Day: June 23, 2025

LINC01783 Promotes Glioma Tumorigenesis by Enhancing GATA3 Expression Through CBP-Mediated H3K27 Acetylation to Suppress PTEN Expression

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LINC01783

In vitro and in vivo molecular mechanistic investigations

Study Summary

Type of Study: In vitro and in vivo molecular mechanistic investigation First Author: Shaocai Hao et al. Author Affiliations:

  • Department of Neurosurgery, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China

Journal: Biofactors DOI: 10.1002/biof.70029 PMID: 40546096 Publication Date: May–June 2025 Title: LINC01783 Promotes Glioma Tumorigenesis by Enhancing GATA3 Expression Through CBP-Mediated H3K27 Acetylation to Suppress PTEN Expression

Purpose

To elucidate the oncogenic function of the long intergenic non-coding RNA LINC01783 in glioma progression, focusing on its effect on GATA3 expression and PTEN suppression via CBP-mediated H3K27 acetylation.

Conclusions

LINC01783 is significantly upregulated in glioma tissues and enhances glioma progression by promoting GATA3 expression through CBP-mediated H3K27 acetylation. This, in turn, transcriptionally represses PTEN, contributing to increased tumor cell proliferation and stemness.

Critical Review

Methodological Weaknesses

  • Sample opacity: No clear details on glioma sample number, subtype stratification, or clinical metadata; undermines reproducibility and clinical significance.
  • In vivo data insufficiently controlled: No information on animal randomization, group sizes, or blinding procedures. Xenograft conclusions are weakly supported.
  • Epigenetic mechanistic oversimplification: Attribution of GATA3 regulation solely to CBP-H3K27ac is unconvincing; alternative pathways and compensatory mechanisms are unexamined.
  • Lack of causal proof: The PTEN axis is emphasized, but whether GATA3 mediates all observed phenotypes is not demonstrated.
  • No translational bridge: No therapeutic agent, inhibitor, or antisense strategy explored. The leap to “potential therapeutic target” is scientifically unfounded.

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Oncolytic virus‑mediated immunomodulation in glioblastoma: Insights from clinical trials and challenges

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In a Review Raziye Piranlioglu *et al.* from

Affiliations Harvey Cushing Neuro‑oncology Laboratories, Dept. Neurosurgery, Brigham and Women’s Hospital, Boston, MA, USA; Dana‑Farber Cancer Institute, Boston, MA, USA

published in *Seminars in Immunology* with the Purpose to synthesize data from clinical trials of oncolytic viruses (OVs) in glioblastoma, evaluating immunomodulatory effects, delivery strategies, and challenges in assessing immune responses. They concluded that Oncolytic virus therapy is well tolerated in GBM trials and can convert the immunosuppressive microenvironment into an immunologically active state. However, limitations in post‑treatment sampling and delivery methods impede full understanding of biological mechanisms.

This review is a rehash of well‑known take‑home messages, offering little in the way of novel synthesis or incisive critique. The authors lean heavily on canonical trials (e.g., oHSV, adenovirus) but fail to integrate preclinical correlates from myeloid-targeting strategies, such as macrophage polarization dynamics or MDSC modulation. There’s no fresh mechanism, no meta‑analysis of response rates, and no exploration of why most trials remain phase I with limited impact. Sample‑scarcity is once again highlighted as a blocker—but no alternative trial designs (e.g., neoadjuvant window cohorts, liquid biopsy) are proposed. In short, the review scratches the surface of challenges without pushing the field forward.

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