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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Sinapaldehyde Induces Mitochondrial Dysfunction and Modulates Autophagy/Mitophagy-Associated Signaling and Apoptosis in MDA-MB-231 Triple-Negative Breast Cancer Cells

  • Hiruni Sandunika Kumarasinghe1
  • Ducdat Le2,3,4
  • Ji-Hyang Kim5
  • Su-Lim Kim6
  • Kyeoung Cheol Kim1
  • Rambukka-na Maggonage Thiruni Dananjana Perera1
  • Yaejun Kim1
  • Mina Lee2,3,4
  • Dong-Sun Lee1,5,6,7
7 affiliations
  1. 1Interdisciplinary Graduate Program in Advanced Convergence Technology & Science, Jeju National University, Jeju 63243, Republic of Korea
  2. 2College of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Suncheon, Jeonnam-Gwangju 57922, Republic of Korea
  3. 3Department of Natural Cosmetics Science and AI Digital Bioscience Research Institute, Sunchon National University, Suncheon, Jeonnam-Gwangju 57922, Republic of Korea
  4. 4AI Bio Autonomous Research Core Facility Center, Sunchon National University, Suncheon, Jeonnam-Gwangju 57922, Republic of Korea
  5. 5Bio-Health Materials Core-Facility Center, Jeju National University, Jeju 63243, Republic of Korea
  6. 6Graduate Program for Bio-Health/Innovative Drug Development Using Subtropical Bio-Resources, Jeju National University, Jeju 63243, Republic of Korea
  7. 7Faculty of Biotechnology, College of Applied Life Sciences, Jeju National University, Jeju 63243, Republic of Korea
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Abstract

Triple-negative breast cancer (TNBC) is highly aggressive and lacks targeted therapies. This study investigated the anti-cancer mechanisms of sinapaldehyde (SNAH). The biological effects of SNAH were evaluated in vitro using MDA-MB-231 TNBC cells. Cellular responses, including autophagy, mitochondrial function, apoptosis, cell-cycle progression, migration, and colony formation were investigated. In silico studies explored associated regulatory networks and binding targets. Sinapaldehyde (SNAH) treatment was associated with mitochondrial dysfunction, characterized by alterations in mitochondrial structural and functional markers, increased reactive oxygen species(ROS) production, and loss of mitochondrial membrane potential. SNAH treatment also altered the expression of PINK1 and Parkin and modulated autophagy-associated markers, including LC3B, p62, LAMP1, Beclin-1, and ATG proteins. Time-dependent changes in autophagy- and apoptosis-associated markers were accompanied by increased Annexin V-positive cells and activation of cleaved caspase-9 and caspase-3. SNAH also altered FTH1 and NCOA4 expression, suggesting modulation of ferritinophagy-associated processes, and inhibited migration and colony formation while inducing G2/M cell-cycle arrest. In silico analyses identified potential breast cancer-related molecular targets and signaling pathways associated with SNAH. SNAH induces mitochondrial dysfunction and is associated with alterations in autophagy/mitophagy-associated signaling and activation of apoptosis in MDA-MB-231 TNBC cells. These findings provide insight into the cellular responses to SNAH treatment, while further functional studies are required to establish changes in mitophagic and ferritinophagic flux and the causal relationship between autophagy and apoptosis.

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Cite

BibTeXRIS
BibTeX
@article{kumarasinghe2026sinapaldehyde,
  title = {{Sinapaldehyde Induces Mitochondrial Dysfunction and Modulates Autophagy/Mitophagy-Associated Signaling and Apoptosis in MDA-MB-231 Triple-Negative Breast Cancer Cells}},
  author = {Hiruni Sandunika Kumarasinghe and Ducdat Le and Ji-Hyang Kim and Su-Lim Kim and Kyeoung Cheol Kim and Rambukka-na Maggonage Thiruni Dananjana Perera and Yaejun Kim and Mina Lee and Dong-Sun Lee},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209359},
  url = {https://www.mdpi.com/1422-0067/27/20/9359},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Sinapaldehyde Induces Mitochondrial Dysfunction and Modulates Autophagy/Mitophagy-Associated Signaling and Apoptosis in MDA-MB-231 Triple-Negative Breast Cancer Cells
AU  - Hiruni Sandunika Kumarasinghe
AU  - Ducdat Le
AU  - Ji-Hyang Kim
AU  - Su-Lim Kim
AU  - Kyeoung Cheol Kim
AU  - Rambukka-na Maggonage Thiruni Dananjana Perera
AU  - Yaejun Kim
AU  - Mina Lee
AU  - Dong-Sun Lee
PY  - 2026
DA  - 2026/10/01
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209359
UR  - https://www.mdpi.com/1422-0067/27/20/9359
AB  - Triple-negative breast cancer (TNBC) is highly aggressive and lacks targeted therapies. This study investigated the anti-cancer mechanisms of sinapaldehyde (SNAH). The biological effects of SNAH were evaluated in vitro using MDA-MB-231 TNBC cells. Cellular responses, including autophagy, mitochondrial function, apoptosis, cell-cycle progression, migration, and colony formation were investigated. In silico studies explored associated regulatory networks and binding targets. Sinapaldehyde (SNAH) treatment was associated with mitochondrial dysfunction, characterized by alterations in mitochondrial structural and functional markers, increased reactive oxygen species(ROS) production, and loss of mitochondrial membrane potential. SNAH treatment also altered the expression of PINK1 and Parkin and modulated autophagy-associated markers, including LC3B, p62, LAMP1, Beclin-1, and ATG proteins. Time-dependent changes in autophagy- and apoptosis-associated markers were accompanied by increased Annexin V-positive cells and activation of cleaved caspase-9 and caspase-3. SNAH also altered FTH1 and NCOA4 expression, suggesting modulation of ferritinophagy-associated processes, and inhibited migration and colony formation while inducing G2/M cell-cycle arrest. In silico analyses identified potential breast cancer-related molecular targets and signaling pathways associated with SNAH. SNAH induces mitochondrial dysfunction and is associated with alterations in autophagy/mitophagy-associated signaling and activation of apoptosis in MDA-MB-231 TNBC cells. These findings provide insight into the cellular responses to SNAH treatment, while further functional studies are required to establish changes in mitophagic and ferritinophagic flux and the causal relationship between autophagy and apoptosis.
SN  - 1422-0067
ER  -