Low vitamin D and high cholesterol facilitate oral carcinogenesis in 4NQO‐induced rat models via regulating glycolysis

Objectives Diets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal origin facilitates carcinogenesis. In this study, we aimed at investigating the possible involvement of vitamin D deficiency (VDD)...

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Published inOral diseases Vol. 29; no. 3; pp. 978 - 989
Main Authors Gumus, Rasim, Capik, Ozel, Gundogdu, Betul, Tatar, Arzu, Altinkaynak, Konca, Ozdemir Tozlu, Ozlem, Karatas, Omer Faruk
Format Journal Article
LanguageEnglish
Published Denmark Wiley Subscription Services, Inc 01.04.2023
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ISSN1354-523X
1601-0825
1601-0825
DOI10.1111/odi.14117

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Abstract Objectives Diets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal origin facilitates carcinogenesis. In this study, we aimed at investigating the possible involvement of vitamin D deficiency (VDD) and high cholesterol (HC) together in oral squamous cell carcinoma (OSCC) through modulating glycolysis. Subjects and Methods We compared total cholesterol, LDL, HDL, triglycerides, LDH, and vitamin D levels of OSCC patients and control individuals. We used GEO datasets for gene set enrichment and 4‐nitroquinoline‐1‐oxide induced in vivo oral carcinogenesis models to investigate contribution of VDD and HC during carcinogenesis via possible modulation of glycolysis. Results We found that VDD and HC co‐exist in OSCC patients, and deregulation of cholesterol and vitamin D levels results in enrichment of genes related to glycolysis. We, then, demonstrated that VDD and HC on their own and together facilitated the formation of larger tumors in 4NQO‐induced in vivo cancer models, which are suppressed by glycolysis inhibition. Conclusion We reported collaborative contribution of HC and VDD during oral carcinogenesis, which is mainly carried out via altering energy metabolism in tumor cells.
AbstractList Diets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal origin facilitates carcinogenesis. In this study, we aimed at investigating the possible involvement of vitamin D deficiency (VDD) and high cholesterol (HC) together in oral squamous cell carcinoma (OSCC) through modulating glycolysis.OBJECTIVESDiets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal origin facilitates carcinogenesis. In this study, we aimed at investigating the possible involvement of vitamin D deficiency (VDD) and high cholesterol (HC) together in oral squamous cell carcinoma (OSCC) through modulating glycolysis.We compared total cholesterol, LDL, HDL, triglycerides, LDH, and vitamin D levels of OSCC patients and control individuals. We used GEO datasets for gene set enrichment and 4-nitroquinoline-1-oxide induced in vivo oral carcinogenesis models to investigate contribution of VDD and HC during carcinogenesis via possible modulation of glycolysis.SUBJECTS AND METHODSWe compared total cholesterol, LDL, HDL, triglycerides, LDH, and vitamin D levels of OSCC patients and control individuals. We used GEO datasets for gene set enrichment and 4-nitroquinoline-1-oxide induced in vivo oral carcinogenesis models to investigate contribution of VDD and HC during carcinogenesis via possible modulation of glycolysis.We found that VDD and HC co-exist in OSCC patients, and deregulation of cholesterol and vitamin D levels results in enrichment of genes related to glycolysis. We, then, demonstrated that VDD and HC on their own and together facilitated the formation of larger tumors in 4NQO-induced in vivo cancer models, which are suppressed by glycolysis inhibition.RESULTSWe found that VDD and HC co-exist in OSCC patients, and deregulation of cholesterol and vitamin D levels results in enrichment of genes related to glycolysis. We, then, demonstrated that VDD and HC on their own and together facilitated the formation of larger tumors in 4NQO-induced in vivo cancer models, which are suppressed by glycolysis inhibition.We reported collaborative contribution of HC and VDD during oral carcinogenesis, which is mainly carried out via altering energy metabolism in tumor cells.CONCLUSIONWe reported collaborative contribution of HC and VDD during oral carcinogenesis, which is mainly carried out via altering energy metabolism in tumor cells.
