Details

Autor(en) / Beteiligte

• Lin, Shuchun
• Mei, Wenfeng
• Lai, Haichun
• Li, Xiufeng
• Weng, Huanjiao
• Xiong, Jiani
• Lin, Xiuyun
• Zeng, Tao
• Zhang, Qiong
• Liu, Xing
• Xu, Yunlu
• Fang, Shubin
• Jin, Rong
• Hu, Xiaohua
• Xie, Jieming
• Yang, Jianbo
• Zheng, Yiqing
• Chen, Yuanzhong
• Lin, Jizhen

Titel

Cigarette smoking promotes keratinocyte malignancy via generation of cancer stem-like cells

Ist Teil von

• Journal of Cancer, 2021, Vol.12 (4), p.1085-1093

Ort / Verlag

Australia: Ivyspring International Publisher Pty Ltd

Erscheinungsjahr

2021

Link zum Volltext

Quelle

Electronic Journals Library - Freely accessible e-journals

Beschreibungen/Notizen

• : Cigarette smoking is involved in the pathogenesis of head and neck squamous cell carcinoma (HNSCC). However, the underlying molecular mechanisms of cigarette smoking-induced HNSCC carcinogenesis are unclear and may involve cancer stem-like cell generation. We examined the effects of cigarette smoke condensate (CSC) on the formation of cancer stem-like cells, which are rich in octamer-binding transcription factor (OCT)-4, inhibitor of differentiation 1 (ID1), nuclear factor (NF)-κB, and B lymphoma Mo-MLV insertion region 1 homolog (BMI-1). : We used , , and archival human HNSCC tissue analysis to evaluate the effects of CSC on cancer stem-like cell formation. We found that CSC regulated OCT-4 expression, which subsequently regulated ID1 and NF-κB, at the promoter, mRNA, and protein levels . Furthermore, OCT-4 knockdown with siRNA reduced ID1 expression. ID1 and NF-κB synergistically increased the expression of BMI-1 and stimulated keratinocyte sphere generation. , ID1 and NF-κB acted together to generate malignant xenograft tumors, which were aggressive locally and systemically metastatic. Clinical data confirmed that ID1- and NF-κB-positive patients had poor clinical outcomes and 5-year disease-free survival. : Our data suggest that smoking cigarettes promoted cancer stem-like cell generation in the head and neck area via the OCT-4/ID1/NF-κB/BMI-1 signaling pathway.