α-Cyperone inhibits the proliferation of human cervical cancer HeLa cells via ROS-mediated PI3K/Akt/mTOR signaling pathway

Eur J Pharmacol. 2020 Sep 15:883:173355. doi: 10.1016/j.ejphar.2020.173355. Epub 2020 Jul 17.

Abstract

Cervical cancer is the fourth leading killer of female cancer patients worldwide. Each year more than half a million women are diagnosed with cervical cancer and the disease results in over 300, 000 deaths. α-Cyperone is known as the principal active ingredient in the Cyperus rotundus (Family: Cyperaceae). However, the effects of α-Cyperone on cancers, especially on cervical cancer, are yet to be explored. In the present study, the underlying mechanism of the anti-tumor activity of α-Cyperone against HeLa cells was investigated. The results showed that α-Cyperone inhibited proliferation and induced apoptosis in HeLa cells. Mechanistically, α-Cyperone promoted HeLa cells apoptosis via a mitochondrial apoptotic pathway, which was proved by increased level of intracellular reactive oxygen species (ROS) and upregulated expression of cytochrome c, cleaved caspase-3, PARP, and Bax. Further RNA-sequencing revealed α-Cyperone inhibited the activation of PI3K/Akt/mTOR signaling pathway in HeLa cells, which confirmed by PI3K inhibitor and agonist. The PI3K inhibitor (LY294002) synergized with α-Cyperone in arresting the growth of HeLa cells, whereas the PI3K agonist (IGF-1) abrogated such an effect. Interestingly, the expression of PD-L1 was attenuated by both α-Cyperone and LY294002, while the supplement of IGF-1 rescued the low expression of PD-L1. In conclusion, our results reveal that the inhibitory effect of α-Cyperone on HeLa cell growth is triggered via the ROS-mediated PI3K/Akt/mTOR signaling pathway and closely related to a decline in the PD-L1 expression.

Keywords: Apoptosis; HeLa cells; PD-L1; PI3K/Akt/mTOR signaling pathway; α-Cyperone.

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis / drug effects
  • B7-H1 Antigen / metabolism
  • Cell Proliferation / drug effects*
  • Female
  • G1 Phase Cell Cycle Checkpoints / drug effects
  • HeLa Cells
  • Humans
  • Mitochondria / drug effects
  • Mitochondria / enzymology
  • Mitochondria / pathology
  • Naphthalenes / pharmacology*
  • Phosphatidylinositol 3-Kinase / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction
  • TOR Serine-Threonine Kinases / metabolism*
  • Uterine Cervical Neoplasms / drug therapy*
  • Uterine Cervical Neoplasms / enzymology
  • Uterine Cervical Neoplasms / pathology

Substances

  • Antineoplastic Agents, Phytogenic
  • B7-H1 Antigen
  • CD274 protein, human
  • Naphthalenes
  • Reactive Oxygen Species
  • MTOR protein, human
  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • alpha-cyperone