Loss of Caveolin-1 Expression in Tumor Cells is Associated with Increased Aggressiveness and Cell Invasion in Oral Squamous Cell Carcinoma

Nascimento, Rebeca Barros; Paiva, Katiúcia Batista Silva; Risteli, Maija; Silva, Luiz Henrique; ro, Maria Fernanda; Cicco, Rafael De; López, Rossana Mendoza; Salo, Tuula; Nunes, Fábio Caixeta; Xavier, Flávia Caló Aquino

doi:10.2139/ssrn.4246445

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“…The dual role of CAV1 in oral carcinogenesis was first suggested by Hung et al, 30 as they observed increasing CAV1 protein levels in normal mucosa, potentially malignant oral lesions, primary oral cancer, and metastatic oral cancer, indicating a connection with lymph node involvement. Recently, Nascimento et al 9…”

Section: Discussionmentioning

confidence: 99%

“…Recently, the increase in invasive capacity in primary OSCC cells (SCC-25) and decrease in metastatic cells (HSC-3) OSCC within human myoma organotypic model were detected after cholesterol depletion. 9 Both CAV1 and CAV2 exhibit dual roles as tumor promoters or suppressors in different cancers. 10,11 Studies in OSCC and head and neck carcinomas suggest a dual role for CAV1 in tumorigenesis (promotion and suppression).…”

Section: Introductionmentioning

confidence: 99%

“…Cell membranes contain cholesterol‐rich microdomains known as caveolae, linked to carcinogenesis mechanisms such as cell signaling, proliferation, motility, invasiveness, and metastasis. Recently, the increase in invasive capacity in primary OSCC cells (SCC‐25) and decrease in metastatic cells (HSC‐3) OSCC within human myoma organotypic model were detected after cholesterol depletion 9 . Both CAV1 and CAV2 exhibit dual roles as tumor promoters or suppressors in different cancers 10,11 .…”

Section: Introductionmentioning

confidence: 99%

“…Studies in OSCC and head and neck carcinomas suggest a dual role for CAV1 in tumorigenesis (promotion and suppression) 12,13 . Previously, Nascimento et al 14 showed that the switch of CAV1 expression from the carcinoma to the spindle cells of the tumor microenvironment may predict the progression of oral cancer. Some studies link CAV1 expression during EMT to altered cell adhesion molecules, enhancing cellular motility and metastasis 15,16 .…”

Section: Introductionmentioning

confidence: 99%

“…Some studies link CAV1 expression during EMT to altered cell adhesion molecules, enhancing cellular motility and metastasis 15,16 . Furthermore, the silencing of CAV1 increased the viability of the primary OSCC cells and induced the invasion of the metastatic OSCC cells 14 . However, CAVs' specific role in OSCC and the impact of cholesterol depletion on OSCC tumorigenesis, CAV expression, and the EMT process remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

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Cholesterol depletion induces mesenchymal properties in oral squamous cell carcinoma cell line

do Nascimento,

Cerqueira,

Silva

et al. 2024

J Oral Pathology Medicine

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BackgroundCholesterol in cell membranes is crucial for cell signaling, adhesion, and migration. Membranes feature cholesterol‐rich caveolae with caveolin proteins, playing roles in epithelial‐mesenchymal transition and cancer progression. Despite elevated cholesterol levels in tumors, its precise function and the effects of its depletion in oral squamous cell carcinoma remain unclear. The aim of this study was to evaluate the influence of cholesterol depletion in oral squamous cell carcinoma cell line and epithelial‐mesenchymal transition process.MethodsCholesterol depletion was induced on SCC‐9 cells by methyl‐β‐cyclodextrin and cell viability, proliferation, apoptosis, and colony formation capacities were evaluated. Gene and protein expressions were evaluated by reverse transcription polymerase chain reaction (RT‐qPCR) and Western Blot, respectively, and cell sublocalization was assessed by immunofluorescence.ResultsCholesterol depletion resulted in alteration of oral squamous cell carcinoma cell morphology at different concentrations of methyl‐β‐cyclodextrin, as well as decreased cell proliferation and viability rates. Analysis of CAV1 transcript expression revealed increased gene expression in the treated SCC‐9 during the 24 h period, at different concentrations of methyl‐β‐cyclodextrin: 5 , 7.5, 10, and 15 mM, in relation to parental SCC‐9. CAV1 protein expression was increased, with subsequent dose‐dependent decrease. A statistically significant difference was observed in samples treated with 5 mM of methyl‐β‐cyclodextrin (p = 0.02, Kruskal–Wallis test). The immunofluorescence assay showed lower cytoplasmic and membrane labeling intensity in the treated samples for CAV1.ConclusionThese findings indicate the modulation of cholesterol as a possible mechanism underlying the regulation of these molecules and activation of epithelial‐mesenchymal transition in oral squamous cell carcinoma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%