Cell cycle progression data on human skin cancer cells with anticancer synthetic peptide LTX-315 treatment

Gloria A Santa-González1,2, Edwin Patiño-González1,2, Marcela Manrique-Moreno2

  • 1Genetic Regeneration and Cancer Group, Faculty of Exact and Natural Sciences, Biology Institute, University of Antioquia, A.A. 1226, Medellin, Colombia.

Data in Brief
|April 8, 2020
PubMed

Insights

LTX-315, an anticancer peptide, affects skin cancer cell cycle differently than normal cells. Non-tumoral cells show a sub-G1 peak, indicating cell death, while tumoral cells exhibit a G1 phase shift, suggesting varied responses to this peptide therapy.

Area of Science:

  • Oncology
  • Dermatology
  • Molecular Biology

Background:

  • Skin cancer, including melanoma and non-melanoma skin cancer (NMSC), is a prevalent malignancy.
  • The synthetic anticancer peptide LTX-315 (Oncopore™) has demonstrated anticancer properties, but its effects on cell cycle progression are not well understood.

Purpose of the Study:

  • To investigate the effects of LTX-315 on the cell cycle progression of skin cancer cell lines (A431 epidermoid carcinoma, A375 melanoma) and a normal keratinocyte cell line (HaCaT).
  • To determine the cytotoxicity of LTX-315 and its relationship with cell cycle distribution.

Main Methods:

  • Flow cytometry analysis of cell cycle distribution.
  • Propidium iodide uptake assay to measure cytotoxicity.

Main Results:

  • LTX-315 treatment induced a sub-G1 cell cycle arrest (indicating cell death) in non-tumoral HaCaT cells.
  • Tumoral cell lines (A431, A375) showed a shift in the G1 phase of the cell cycle without a distinct sub-G1 peak in response to LTX-315.
  • A significant decrease in cell viability was observed in non-cancer cells, correlating with the observed cell cycle changes.

Conclusions:

  • LTX-315 exhibits differential effects on the cell cycle of normal versus skin cancer cells.
  • The peptide induces cell death in normal keratinocytes, while its primary effect on tumoral cells involves alterations in G1 phase progression.