<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13(3)</volume><submitter>Zang Y</submitter><pubmed_abstract>Lumican (&lt;i>LUM&lt;/i>), a small leucine-rich proteoglycan, is a component of the extracellular matrix. Abnormal &lt;i>LUM&lt;/i> expression is potentially associated with cancer progression. In the present study, we confirmed high &lt;i>LUM&lt;/i> mRNA expression in colorectal adenocarcinoma (COAD) through the UALCAN database. The Kaplan-Meier method, univariate, and multivariate COX analysis showed that high &lt;i>LUM&lt;/i> expression is an independent determinant of poor prognosis in COAD. A COX regression model was constructed based on clinical information and &lt;i>LUM&lt;/i> expression. The receiver operating characteristic (ROC) curve indicated that this model was highly accurate in monitoring COAD prognosis. The co-expression network of &lt;i>LUM&lt;/i> was determined by LinkedOmics, which showed that &lt;i>LUM&lt;/i> expression was closely related to immune escape and the miR200 family. Furthermore, we studied the co-expression network of &lt;i>LUM&lt;/i> and found that &lt;i>LUM&lt;/i> could promote tumor metastasis and invasion. The Tumor Immune Estimation Resource website showed that &lt;i>LUM&lt;/i> was closely related to immune infiltration and correlated with regulatory T cells, tumour-associated macrophages, and dendritic cells. We found that &lt;i>LUM&lt;/i> cultivated cancer progression by targeting the miR200 family to promote epithelial-to-mesenchymal transition. These findings suggest that &lt;i>LUM&lt;/i> is a potential target for inhibiting immune escape and carcinogenic pathways.</pubmed_abstract><journal>Aging</journal><pagination>4388-4408</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7906189</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Lumican inhibits immune escape and carcinogenic pathways in colorectal adenocarcinoma.</pubmed_title><pmcid>PMC7906189</pmcid><pubmed_authors>Wang R</pubmed_authors><pubmed_authors>Lu Y</pubmed_authors><pubmed_authors>Dong K</pubmed_authors><pubmed_authors>Zang Y</pubmed_authors><pubmed_authors>Liang Z</pubmed_authors><pubmed_authors>Dong Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>Lumican inhibits immune escape and carcinogenic pathways in colorectal adenocarcinoma.</name><description>Lumican (&lt;i>LUM&lt;/i>), a small leucine-rich proteoglycan, is a component of the extracellular matrix. Abnormal &lt;i>LUM&lt;/i> expression is potentially associated with cancer progression. In the present study, we confirmed high &lt;i>LUM&lt;/i> mRNA expression in colorectal adenocarcinoma (COAD) through the UALCAN database. The Kaplan-Meier method, univariate, and multivariate COX analysis showed that high &lt;i>LUM&lt;/i> expression is an independent determinant of poor prognosis in COAD. A COX regression model was constructed based on clinical information and &lt;i>LUM&lt;/i> expression. The receiver operating characteristic (ROC) curve indicated that this model was highly accurate in monitoring COAD prognosis. The co-expression network of &lt;i>LUM&lt;/i> was determined by LinkedOmics, which showed that &lt;i>LUM&lt;/i> expression was closely related to immune escape and the miR200 family. Furthermore, we studied the co-expression network of &lt;i>LUM&lt;/i> and found that &lt;i>LUM&lt;/i> could promote tumor metastasis and invasion. The Tumor Immune Estimation Resource website showed that &lt;i>LUM&lt;/i> was closely related to immune infiltration and correlated with regulatory T cells, tumour-associated macrophages, and dendritic cells. We found that &lt;i>LUM&lt;/i> cultivated cancer progression by targeting the miR200 family to promote epithelial-to-mesenchymal transition. These findings suggest that &lt;i>LUM&lt;/i> is a potential target for inhibiting immune escape and carcinogenic pathways.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jan</publication><modification>2024-11-20T09:45:03.306Z</modification><creation>2021-03-07T08:15:20Z</creation></dates><accession>S-EPMC7906189</accession><cross_references><pubmed>33493133</pubmed><doi>10.18632/aging.202401</doi></cross_references></HashMap>