Medicina · 2026
Omega-3 fatty acids reduce viability and modulate miR-34 in dysplastic oral keratinocytes.
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Don Julieta, Ferrero Victoria, Mazo Tamara, Roldán Franco, Barotto Nelso N, Flores Tania, Torres Vicente A, Pasqualini María Eugenia, Brunotto Mabel
Аннотация
INTRODUCTION: This study aimed to evaluate whether diet-relevant polyunsaturated fatty acids modulate the tumor suppressor miR-34 family during early stages of oral carcinogenesis.
MATERIALS AND METHODS: Oral dysplastic keratinocytes (DOK) were incubated with arachidonic acid (AA, omega- 6), eicosapentaenoic acid (EPA, omega-3), and docosahexaenoic acid (DHA, omega-3) at different concentrations ranging from 10 to 200 uM, or with vehicle control (ethanol). Cell viability was assessed using the resazurin assay, cell migration through the wound healing assay, and membrane lipid composition was analyzed by gas chromatography. Genotyping of TP53 and pri-miR-34b/c was performed by polymerase chain reaction (PCR), and RT-qPCR quantified miR-34 expression levels.
RESULTS: EPA and DHA reduced cell viability at all concentrations tested, while AA enhanced cell migration and increased the omega-6/omega-3 ratio. No significant changes were observed in TP53 and pri-miR-34b/c genotyping. Nevertheless, miR-34a expression was significantly upregulated in cells exposed to omega-3 fatty acids compared with control and omega-6 fatty acids.
CONCLUSION: Omega-3 fatty acids are associated with upregulation of the tumor suppressor miRNA-34 family in dysplastic oral keratinocytes, suggesting a biologically plausible protective molecular mechanism, consistent with epidemiological evidence linking omega-3 intake to a reduced risk of cancer.
MATERIALS AND METHODS: Oral dysplastic keratinocytes (DOK) were incubated with arachidonic acid (AA, omega- 6), eicosapentaenoic acid (EPA, omega-3), and docosahexaenoic acid (DHA, omega-3) at different concentrations ranging from 10 to 200 uM, or with vehicle control (ethanol). Cell viability was assessed using the resazurin assay, cell migration through the wound healing assay, and membrane lipid composition was analyzed by gas chromatography. Genotyping of TP53 and pri-miR-34b/c was performed by polymerase chain reaction (PCR), and RT-qPCR quantified miR-34 expression levels.
RESULTS: EPA and DHA reduced cell viability at all concentrations tested, while AA enhanced cell migration and increased the omega-6/omega-3 ratio. No significant changes were observed in TP53 and pri-miR-34b/c genotyping. Nevertheless, miR-34a expression was significantly upregulated in cells exposed to omega-3 fatty acids compared with control and omega-6 fatty acids.
CONCLUSION: Omega-3 fatty acids are associated with upregulation of the tumor suppressor miRNA-34 family in dysplastic oral keratinocytes, suggesting a biologically plausible protective molecular mechanism, consistent with epidemiological evidence linking omega-3 intake to a reduced risk of cancer.