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Dihydroartemisinin Suppresses Hepatocellular Carcinoma Progression by Acting on KIF11 with PI3K/Akt Modulation

Aina Xiao1, Yu'E Liu2, Wenjia Guo3

  • 1Department of Blood Transfusion, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan 750002, China.

Cancers
|May 27, 2026
PubMed

Insights

Dihydroartemisinin (DHA) shows promise for treating hepatocellular carcinoma (HCC) by targeting KIF11 and the PI3K/Akt pathway. This research reveals a novel therapeutic strategy for this deadly cancer.

Area of Science:

  • Hepatocellular Carcinoma Research
  • Molecular Oncology
  • Drug Discovery

Background:

  • Hepatocellular carcinoma (HCC) is a major global cancer mortality cause with limited treatment options.
  • Dihydroartemisinin (DHA), an artemisinin derivative, has shown antitumor potential, but its mechanism in HCC is not fully understood.
  • Kinesin family member 11 (KIF11) has been identified as a key mediator of DHA's effects in HCC.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying Dihydroartemisinin's (DHA) antitumor activity in Hepatocellular Carcinoma (HCC).
  • To investigate the role of Kinesin family member 11 (KIF11) in mediating DHA's effects.
  • To explore the potential of DHA as a therapeutic agent for HCC targeting KIF11 and the PI3K/Akt pathway.

Main Methods:

  • Bioinformatic analysis of KIF11 expression in HCC and its correlation with prognosis.
  • In vitro functional assays to assess DHA's impact on HCC cell proliferation, migration, invasion, and apoptosis.
  • In vivo studies using xenograft models in nude mice to validate therapeutic efficacy.
  • Gene expression profiling to identify pathways involved, including PI3K/Akt.

Main Results:

  • KIF11 is upregulated in HCC and linked to poor prognosis, suggesting an oncogenic role.
  • DHA effectively inhibits HCC cell growth, migration, invasion, and colony formation while promoting apoptosis.
  • DHA downregulates KIF11 and epithelial-mesenchymal transition (EMT) markers; KIF11 overexpression counteracts DHA's effects.
  • PI3K inhibition restores sensitivity to DHA in KIF11-overexpressing cells, and in vivo studies confirm tumor suppression by DHA.

Conclusions:

  • Dihydroartemisinin (DHA) exerts significant antitumor effects in Hepatocellular Carcinoma (HCC).
  • DHA's mechanism involves the modulation of Kinesin family member 11 (KIF11) and the PI3K/Akt signaling pathway.
  • Targeting KIF11 and PI3K/Akt with DHA presents a promising therapeutic strategy for HCC.
Abstract

Keywords:
KIF11PI3K/Akt signalingapoptosisdihydroartemisininhepatocellular carcinoma

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