreatic cancer.
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