KHDRBS1 regulates the pentose phosphate pathway and malignancy of GBM through SNORD51-mediated polyadenylation of ZBED6 pre-mRNA DOI Creative Commons

Xiaoyu Liu,

Xiaobai Liu,

Weiwei Dong

et al.

Cell Death and Disease, Journal Year: 2024, Volume and Issue: 15(11)

Published: Nov. 8, 2024

Glioblastoma is one of the most common and aggressive primary brain tumors. The aberration metabolism important character GBM cells tightly related to malignancy GBM. We mainly verified regulatory effects KHDRBS1, SNORD51 ZBED6 on pentose phosphate pathway malignant biological behavior in glioblastoma cells, such as proliferation, migration invasion. KHDRBS1 were upregulated tissues cells. But had opposite tendency may improve stability by binding SNORD51, thus elevating expression SNORD51. More importantly, can competitively bind WDR33 with 3'UTR pre-mRNA which inhibit 3' end processing pre-mRNA, thereby inhibiting mRNA. inhibited transcription G6PD promoter region G6PD. Therefore, KHDRBS1/SNORD51/ZBED6 performs an part regulating influence providing new insights potential targets for treatment

Language: Английский

Importance of long non-coding RNAs in the pathogenesis, diagnosis, and treatment of prostate cancer DOI Creative Commons
Mohammad Taheri, Elham Badrlou, Bashdar Mahmud Hussen

et al.

Frontiers in Oncology, Journal Year: 2023, Volume and Issue: 13

Published: March 21, 2023

Long non-coding RNAs (lncRNAs) are regulatory transcripts with essential roles in the pathogenesis of almost all types cancers, including prostate cancer. They can act as either oncogenic lncRNAs or tumor suppressor ones Small nucleolar RNA host genes among mostly assessed this PCA3 is an example that has been approved a diagnostic marker A number well-known other cancers such DANCR, MALAT1, CCAT1, PVT1, TUG1 and NEAT1 have also shown to oncogenes On hand, LINC00893, LINC01679, MIR22HG, RP1-59D14.5, MAGI2-AS3, NXTAR, FGF14-AS2 ADAMTS9-AS1 suppressors LncRNAs contribute cancer via modulation androgen receptor (AR) signaling, ubiquitin-proteasome degradation process AR important signaling pathways. The current review summarizes role evolution especial focus on their importance design novel biomarker panels therapeutic targets.

Language: Английский

Citations

16
Musashi-2 potentiates colorectal cancer immune infiltration by regulating the post-translational modifications of HMGB1 to promote DCs maturation and migration DOI Creative Commons

Xiaole Meng,

Risi Na,

Peng Xiao

et al.

Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)

Published: Feb. 12, 2024

Abstract Post-translational modifications (PTMs) of the non-histone protein high-mobility group B1 (HMGB1) are involved in modulating inflammation and immune responses. Recent studies have implicated that RNA-binding (RBP) Musashi-2 (MSI2) regulates multiple critical biological metabolic immunoregulatory functions. However, precise role MSI2 regulating PTMs tumor immunity colorectal cancer (CRC) remains unclear. Here, we present data indicating potentiates CRC immunopathology colitis-associated colon (CAC) mouse models, cell lines clinical specimens, specifically via HMGB1-mediated dendritic (DC) maturation migration, further contributes to infiltration CD4 + CD8 T cells inflammatory Under stress conditions, can exacerbate production, nucleocytoplasmic transport extracellular release damage-associated molecular patterns (DAMPs)-HMGB1 cells. Mechanistically, mainly enhances disulfide HMGB1 production translation direct binding nucleotides 1403–1409 3′ UTR, interacts with cytoplasmic acetyltransferase P300 upregulate its expression, promoting acetylation K29 residue HMGB1, thus leading K29-HMGB1 translocation release. Furthermore, blocking activity glycyrrhizic acid (Gly) attenuates MSI2-mediated vitro vivo. Collectively, this study suggests may improve prognosis patients by reprogramming microenvironment (TIME) through PTMs, which might be a novel therapeutic option for immunotherapy.

Language: Английский

Citations

6
Silencing BMAL1 promotes M1/M2 polarization through the LDHA/lactate axis to promote GBM sensitivity to bevacizumab DOI
Fan Wang, Wenjun Liao, Caiyan Li

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 134, P. 112187 - 112187

Published: May 11, 2024

Language: Английский

Citations

6
Glioma glycolipid metabolism: MSI2–SNORD12B–FIP1L1–ZBTB4 feedback loop as a potential treatment target DOI Creative Commons

Weiwei Dong,

Xiaobai Liu,

Chunqing Yang

et al.

