Fucoidan induces ROS-dependent epigenetic modulation in cervical cancer HeLa cell

Saad Mustafa1, Jogendra Singh Pawar1, Ilora Ghosh1

  • 1Biochemistry and Environmental Toxicology, Laboratory # 103, School of Environmental Sciences, Jawaharlal Nehru University, New Delhi 110067, India.

Insights

Fucoidan, a marine algae compound, effectively targets HDACs in cervical cancer cells, inducing cell death through autophagy and senescence. This study highlights Fucoidan

Area of Science:

  • Marine Biotechnology
  • Cancer Biology
  • Pharmacology

Background:

  • Fucoidan, a sulfated polysaccharide from marine algae, exhibits diverse pharmacological activities.
  • Cervical cancer remains a significant global health concern, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To investigate Fucoidan's therapeutic potential against human cervical cancer (HeLa) cells.
  • To elucidate the mechanisms underlying Fucoidan's anti-cancer effects, including cytotoxicity, autophagy, and senescence induction.

Main Methods:

  • Utilized flow cytometry, fluorescence microscopy, and western blotting to assess cell viability, redox balance, and protein expression.
  • Employed colorimetrical studies and molecular docking to evaluate HDAC inhibition and Fucoidan-HDAC1 interaction.

Main Results:

  • Fucoidan induced cytotoxicity in HeLa cells via reactive oxygen species (ROS) and mitochondrial superoxide generation, leading to ATP depletion.
  • Observed Fucoidan-impaired HDAC expression, induced senescence-associated heterochromatin foci, and triggered autophagosome formation, indicating autophagy.
  • Confirmed Fucoidan-HDAC1 association through molecular docking and observed changes in senescence and autophagy markers (p21, p16, BECN1, HDAC1).

Conclusions:

  • Fucoidan demonstrates significant anti-cancer properties against cervical cancer cells.
  • Fucoidan's mechanism involves HDAC inhibition, induction of autophagy, and promotion of cellular senescence.
  • Fucoidan presents a promising therapeutic candidate for targeting HDACs in cervical cancer treatment.