Objectives Diets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal origin facilitates carcinogenesis. In this study, we aimed at investigating the possible involvement of vitamin D deficiency (VDD) and high cholesterol (HC) together in oral squamous cell carcinoma (OSCC) through modulating glycolysis. Subjects and Methods We compared total cholesterol, LDL, HDL, triglycerides, LDH, and vitamin D levels of OSCC patients and control individuals. We used GEO datasets for gene set enrichment and 4‐nitroquinoline‐1‐oxide induced in vivo oral carcinogenesis models to investigate contribution of VDD and HC during carcinogenesis via possible modulation of glycolysis. Results We found that VDD and HC co‐exist in OSCC patients, and deregulation of cholesterol and vitamin D levels results in enrichment of genes related to glycolysis. We, then, demonstrated that VDD and HC on their own and together facilitated the formation of larger tumors in 4NQO‐induced in vivo cancer models, which are suppressed by glycolysis inhibition. Conclusion We reported collaborative contribution of HC and VDD during oral carcinogenesis, which is mainly carried out via altering energy metabolism in tumor cells.
Diets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal origin facilitates carcinogenesis. In this study, we aimed at investigating the possible involvement of vitamin D deficiency (VDD) and high cholesterol (HC) together in oral squamous cell carcinoma (OSCC) through modulating glycolysis. We compared total cholesterol, LDL, HDL, triglycerides, LDH, and vitamin D levels of OSCC patients and control individuals. We used GEO datasets for gene set enrichment and 4-nitroquinoline-1-oxide induced in vivo oral carcinogenesis models to investigate contribution of VDD and HC during carcinogenesis via possible modulation of glycolysis. We found that VDD and HC co-exist in OSCC patients, and deregulation of cholesterol and vitamin D levels results in enrichment of genes related to glycolysis. We, then, demonstrated that VDD and HC on their own and together facilitated the formation of larger tumors in 4NQO-induced in vivo cancer models, which are suppressed by glycolysis inhibition. We reported collaborative contribution of HC and VDD during oral carcinogenesis, which is mainly carried out via altering energy metabolism in tumor cells.
ObjectivesDiets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal origin facilitates carcinogenesis. In this study, we aimed at investigating the possible involvement of vitamin D deficiency (VDD) and high cholesterol (HC) together in oral squamous cell carcinoma (OSCC) through modulating glycolysis.Subjects and MethodsWe compared total cholesterol, LDL, HDL, triglycerides, LDH, and vitamin D levels of OSCC patients and control individuals. We used GEO datasets for gene set enrichment and 4‐nitroquinoline‐1‐oxide induced in vivo oral carcinogenesis models to investigate contribution of VDD and HC during carcinogenesis via possible modulation of glycolysis.ResultsWe found that VDD and HC co‐exist in OSCC patients, and deregulation of cholesterol and vitamin D levels results in enrichment of genes related to glycolysis. We, then, demonstrated that VDD and HC on their own and together facilitated the formation of larger tumors in 4NQO‐induced in vivo cancer models, which are suppressed by glycolysis inhibition.ConclusionWe reported collaborative contribution of HC and VDD during oral carcinogenesis, which is mainly carried out via altering energy metabolism in tumor cells.
Author Altinkaynak, Konca
Karatas, Omer Faruk
Gundogdu, Betul
Tatar, Arzu
Capik, Ozel
Gumus, Rasim
Ozdemir Tozlu, Ozlem
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Keywords 4NQO
cholesterol
oral squamous cell carcinoma
LDL
vitamin D deficiency
glycolysis
Language English
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Notes Funding information
This work was supported by the Scientific and Technological Research Council of Turkey, Grant/Award Number: 119Z195
Rasim Gumus and Ozel Capik authors contributed equally to this work.
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Snippet Objectives Diets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods...
Diets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal...
ObjectivesDiets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods...
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SubjectTerms 4NQO
Animal models
Animals
Carcinogenesis
Carcinogenesis - metabolism
Carcinoma, Squamous Cell - chemically induced
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - metabolism
Cholesterol
Diet
Energy metabolism
Glycolysis
Head and Neck Neoplasms
High density lipoprotein
Hyperlipidemia
LDL
Low density lipoprotein
Mouth Neoplasms - genetics
Nutrient deficiency
Nutrition
Oral cancer
Oral carcinoma
Oral squamous cell carcinoma
Rats
Squamous cell carcinoma
Squamous Cell Carcinoma of Head and Neck
Triglycerides
Tumor cells
Vitamin D
vitamin D deficiency
Vitamin D Deficiency - complications
Vitamin deficiency
Title Low vitamin D and high cholesterol facilitate oral carcinogenesis in 4NQO‐induced rat models via regulating glycolysis
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fodi.14117
https://www.ncbi.nlm.nih.gov/pubmed/34954855
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https://www.proquest.com/docview/2614757238
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