ArticleJournal of translational medicine2022
miR-1297 sensitizes glioma cells to temozolomide (TMZ) treatment through targeting adrenomedullin (ADM).
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Integrative Proteome-Wide Mendelian Randomization and Multi-Omics Analysis Identify ADM and CFH as Candidate Genes for Osteoarthritis.Biomedicines · 2026Article
- Overexpression of miR-219 as a potential therapeutic strategy of glioblastoma cells in vitro.Scientific reports · 2026Article
- E3 ligase LMO7 enhances temozolomide sensitivity by promoting MGMT degradation in lung cancer.The Journal of biological chemistry · 2026Article
- Loss of CD99L2 Contributed to Temozolomide Resistance and Glioblastoma Tumorigenesis Based on Genome-scale CRISPR/Cas9 Screening.Current pharmaceutical design · 2026Article
- Spatial transcriptomics of glioblastoma defines biologically and clinically significant reprogramming patterns across unique spatial microenvironments.bioRxiv : the preprint server for biology · 2025Article
- Biomimetic cancer cell membrane engineered lipid nanoparticles for enhanced chemotherapy of homologous malignant tumor.BMC cancer · 2025Article
- Adrenomedullin in Tumorigenesis and Cancer Progression.International journal of molecular sciences · 2025Review
- Androgen receptor inhibition sensitizes glioblastoma stem cells to temozolomide by the miR-1/miR-26a-1/miR-487b signature mediated WT1 and FOXA1 silencing.Cell death discovery · 2025Article
- Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature review.Frontiers in immunology · 2025Review
- ICAM1-Mediated Endothelial Cells and Macrophage Interactions in Modulating GBM Malignant Transformation.Journal of inflammation research · 2025Article
- The effect of Licochalcone A on proliferation, invasion, and drug resistance of glioma cells by regulating TLR4/NF-κB signaling pathway.Clinics (Sao Paulo, Brazil) · 2025Article
- Integrative single-cell and bulk transcriptome analyses identify a distinct pro-tumor macrophage signature that has a major prognostic impact on glioblastomas.Clinical and experimental medicine · 2024Article
- Glioma and Peptidergic Systems: Oncogenic and Anticancer Peptides.International journal of molecular sciences · 2024Review
- MicroRNAs as the pivotal regulators of Temozolomide resistance in glioblastoma.Molecular brain · 2024Review
- CRISPR-Cas9 identifies growth-related subtypes of glioblastoma with therapeutical significance through cell line knockdown.BMC cancer · 2023Article
- Peptidergic Systems and Cancer: Focus on Tachykinin and Calcitonin/Calcitonin Gene-Related Peptide Families.Cancers · 2023Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGliomas account for about 80% of all malignant brain and other central nervous system (CNS) tumors. Temozolomide (TMZ) resistance represents a major treatment hurdle. Adrenomedullin (ADM) has been reported to induce glioblastoma cell growth.
methodsCell viability was measured using the CCK-8 assay. The apoptosis analysis was performed using the Annexin V-FITC Apoptosis Detection Kit. The mitochondrial membrane potential was determined by JC-1 staining. A nude mouse tumor assay was used to detect tumor formation. Hematoxylin and eosin (H&E) and immunohistochemical (IHC) staining were performed in tissue sections. Activation of Akt and Erk and expression of apoptosis-related proteins were determined by immunoblotting.
resultsADM expression has been found upregulated in TMZ -resistant glioma samples based on bioinformatics and experimental analyses. Knocking down ADM in glioma cells enhanced the suppressive effects of TMZ on glioma cell viability, promotive effects on cell apoptosis, and inhibitory effects on mitochondrial membrane potential. Moreover, ADM knockdown also enhanced TMZ effects on Bax/Bcl-2, Akt phosphorylation, and Erk1/2 phosphorylation. Bioinformatics and experimental investigation indicated that miR-1297 directly targeted ADM and inhibited ADM expression. miR-1297 overexpression exerted similar effects to ADM knockdown on TMZ-treated glioma cells. More importantly, under TMZ treatment, inhibition of miR-1297 attenuated TMZ treatment on glioma cells; ADM knockdown partially attenuated the effects of miR-1297 inhibition on TMZ-treated glioma cells.
conclusionsmiR-1297 sensitizes glioma cells to TMZ treatment through targeting ADM. The Bax/Bcl-2, Akt, and Erk1/2 signaling pathways, as well as mitochondrial functions might be involved.
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