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Background <p>Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies, and the treatment options are limited. Growing evidence shows that long non-coding RNAs (LncRNAs) encode peptides, suggesting that lncRNAs-derived peptides may play a role in HCC progression and explore their potential as therapeutic targets.</p> Methods <p>We used RNA-sequencing and bioinformatics analysis to identify a 107-amino acid peptide, SMIM45-107aa, encoded by LINC00634. The expression levels and prognostic significance of SMIM45-107aa in HCC tissues were assessed by immunohistochemistry (IHC) and Kaplan-Meier. Wound-healing and cell colony formation evaluate the effects of SMIM45-107aa on cell migration and proliferation. A mouse xenograft model was used to examine the tumor formation. Interactions between SMIM45-107aa and MTDH were explored and the effects on MTDH ubiquitination were investigated by immunoprecipitation. Proteomic analysis and Western blotting confirmed the mechanism of SMIM45-107aa effected HCC. Additionally, a short peptide, peptide 5 derived from SMIM45-107aa was analyzed by cell migration in SK-Hep1 cells and by zebrafish model.</p> Results <p>SMIM45-107aa was highly expressed in HCC tissues and associated with poor prognosis. It promoted cell migration and proliferation in vitro and tumor formation in vivo. SMIM45-107aa interacted with MTDH, inhibiting its ubiquitination and stabilizing the protein. Proteomic and Western blot analysis revealed that SMIM45-107aa upregulated MGST1 and phosphorylated AKT (pAKT). Importantly, peptide 5 inhibited SMIM45-107aa-induced cell migration and demonstrated anticancer activity in zebrafish models.</p> Conclusion <p>We identified SMIM45-107aa, a novel peptide encoded by LINC00634, which promoted HCC progression via the MGST1-pAKT-MTDH axis. The derived peptide 5 exhibited anticancer activity, suggesting a potential therapeutic strategy for HCC.</p>

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–A novel peptide SMIM45-107aa promotes HCC progression via MTDH pathways and its anticancer peptide derivative

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月11日

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  • Yan An,
  • Xiangyang Shi,
  • Wentao Huang,
  • Mingyi Shang,
  • Guang-Zhi Jin

摘要

Background

Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies, and the treatment options are limited. Growing evidence shows that long non-coding RNAs (LncRNAs) encode peptides, suggesting that lncRNAs-derived peptides may play a role in HCC progression and explore their potential as therapeutic targets.

Methods

We used RNA-sequencing and bioinformatics analysis to identify a 107-amino acid peptide, SMIM45-107aa, encoded by LINC00634. The expression levels and prognostic significance of SMIM45-107aa in HCC tissues were assessed by immunohistochemistry (IHC) and Kaplan-Meier. Wound-healing and cell colony formation evaluate the effects of SMIM45-107aa on cell migration and proliferation. A mouse xenograft model was used to examine the tumor formation. Interactions between SMIM45-107aa and MTDH were explored and the effects on MTDH ubiquitination were investigated by immunoprecipitation. Proteomic analysis and Western blotting confirmed the mechanism of SMIM45-107aa effected HCC. Additionally, a short peptide, peptide 5 derived from SMIM45-107aa was analyzed by cell migration in SK-Hep1 cells and by zebrafish model.

Results

SMIM45-107aa was highly expressed in HCC tissues and associated with poor prognosis. It promoted cell migration and proliferation in vitro and tumor formation in vivo. SMIM45-107aa interacted with MTDH, inhibiting its ubiquitination and stabilizing the protein. Proteomic and Western blot analysis revealed that SMIM45-107aa upregulated MGST1 and phosphorylated AKT (pAKT). Importantly, peptide 5 inhibited SMIM45-107aa-induced cell migration and demonstrated anticancer activity in zebrafish models.

Conclusion

We identified SMIM45-107aa, a novel peptide encoded by LINC00634, which promoted HCC progression via the MGST1-pAKT-MTDH axis. The derived peptide 5 exhibited anticancer activity, suggesting a potential therapeutic strategy for HCC.