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<p>Hepatocellular carcinoma (HCC) is characterized by aggressive progression and metastasis, driven by complex molecular interactions. This study elucidates the functional roles of slit guidance ligand 2 (SLIT2) and non-muscle myosin IIA (NMIIA) in HCC and explores their mechanistic interplay. Immunofluorescence and quantitative PCR (Q-PCR) analyses demonstrated significant downregulation of SLIT2 and upregulation of NMIIA in HCC tissues, with SLIT2 expression inversely correlating with tumor stage and metastatic propensity, as validated by The Cancer Genome Atlas (TCGA) dataset. Functional assays revealed that SLIT2 overexpression attenuated HCC cell proliferation, migration, and invasion, whereas NMIIA overexpression markedly enhanced these oncogenic properties. Mechanistically, NMIIA facilitated epithelial-mesenchymal transition (EMT) and mitophagy, potentiating tumor progression. Conversely, SLIT2 overexpression inhibited myosin regulatory light chain (MRLC) phosphorylation, thereby suppressing NMIIA activity, EMT, and mitophagy. SLIT2 also diminished cell adhesion, while NMIIA enhanced adhesion and colony-forming capacity. In vivo xenograft studies corroborated that SLIT2 depletion accelerated tumor growth. These findings establish the SLIT2/NMIIA axis as a critical modulator of HCC progression and a promising therapeutic target.</p>

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SLIT2 modulates NMIIA to regulate mitophagy and suppress hepatocellular carcinoma progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月14日

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  • Yong Qin,
  • Junbin Zhou,
  • Shimiao Li,
  • Xiaofeng Liu,
  • Shengqian Xu

摘要

Hepatocellular carcinoma (HCC) is characterized by aggressive progression and metastasis, driven by complex molecular interactions. This study elucidates the functional roles of slit guidance ligand 2 (SLIT2) and non-muscle myosin IIA (NMIIA) in HCC and explores their mechanistic interplay. Immunofluorescence and quantitative PCR (Q-PCR) analyses demonstrated significant downregulation of SLIT2 and upregulation of NMIIA in HCC tissues, with SLIT2 expression inversely correlating with tumor stage and metastatic propensity, as validated by The Cancer Genome Atlas (TCGA) dataset. Functional assays revealed that SLIT2 overexpression attenuated HCC cell proliferation, migration, and invasion, whereas NMIIA overexpression markedly enhanced these oncogenic properties. Mechanistically, NMIIA facilitated epithelial-mesenchymal transition (EMT) and mitophagy, potentiating tumor progression. Conversely, SLIT2 overexpression inhibited myosin regulatory light chain (MRLC) phosphorylation, thereby suppressing NMIIA activity, EMT, and mitophagy. SLIT2 also diminished cell adhesion, while NMIIA enhanced adhesion and colony-forming capacity. In vivo xenograft studies corroborated that SLIT2 depletion accelerated tumor growth. These findings establish the SLIT2/NMIIA axis as a critical modulator of HCC progression and a promising therapeutic target.