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Background <p>Lung adenocarcinoma (LUAD) is characterized by poor prognosis and limited treatment options. The homologous recombination factor with OB-fold (HROB) is reportedly associated with DNA repair, playing an essential role in a variety of cancers. However, the functional impact, clinical relevance, and underlying mechanisms of HROB in LUAD remain elusive, prompting this study to comprehensively characterize its expression profile and pathogenetic contributions.</p> Methods <p>We first systematically profiled HROB expression across pan-cancer contexts and multiple cell lines. To characterize its clinical relevance in LUAD, we employed receiver operator characteristic (ROC) curves, Kaplan–Meier survival analyses, and univariate and multivariate Cox regression modeling. Potential molecular mechanisms underlying HROB function were interrogated enrichment analyses and immune correlation studies. Using RT-PCR, we quantified HROB expression in different LUAD cell lines, followed by functional characterization through Cell Counting Kit-8(CCK-8), 5-Ethynyl-2’-deoxyuridine (EdU), wound-healing, and Transwell assays.</p> Results <p>HROB exhibited significant overexpression in LUAD tissues compared to normal, with high diagnostic accuracy. Elevated HROB expression was strongly associated with adverse clinical outcomes. Bioinformatics analysis revealed HROB’s involvement in modulating immune cell infiltration, regulating cell cycle progression and DNA repair pathways. Besides, BUB1B, BUB1, NUF2, CCNB2, CCNB1, KIF11, KIF2C, TPX2, DLGAP5, and CDCA8 were identified as potential hub genes within HROB-associated signaling modules. Knocking down HROB expression inhibited LUAD cell proliferation, migration, and invasion.</p> Conclusions <p>HROB is upregulated in LUAD and represents a promising prognostic biomarker, driving tumor proliferation, migration, and invasion.</p>

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HROB is a novel prognostic biomarker correlated with immune cell infiltration and tumor progression in lung adenocarcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月3日

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  • Yongjie Zhu,
  • Chaoqiang Wu,
  • Qiwei Li,
  • Yingxue Hu,
  • Yue Li,
  • Zuotao Wu,
  • Honglin Lu,
  • Ye jun Chen,
  • Bo Chen

摘要

Background

Lung adenocarcinoma (LUAD) is characterized by poor prognosis and limited treatment options. The homologous recombination factor with OB-fold (HROB) is reportedly associated with DNA repair, playing an essential role in a variety of cancers. However, the functional impact, clinical relevance, and underlying mechanisms of HROB in LUAD remain elusive, prompting this study to comprehensively characterize its expression profile and pathogenetic contributions.

Methods

We first systematically profiled HROB expression across pan-cancer contexts and multiple cell lines. To characterize its clinical relevance in LUAD, we employed receiver operator characteristic (ROC) curves, Kaplan–Meier survival analyses, and univariate and multivariate Cox regression modeling. Potential molecular mechanisms underlying HROB function were interrogated enrichment analyses and immune correlation studies. Using RT-PCR, we quantified HROB expression in different LUAD cell lines, followed by functional characterization through Cell Counting Kit-8(CCK-8), 5-Ethynyl-2’-deoxyuridine (EdU), wound-healing, and Transwell assays.

Results

HROB exhibited significant overexpression in LUAD tissues compared to normal, with high diagnostic accuracy. Elevated HROB expression was strongly associated with adverse clinical outcomes. Bioinformatics analysis revealed HROB’s involvement in modulating immune cell infiltration, regulating cell cycle progression and DNA repair pathways. Besides, BUB1B, BUB1, NUF2, CCNB2, CCNB1, KIF11, KIF2C, TPX2, DLGAP5, and CDCA8 were identified as potential hub genes within HROB-associated signaling modules. Knocking down HROB expression inhibited LUAD cell proliferation, migration, and invasion.

Conclusions

HROB is upregulated in LUAD and represents a promising prognostic biomarker, driving tumor proliferation, migration, and invasion.