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Surfactin induces autophagy, apoptosis, and cell cycle arrest in human oral squamous cell carcinoma.
Vo, Thi Thuy Tien; Wee, Yinshen; Cheng, Hsin-Chung; Wu, Ching-Zong; Chen, Yuh-Lien; Tuan, Vo Phuoc; Liu, Ju-Fang; Lin, Wei-Ning; Lee, I-Ta.
Afiliación
  • Vo TTT; School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
  • Wee Y; Department of Pathology, University of Utah, Salt Lake City, UT, USA.
  • Cheng HC; School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
  • Wu CZ; Department of Dentistry, Taipei Medical University Hospital, Taipei, Taiwan.
  • Chen YL; School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
  • Tuan VP; Department of Dentistry, Taipei Medical University Hospital, Taipei, Taiwan.
  • Liu JF; Department of Dentistry, Lotung Poh-Ai Hospital, Yilan, Taiwan.
  • Lin WN; Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan.
  • Lee IT; Endoscopy Department, Cho Ray Hospital, Ho Chi Minh City, Vietnam.
Oral Dis ; 29(2): 528-541, 2023 Mar.
Article en En | MEDLINE | ID: mdl-34181793
OBJECTIVES: To investigate the anticancer effects and underlying mechanisms of surfactin on human oral squamous cell carcinoma (OSCC). MATERIALS AND METHODS: The capacity of surfactin to induce apoptosis, autophagy, and cell cycle arrest of two different human OSCC cell lines was investigated by cell viability, acridine orange staining, and cell cycle regulatory protein expression, respectively. The signaling network underlying these processes were determined by the analysis of reactive oxygen species (ROS) generation, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, endoplasmic reticulum (ER) stress-related protein levels, calcium release, mitogen-activated protein kinases activation, and cell cycle regulatory protein expression through corresponding reagents and experiments under various experimental conditions using specific pharmaceutical inhibitors or small interfering RNAs. RESULTS: Surfactin was able to induce apoptosis through NADPH oxidase/ROS/ER stress/calcium-downregulated extracellular signal-regulated kinases 1/2 pathway. Surfactin could also lead to autophagy that shared the common regulatory signals with apoptosis pathway until calcium node. Cell cycle arrest at G2 /M phase caused by surfactin was demonstrated through p53 and p21 accumulation combined p34cdc2 , phosphorylated p34cdc2 , and cyclin B1 inhibition, which was regulated by NADPH oxidase-derived ROS. CONCLUSION: Surfactin could induce apoptosis, autophagy, and cell cycle arrest in ROS-dependent manner, suggesting a multifaced anticancer agent for OSCC.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias de la Boca / Carcinoma de Células Escamosas / Neoplasias de Cabeza y Cuello Límite: Humans Idioma: En Revista: Oral Dis Asunto de la revista: ODONTOLOGIA Año: 2023 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Dinamarca
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias de la Boca / Carcinoma de Células Escamosas / Neoplasias de Cabeza y Cuello Límite: Humans Idioma: En Revista: Oral Dis Asunto de la revista: ODONTOLOGIA Año: 2023 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Dinamarca