Lumican inhibits immune escape and carcinogenic pathways in colorectal adenocarcinoma.

Lumican (LUM), a small leucine-rich proteoglycan, is a component of the extracellular matrix. Abnormal LUM expression is potentially associated with cancer progression. In the present study, we confirmed high LUM mRNA expression in colorectal adenocarcinoma (COAD) through the UALCAN database. The Kaplan-Meier method, univariate, and multivariate COX analysis showed that high LUM expression is an independent determinant of poor prognosis in COAD. A COX regression model was constructed based on clinical information and LUM expression. The receiver operating characteristic (ROC) curve indicated that this model was highly accurate in monitoring COAD prognosis. The co-expression network of LUM was determined by LinkedOmics, which showed that LUM expression was closely related to immune escape and the miR200 family. Furthermore, we studied the co-expression network of LUM and found that LUM could promote tumor metastasis and invasion. The Tumor Immune Estimation Resource website showed that LUM was closely related to immune infiltration and correlated with regulatory T cells, tumour-associated macrophages, and dendritic cells. We found that LUM cultivated cancer progression by targeting the miR200 family to promote epithelial-to-mesenchymal transition. These findings suggest that LUM is a potential target for inhibiting immune escape and carcinogenic pathways.

Analysis of proteoglycan expression in human dental pulp.

Proteoglycans are glycosylated proteins which have covalently attached highly anionic glycosaminoglycans. They can be located on the extracellular matrix, cell membrane or intracellular granules. To date, few studies have reported the presence of proteoglycans in human dental pulp. OBJECTIVE: The aim of this study was, therefore, to analyze the expression of lumican, versican and glypican proteoglycans in deciduous and permanent human dental pulp by real-time polymerase chain reaction (q-PCR) and immunofluorescence. DESIGN: Healthy human dental pulps were used: 13 from permanent teeth (group 1) and eight from deciduous teeth (group 2). Versican, lumican and glypican (glypican-1 to 6) gene expressions were quantitatively evaluated by real-time PCR technique, using the expression of the endogenous gene GAPDH as control. Pulp sections were submitted to immunostaining procedure with fluorescence labelling, the tissues being fixed and incubated with well-characterized monoclonal and polyclonal antibodies against proteoglycan epitopes, including anti-versican and anti-lumican. Comparisons among the groups of the quantitative scores for each proteoglycan were analyzed using the t-test and ANOVA (P < 0.05). RESULTS: The real-time PCR analysis showed expression of versican and lumican proteoglycans in the two groups, with significant predominance of lumican gene (P = 0.03). Considering the glypican genes, glypican-3 was the proteoglycan most significantly expressed in permanent pulps (P < 0.001), while glypican-2 was not expressed in this tissue. The immunofluorescence quantification exhibited no significant differences between lumican and versican among the pulps and groups. CONCLUSIONS: The lumican gene was more expressed than versican and glypican-3 was the isoform more expressed in permanent pulp compared to deciduous.

Immunolocalization and distribution of proteoglycans in carious dentine.

BACKGROUND: Collagen type I, proteoglycans (PG) and non-collagenous proteins represent important building blocks of the dentine matrix. While different PGs have been identified in dentine, changes in the distribution of these macromolecules with the progression of caries have been poorly characterized. The aim of this study was to compare the immunolocalization of three small collagen-binding PGs (biglycan, fibromodulin and lumican) as well as collagen (types I and VI) in healthy versus carious dentine. METHODS: Longitudinal demineralized sections of extracted teeth were stained with antibodies recognizing specific PG core proteins and collagens, as well as glycosaminoglycans (GAGs) with toluidine blue. RESULTS: In healthy dentine, PGs appeared to be more abundant near the tubule walls and directly under the cusps. Conversely, in carious dentine, specific locations appeared to be more prone to PG degradation than others. These degradation patterns were well correlated with the progression of caries into the tissue, and also appeared to trigger interesting morphological changes in the tissue structure, such as the deformation of dentine tubules near highly infected areas and the lower concentration of PG in tertiary dentine. CONCLUSIONS: This study presents new insights into the involvement of PGs in the progression of caries.