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<p>Growth-regulated oncogene‑α (GRO‑α) has been widely reported in tumorigenesis. However, the specific contribution of GRO‑α to the malignant behaviors of triple-negative breast cancer (TNBC) remains unclear. Bioinformatics analyses were conducted using the UALCAN and TIMER databases. The underlying mechanism of action of GRO‑α on the progression of TNBC MDA-MB-231 cells was investigated using CCK‑8, EdU, transwell and Western blotting assays. TNBC tissues exhibited elevated expression of GRO‑α, and its high expression was positively correlated with tumor immune cytokines and immune cell recruitment. The growth and migration of TNBC MDA-MB-231 cells were significantly enhanced following treatment with recombinant GRO‑α. Consistently, the protein levels of AKT, p‑mTOR, and mTOR in MDA-MB-231 cells were extremely elevated by recombinant GRO‑α. In addition, the malignant behaviors induced by GRO‑α were surprisingly attenuated following treatment with mTOR inhibitor Torin1. GRO‑α may play a role in the malignant progression of TNBC in an AKT-mTOR-dependent manner.</p>

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GRO‑α Promotes the Proliferation and Migration of Triple-Negative Breast Cancer Cells through AKT-mTOR Signaling Pathway

  • 期刊论文

  • 发表日期：

    2026年6月2日

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  • Shengyang Sun,
  • Lichun Liang,
  • Bing Han,
  • Ziteng Cai,
  • Weiqun Wang,
  • Yikun Qu

摘要

Growth-regulated oncogene‑α (GRO‑α) has been widely reported in tumorigenesis. However, the specific contribution of GRO‑α to the malignant behaviors of triple-negative breast cancer (TNBC) remains unclear. Bioinformatics analyses were conducted using the UALCAN and TIMER databases. The underlying mechanism of action of GRO‑α on the progression of TNBC MDA-MB-231 cells was investigated using CCK‑8, EdU, transwell and Western blotting assays. TNBC tissues exhibited elevated expression of GRO‑α, and its high expression was positively correlated with tumor immune cytokines and immune cell recruitment. The growth and migration of TNBC MDA-MB-231 cells were significantly enhanced following treatment with recombinant GRO‑α. Consistently, the protein levels of AKT, p‑mTOR, and mTOR in MDA-MB-231 cells were extremely elevated by recombinant GRO‑α. In addition, the malignant behaviors induced by GRO‑α were surprisingly attenuated following treatment with mTOR inhibitor Torin1. GRO‑α may play a role in the malignant progression of TNBC in an AKT-mTOR-dependent manner.