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TAF15 mediates ROP16-induced apoptosis and cell cycle arrest in lung cancer

Guangqi Li1,2, Mei Tian3, Yuning Zhou4

  • 1Medical Laboratory Center, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.

Parasites & Vectors
|July 19, 2025
PubMed
Abstract

Insights

Toxoplasma gondii ROP16 (ROP16) protein, specifically types I and III, induces lung adenocarcinoma cell death and cell cycle arrest by interacting with host TAF15. This interaction highlights the oncosuppressive potential of parasite proteins.

Area of Science:

  • Molecular biology
  • Cancer research
  • Parasitology

Background:

  • Lung adenocarcinoma is a major cause of cancer mortality.
  • Toxoplasma gondii secretory proteins, like ROP16, are investigated for their biological functions.
  • Understanding host-pathogen interactions is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the interaction between ROP16 and TAF15 in A549 lung adenocarcinoma cells.
  • To determine the effects of this interaction on apoptosis and cell cycle regulation.
  • To explore the potential oncosuppressive role of parasite-derived proteins.

Main Methods:

  • Established lentivirus-infected A549 cell lines overexpressing ROP16 types I, II, and III.
  • Identified ROP16 interacting proteins using co-immunoprecipitation (Co-IP) and liquid chromatography-mass spectrometry (LC-MS).
  • Confirmed ROP16-TAF15 interaction and assessed apoptosis and cell cycle changes via flow cytometry, RT-qPCR, and western blotting after TAF15 silencing.

Main Results:

  • Confirmed interaction between ROP16 and TAF15.
  • Type I and III ROP16 promoted apoptosis and cell cycle arrest in A549 cells, modulating key regulatory proteins.
  • Type II ROP16 had no significant effect; TAF15 silencing attenuated the effects of type I/III ROP16.

Conclusions:

  • Type I/III ROP16 induce apoptosis and cell cycle arrest in lung adenocarcinoma cells via interaction with TAF15.
  • This interaction reveals a mechanism where parasite effectors hijack host transcriptional regulators.
  • Toxoplasma gondii-derived secretory proteins exhibit oncosuppressive potential against cancer cell survival.
Keywords:
ApoptosisCell cycleLung adenocarcinomaROP16TAF15Toxoplasma gondii

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