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BACE2 facilitates lung adenocarcinoma progression by enhancing mTORC1 signalling

Zhixin You1, Wei He1, Yanfei Zhou2

  • 1Respiratory Department, Shaoxing Hospital of Traditional Chinese Medicine, Shaoxing, China.

Translational Cancer Research
|March 12, 2026
PubMed
Abstract

Insights

Beta-secretase 2 (BACE2) promotes lung adenocarcinoma (LUAD) progression by activating the mTORC1 pathway. Targeting BACE2 offers a new therapeutic strategy for LUAD patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Lung adenocarcinoma (LUAD) presents a significant clinical challenge due to resistance to conventional therapies.
  • Identifying novel oncogenic drivers and therapeutic targets is crucial for improving LUAD patient outcomes.
  • The role of Beta-secretase 2 (BACE2) in LUAD pathogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate the expression patterns of BACE2 in LUAD.
  • To elucidate the biological functions and underlying molecular mechanisms of BACE2 in LUAD.
  • To evaluate BACE2 as a potential therapeutic target for LUAD.

Main Methods:

  • Bioinformatic analysis and immunohistochemistry were used to assess BACE2 expression in LUAD tissues and cell lines.
  • In vitro assays (CCK-8, EdU, flow cytometry, Transwell, scratch) evaluated the effects of BACE2 on cell viability, proliferation, apoptosis, migration, and cell cycle.
  • Gene set enrichment analysis (GSEA) and Western blotting identified the downstream signaling pathways regulated by BACE2.
  • An in vivo xenograft model was utilized to confirm the role of BACE2 in tumor growth.

Main Results:

  • BACE2 expression was significantly elevated in LUAD tissues and cell lines, correlating with poorer patient survival.
  • BACE2 knockdown resulted in increased apoptosis, reduced cell viability, proliferation, and migration, and G2 phase cell cycle arrest.
  • BACE2 activates the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway, as evidenced by GSEA and Western blot analyses.
  • Inhibition of mTORC1 abrogated the oncogenic effects of BACE2, and BACE2 knockdown suppressed tumor growth in vivo.

Conclusions:

  • BACE2 plays a critical role in promoting LUAD progression through the activation of the mTORC1 signaling pathway.
  • BACE2 represents a novel and promising therapeutic target for the treatment of lung adenocarcinoma.
  • Targeting BACE2 may offer a new strategy to overcome resistance to existing LUAD therapies.
Keywords:
Lung adenocarcinoma (LUAD)beta-secretase 2 (BACE2)mammalian target of rapamycin complex 1 signalling pathway (mTORC1 signalling pathway)migration

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