PLEKHA4 promotes glioblastoma progression through apoptosis inhibition, tumor cell migration, and macrophage infiltration.

Immunobiology

Lanzhou University Second Hospital, The Second Clinical Medical College of Lanzhou University, Lanzhou University, Lanzhou, Gansu, China. Electronic address:

Published: November 2023

AI Article Synopsis

  • PLEKHA4 has been linked to glioblastoma (GBM) development, with its increased expression in tumor tissues correlating to higher disease severity and worse prognosis.
  • Analysis of data from TCGA and GEO indicated that silencing PLEKHA4 in laboratory settings decreased GBM cell migration and increased cell death while also affecting immune cell behavior.
  • These findings suggest that PLEKHA4 could serve as a significant biomarker for diagnosing and treating GBM.

Article Abstract

Background: Glioblastoma(GBM) has a profound impact on human health, making the identification of reliable prognostic biomarkers pivotal. While PLEKHA4 has been associated with tumor genesis and development, its role in gliomas is still uncertain.

Methods: We analyzed PLEKHA4 expression in tumor tissues using the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Additionally, we utilized TCGA data to investigate its impact on prognosis, pathway enrichment, and immune infiltration. In vitro loss-of-function experiments were conducted to elucidate the effect of PLEKHA4 silencing on GBM cell behavior.

Results: TCGA and GEO data sets revealed increased levels of PLEKHA4 expression in glioma tissues. Furthermore, we identified a correlation between PLEKHA4 expression and higher disease classification, pathological grading, and poorer prognosis. Silencing PLEKHA4 in vitro resulted in decreased glioma cell migration and increased apoptosis. It also reduced macrophage infiltration and hindered M2 polarization of macrophages.

Conclusion: Our findings highlight the pivotal role of PLEKHA4 in GBM pathogenesis and suggest its potential as a diagnostic and therapeutic target for GBM.

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Source
http://dx.doi.org/10.1016/j.imbio.2023.152746DOI Listing

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