Lactonic sophorolipid-induced apoptosis in human HepG2 cells through the Caspase-3 pathway

Xiao Wang1,2, Na Xu3,4, Qinglin Li1

  • 1Key Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei, 230038, Anhui, China.

Insights

Lactonic sophorolipids (LSL) show potential as a liver cancer treatment by inhibiting HepG2 cell proliferation and inducing apoptosis. LSL activates the Caspase-3 pathway, offering a promising therapeutic strategy with fewer side effects.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Liver cancer is a leading cause of cancer-related mortality worldwide, necessitating novel therapeutic agents with reduced toxicity.
  • Lactonic sophorolipids (LSL) possess known biological activities and are being investigated for their anticancer potential.

Purpose of the Study:

  • To investigate the in vitro effects of Lactonic sophorolipids (LSL) on HepG2 liver cancer cell proliferation.
  • To elucidate the mechanism by which LSL affects HepG2 cells, focusing on apoptosis induction and related pathways.

Main Methods:

  • Cell proliferation was assessed using MTT assays on HepG2 cells treated with LSL.
  • Apoptosis was evaluated through morphological observation, flow cytometry, and analysis of Caspase-3 and Caspase-9 activity.
  • Gene and protein expression related to apoptosis (Apaf-1, Caspase-3, Bax, Bcl-2) were measured via RT-PCR and Western blot.

Main Results:

  • Lactonic sophorolipids (LSL) significantly inhibited HepG2 cell proliferation.
  • LSL induced typical apoptotic morphology and increased the apoptosis rate in HepG2 cells.
  • LSL treatment led to elevated activity of Caspase-3 and Caspase-9, and modulated the expression of apoptosis-related genes and proteins via the Caspase-3 pathway.

Conclusions:

  • Lactonic sophorolipids (LSL) demonstrate significant potential in inhibiting liver cancer cell proliferation and inducing apoptosis.
  • The Caspase-3 pathway is implicated in the mechanism of LSL-induced apoptosis in HepG2 cells.
  • LSL represents a promising candidate for further development as a therapeutic agent for liver cancer.

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