Clinical and Translational Medicine, Journal Year: 2021, Volume and Issue: 11(5)

Published: May 1, 2021

Abstract Abnormal energy metabolism, including enhanced aerobic glycolysis and lipid synthesis, is a well‐established feature of glioblastoma (GBM) cells. Thus, targeting the cellular glycolipid metabolism can be feasible therapeutic strategy for GBM. This study aimed to evaluate roles MSI2, SNORD12B, ZBTB4 in regulating proliferation GBM MSI2 SNORD12B expression was significantly upregulated low tissues Knockdown or overexpression inhibited cell proliferation. may improve by increasing its stability. Importantly, increased utilization mRNA transcript distal polyadenylation signal alternative processing competitively combining with FIP1L1, which decreased because proportion 3′ untranslated region long transcript. transcriptionally suppressed HK2 ACLY binding directly promoter regions. Additionally, bound MSI suppress expression, thereby forming an MSI2/SNORD12B/FIP1L1/ZBTB4 feedback loop regulate In conclusion, stability regulated FIP1L1. positive plays crucial role cells provides potential drug target glioma treatment.

Language: Английский

Citations

33
Effect of SNORD113-3/ADAR2 on glycolipid metabolism in glioblastoma via A-to-I editing of PHKA2 DOI Creative Commons
Zheng Cui, Xiaobai Liu,

E Tiange

et al.

Cellular & Molecular Biology Letters, Journal Year: 2025, Volume and Issue: 30(1)

Published: Jan. 10, 2025

Abstract Background Glioblastoma multiforme (GBM) is a highly aggressive brain tumor, characterized by its poor prognosis. Glycolipid metabolism strongly associated with GBM development and malignant behavior. However, the precise functions of snoRNAs ADARs in glycolipid within cells remain elusive. The objective present study to delve into underlying mechanisms through which exert regulatory effects on cells. Methods RNA immunoprecipitation pull-down experiments were conducted verify homodimerization ADAR2 SNORD113-3, Sanger sequencing Western blot used detect A-to-I editing PHKA2 mRNA ADAR2. Furthermore, phosphorylation EBF1 was measured vitro kinase assay. Finally, vivo studies using nude mice confirmed that SNORD113-3 overexpression, along knockdown, could suppress formation subcutaneous xenograft tumors improve outcome tumor-bearing mice. Results We found significantly promoted metabolism, while ADAR2, inhibited metabolism. promotes protein expression promoting homodimer formation. mediates mRNA. Mass spectrometry analysis testing revealed phosphorylates Y256, reducing stability EBF1. direct binding PKM2 ACLY promoters observed, suggesting inhibition their These findings suggest existence SNORD113-3/ADAR2/PHKA2/EBF1 pathway collectively regulates growth knockdown PHKA2, overexpression obviously tumor those Conclusions Herein, we clarified mechanism involving regulation cell Our results provide framework for innovative therapeutic interventions prognosis patients GBM.

Language: Английский

Citations

0
Current Research on the Regulation of Glycolipid Metabolism by Plant-Derived Active Polysaccharides DOI
Jie Xu, Zebin Weng, Qi Cui

et al.

Trends in Food Science & Technology, Journal Year: 2025, Volume and Issue: 159, P. 104959 - 104959

Published: March 5, 2025

Language: Английский

Citations

0
Exosomes: efficient macrophage-related immunomodulators in chronic lung diseases DOI Creative Commons
Jianxiong Kang, Peiyan Hua,

Xiaojing Wu

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: April 9, 2024

Macrophages, the predominant immune cells in lungs, play a pivotal role maintaining delicate balance of pulmonary microenvironment. However, chronic inflammatory lung diseases and cancer, macrophage phenotypes undergo distinct transitions, with M1-predominant macrophages promoting damage M2-predominant fostering cancer progression. Exosomes, as critical mediators intercellular signaling substance exchange, participate pathological reshaping during development cancer. Specifically, diseases, exosomes promote pro-inflammatory phenotype macrophages, suppress anti-inflammatory phenotype, subsequently, released by reshaped further exacerbate damage. In pro-tumor tumor-associated (TAMs); inhibit anti-tumor TAMs; TAMs enhance tumor proliferation, metastasis, resistance to chemotherapy. Simultaneously, exhibit dual role, holding potential transmit immune-modulating molecules load therapeutic agents offering prospects for restoring dysregulation this is manifested inhibiting alleviating post-reshaping. reshape secrete that development. Looking ahead, efficient targeted exosome-based therapies may emerge promising direction treatment diseases.

Language: Английский

Citations

4
Update on the Progress of Musashi-2 in Malignant Tumors DOI Creative Commons
Yulian Niu, Tao Zhou, Yanjun Li

et al.

