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DLGAP5 promotes lung adenocarcinoma growth via upregulating PLK1 and serves as a therapeutic target.

Maojian Chen1,2, Shaoping Zhang1, Fan Wang1

  • 1Department of Medical Oncology, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, Guangdong, People's Republic of China.

Journal of Translational Medicine
|February 27, 2024
PubMed
Summary

Human discs large-associated protein 5 (DLGAP5) is upregulated in lung adenocarcinoma (LUAD), correlating with poor prognosis and immune infiltration. Targeting DLGAP5 with AT9283 inhibits LUAD growth by downregulating PLK1, suggesting DLGAP5 as a therapeutic target.

Keywords:
AT9283DLGAP5LUADPLK1

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Area of Science:

  • Oncology
  • Molecular Biology
  • Bioinformatics

Background:

  • Human discs large-associated protein 5 (DLGAP5) is implicated in cell cycle regulation and cancer progression.
  • Understanding DLGAP5's role in lung adenocarcinoma (LUAD) is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the prognostic value, immune implications, biological functions, and therapeutic targeting strategies of DLGAP5 in LUAD.
  • To explore DLGAP5's role in LUAD cell proliferation and its relationship with Polo-like kinase 1 (PLK1).

Main Methods:

  • Utilized multiple databases (TCGA, GEO, CPTAC, Human Protein Atlas) for expression and clinical significance analysis.
  • Performed bioinformatics analysis, network pharmacology, and in vitro/in vivo experiments to assess DLGAP5 function and identify inhibitors.
  • Screened for DLGAP5 inhibitors using virtual screening and evaluated their efficacy in LUAD models.

Main Results:

  • DLGAP5 was highly expressed in LUAD, associated with poor prognosis, increased immune infiltration, and higher drug resistance.
  • DLGAP5 promotes LUAD cell proliferation by upregulating PLK1; PLK1 can rescue DLGAP5 knockdown effects.
  • AT9283 identified as a DLGAP5 inhibitor, effectively suppressing LUAD growth in vitro and in vivo, and its effects were linked to DLGAP5 and PLK1 expression.

Conclusions:

  • DLGAP5 is upregulated in LUAD, linked to poor prognosis and immune evasion.
  • DLGAP5 promotes LUAD proliferation via PLK1, highlighting a potential therapeutic pathway.
  • DLGAP5 inhibition by AT9283 shows promise as a therapeutic strategy for LUAD.