{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lin S"],"funding":["NCI NIH HHS"],"pagination":["1085-1093"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7797662"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(4)"],"pubmed_abstract":["<b>Objectives</b>: 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). <b>Materials and Methods</b>: We used <i>in vitro</i>, <i>in vivo</i>, and archival human HNSCC tissue analysis to evaluate the effects of CSC on cancer stem-like cell formation. <b>Results:</b> We found that CSC regulated OCT-4 express"],"journal":["Journal of Cancer"],"pubmed_title":["Cigarette smoking promotes keratinocyte malignancy via generation of cancer stem-like cells."],"pmcid":["PMC7797662"],"funding_grant_id":["R03 CA107989"],"pubmed_authors":["Lai H","Xiong J","Yang J","Zheng Y","Lin S","Mei W","Jin R","Hu X","Lin X","Zeng T","Zhang Q","Liu X","Li X","Weng H","Xie J","Fang S","Chen Y","Lin J","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"Cigarette smoking promotes keratinocyte malignancy via generation of cancer stem-like cells.","description":"<b>Objectives</b>: 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). <b>Materials and Methods</b>: We used <i>in vitro</i>, <i>in vivo</i>, and archival human HNSCC tissue analysis to evaluate the effects of CSC on cancer stem-like cell formation. <b>Results:</b> We found that CSC regulated OCT-4 express","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021","modification":"2026-06-04T03:04:13.946Z","creation":"2025-05-29T21:04:39.014Z"},"accession":"S-EPMC7797662","cross_references":{"pubmed":["33442406"],"doi":["10.7150/jca.50746"]}}