Frontiers in Bioscience-Landmark, Journal Year: 2025, Volume and Issue: 30(1)

Published: Jan. 17, 2025

Since the discovery of Musashi (MSI) protein, its ability to affect mitosis Drosophila progenitor cells has garnered significant interest among scientists. In following 20 years, it lived up expectations. A substantial body evidence demonstrated that is closely related development, metastasis, migration, and drug resistance malignant tumors. recent research on MSI protein advanced, many novel viewpoints attempts have been derived; for example, tumor p53 mutations MSI-binding proteins lead arginine N-methyltransferase 5-targeted therapy in lymphoma patients. Moreover, high expression MSI2 pancreatic cancer might suppress development progression. As a member family, associated with multiple tumors, including hematological disorders, common abdominal other types (e.g., glioblastoma, breast cancer). highly expressed majority tumors poor disease prognosis. However, specific levels regulatory mechanisms may differ based type. This review summarizes progress occurrence, migration mechanism, resistance, as well prospect developing immunosuppressants biomarkers.

Language: Английский

Citations

0
Characterization of circRNA-Associated-ceRNA Networks Involved in the Pathogenesis of Postoperative Cognitive Dysfunction in Aging Mice DOI Creative Commons
Mengxue Zhang,

Jing-Run Lin,

Shuting Yang

et al.

Frontiers in Aging Neuroscience, Journal Year: 2022, Volume and Issue: 14

Published: April 4, 2022

Postoperative cognitive dysfunction (POCD) is a clinical entity associated with declined function following surgery. It occurs more frequently in elderly patients. Recent studies have shown that circRNA-associated-ceRNA networks, constructed based on interactions between circRNA-miRNA and miRNA-mRNA, provide key insight into the molecular mechanisms underlying pathogenesis of several neurological diseases. However, mechanism POCD remains undetermined. In this study, laparotomies were performed under isoflurane anesthesia young (2-month-old) aging (17-month-old) male C57BL/6 mice. The results showed mice likely than to develop POCD. Subsequently, differentially expressed circRNAs, miRNAs, mRNAs characterized by RNA sequencing hippocampi control surgery conditions. Six 6 203 identified construct network for condition, while 13 8 189 used condition. Further Gene Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) pathway enrichment analysis these two networks revealed are involved though modulating Wnt VEGF signaling pathways, as well neural processes long-term synaptic depression transmission. particular, mmu-miR-298-5P regulatory study's mouse model suggests mm9_circ_009789- mm9_circ_004229-associated-ceRNA closely related occurrence through regulating PKC pathway, cell apoptosis glycolipid metabolism pathway. These findings possible role helping unravel complexity

Language: Английский

Citations

16
High expression of SRSF1 facilitates osteosarcoma progression and unveils its potential mechanisms DOI Creative Commons
Shuqi Li,

Xinyi Huang,

Shuang Zheng

et al.

BMC Cancer, Journal Year: 2024, Volume and Issue: 24(1)

Published: May 12, 2024

Abstract Background SRSF1, a member of Serine/Arginine-Rich Splicing Factors (SRSFs), has been observed to significantly influence cancer progression. However, the precise role SRSF1 in osteosarcoma (OS) remains unclear. This study aims investigate functions and its underlying mechanism OS. Methods expression level OS was evaluated on TCGA dataset, TAGET-OS database. qRT-PCR Western blotting were employed assess human cell lines as well interfered ectopic states. The effect migration, invasion, proliferation, apoptosis cells measured by transwell assay flow cytometry. RNA sequence bioinformatic analyses conducted elucidate targeted genes, relevant biological pathways, alternative splicing (AS) events regulated SRSF1. Results consistently upregulated both samples lines. Diminishing resulted reduced invasion increased while overexpressing led enhanced growth, decreased apoptosis. Mechanistically, Gene Ontology (GO) analysis, Kyoto Encyclopedia Genes Genomes (KEGG) Set Enrichment Analysis (GSEA) revealed that closely associated with dysregulation protein targeting processes, location cytosolic ribosome, extracellular matrix (ECM), proteinaceous matrix, along PI3K-AKT pathway, Wnt HIPPO pathway. Transcriptome analysis identified AS modulated especially (Skipped Exon) SE (Mutually exclusive Exons) MXE events, revealing potential roles molecules mRNA surveillance, degradation, transport during development. confirmed knockdown occurrence SRRM2, DMKN, SCAT1 Conclusions Our results highlight oncogenic high promoting progression, further explore mechanisms action. significant involvement development suggests utility therapeutic target

Language: Английский

Citations

3