Integrated spectroscopic and morphological analyses reveal cellular shifts in gene-silenced melanoma CSCs

Berrin Ozdil1,2,3, Günnur Güler3, Evren Ataman3

  • 1Department of Histology and Embryology, Faculty of Medicine, Ege University, Izmir, 35100, Turkey.

Scientific Reports
|August 25, 2025
PubMed

Insights

Targeting key genes in melanoma cancer stem cells (CSCs) with siRNA altered cell structure and biochemistry, reducing stem-like traits. This research offers new insights into cellular plasticity and potential therapeutic strategies.

Area of Science:

  • Oncology
  • Cancer Stem Cell Biology
  • Biophysics

Background:

  • Intratumoral heterogeneity driven by cancer stem cells (CSCs) impedes effective cancer therapies.
  • Melanoma CSCs exhibit unique properties that contribute to treatment resistance.

Purpose of the Study:

  • To investigate the structural and biochemical effects of silencing KLF4, SHH, and HIF1α in melanoma CSCs.
  • To explore the potential of multi-scale analyses, including spectroscopy, for characterizing CSC responses.

Main Methods:

  • siRNA-mediated gene silencing of KLF4, SHH, and HIF1α in melanoma CSCs.
  • Integrated multi-scale analyses: morphological, molecular, ATR-FTIR spectroscopy, SEM-EDS, and XPS.
  • Assessment of cytoskeletal organization (F-actin) and protein expression (PFN1).

Main Results:

  • Gene silencing led to significant alterations in cell morphology and reduced F-actin organization, indicative of decreased stemness.
  • ATR-FTIR spectroscopy revealed changes in biomolecular composition, including reduced amide III and increased lipid ester signals.
  • SEM-EDS and XPS analyses showed differences in elemental composition (carbon, nitrogen) between silenced and control cells.

Conclusions:

  • Targeting KLF4, SHH, and HIF1α induces significant cytoskeletal and biochemical remodeling in melanoma CSCs.
  • Multi-scale analytical approaches, particularly FTIR spectroscopy, provide valuable insights into CSC plasticity.
  • These findings highlight potential therapeutic strategies by targeting regulatory pathways in melanoma CSCs.