Fig 1: Correlation between LSM1 expression and immune cell infiltration in GBM using TCGA dataset. (a) Analysis of LSM1 expression reveals correlations with immune cell infiltration in GBM. Representative correlations are shown: (b) negative correlation with TFH cell infiltration; (c) negative correlation with CD56bright cell infiltration; (d) positive correlation with macrophage infiltration; and (e) positive correlation with Th2 cell enrichment. These findings indicate that LSM1 expression in GBM is linked to distinct patterns of immune cell infiltration, shed light on the potential immunoregulatory role of LSM1 in the GBM tumor microenvironment, and provide insights into its impact on immune cell interactions.
Fig 2: Impact of LSM1 expression on survival outcomes in glioma patients. The analysis of overall survival (a), disease-specific survival (b), and progression-free survival (c) based on LSM1 expression levels in glioma patients was conducted. Kaplan-Meier survival curves are depicted for patients with either high or low LSM1 expression. The consistent results demonstrate that patients with higher LSM1 expression exhibit significantly worse clinical outcomes in terms of overall survival (a), disease-specific survival (b), and progression-free survival (c).
Fig 3: Comparison of LSM1 expression levels in different glioma subtypes. This figure showcases the analysis of LSM1 expression levels in glioma subtypes based on histological type (a), WHO grade (b), age (c), IDH status (d), and 1p/19q codeletion (e). Bar graphs depict the relative expression of LSM1 in each glioma subgroup. The findings demonstrate a marked increase in LSM1 expression in glioblastoma (a), higher WHO grades (b), older age (c), wild-type IDH status (d), and gliomas without 1p/19q codeletion (e). These results suggest a potential association between LSM1 upregulation and more aggressive glioma characteristics (all p < 0.05), highlighting its promise as a prognostic biomarker and a potential therapeutic target.
Fig 4: Comparative analysis of LSM1 expression in glioblastoma (GBM) and normal brain tissues. Comparison of LSM1 expression levels between GBM (N = 163) and normal brain tissues (N = 207) using TCGA and GTEx datasets. (a) A box plot representation of LSM1 expression levels in GBM and normal brain tissues is presented, measured in transcripts per million (TPM). The box plot visualizes the distribution of expression levels, with the median indicated by a horizontal line within the box. Outliers are represented as individual data points. (b) A bar graph displays the statistical significance of the differential LSM1 expression between GBM and normal brain tissues. The figure emphasizes the significantly higher expression of LSM1 in GBM compared to normal brain tissues.
Fig 5: Effects of LSM1 modulation on U87 GBM cell behavior. Cellular consequences of LSM1 modulation in U87 GBM cells were evaluated. (a) Western blot analysis confirms the efficiency of LSM1 knockdown and overexpression, using scrambled-siRNA and vector controls, respectively. (b) Semiquantification of the western blot results demonstrates successful LSM1 knockdown and overexpression. (c) The impact on cell proliferation is evaluated using the CCK-8 assay, revealing that LSM1 overexpression promotes cell proliferation, while knockdown of LSM1 inhibits cell growth in U87 GBM cells. (d) Cell invasion capacity is assessed, indicating that LSM1 overexpression enhances GBM cell invasion, while LSM1 knockdown significantly inhibits this process. These findings elucidate the functional implications of LSM1 in GBM, where overexpression promotes cell proliferation and invasion, while knockdown exerts suppressive effects. LSM1 emerges as a potential therapeutic target for GBM. ∗ indicates p < 0.05 by the Student's t-test between the two groups.
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