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<p>Hepatocellular carcinoma (HCC) is a common liver cancer often diagnosed at an advanced stage. While chemotherapies such as sorafenib is effective for some patients, others show poor responses, necessitating new treatments. Overexpression of MYCN/NCYM was recently shown to contribute to the development of HCC. This study investigated the effects of Pentagamavunone-1 (PGV-1), a curcumin analog with strong antiproliferative properties, on HCC cells expressing MYCN/NCYM. PGV-1 was more effective than curcumin and sorafenib in inhibiting HCC cell proliferation by inducing mitotic arrest, oxidative stress, and senescence. In MYCN-positive JHH-7 cells, PGV-1 treatment increased phosphorylation of aurora A, cyclin B1, and PLK1. PGV-1 also suppressed MYCN/NCYM transcription and destabilized MYCN protein by inducing phosphorylation at Ser54 and Thr58. In a xenograft model, PGV-1 significantly reduced tumor formation and growth. These findings highlight PGV-1’s potential as a targeted therapy for MYCN-overexpressing HCC, warranting further development.</p>

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Pentagamavunone-1 targets excessive MYCN/NCYM expression mediated by mitotic arrest to suppress hepatocellular carcinoma proliferation

  • 期刊论文

  • 发表日期：

    2025年9月1日

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  • Dhania Novitasari,
  • Ikuko Nakamae,
  • Noriko Yoneda-Kato,
  • Edy Meiyanto,
  • Jun-ya Kato

摘要

Hepatocellular carcinoma (HCC) is a common liver cancer often diagnosed at an advanced stage. While chemotherapies such as sorafenib is effective for some patients, others show poor responses, necessitating new treatments. Overexpression of MYCN/NCYM was recently shown to contribute to the development of HCC. This study investigated the effects of Pentagamavunone-1 (PGV-1), a curcumin analog with strong antiproliferative properties, on HCC cells expressing MYCN/NCYM. PGV-1 was more effective than curcumin and sorafenib in inhibiting HCC cell proliferation by inducing mitotic arrest, oxidative stress, and senescence. In MYCN-positive JHH-7 cells, PGV-1 treatment increased phosphorylation of aurora A, cyclin B1, and PLK1. PGV-1 also suppressed MYCN/NCYM transcription and destabilized MYCN protein by inducing phosphorylation at Ser54 and Thr58. In a xenograft model, PGV-1 significantly reduced tumor formation and growth. These findings highlight PGV-1’s potential as a targeted therapy for MYCN-overexpressing HCC, warranting further development.