<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>17(3)</volume><submitter>Shahid A</submitter><funding>western university of health sciences intramural student funds as part of the graduate program.</funding><funding>beijing tong ren tang chinese medicine co., ltd</funding><pubmed_abstract>The medicinal mushroom Ganoderma lucidum is traditionally used for treating multiple diseases, including cancer. This study examined skin cancer preventive activity of a commercial product containing spore and fruiting body in 30:8 ratio (GLSF). Extracts of GLSF and spore component (GLS) were prepared using artificial gastrointestinal juice and examined on JB6 cells. GLSF and GLS dose-dependently inhibited epidermal growth factor-induced JB6 transformation at non-toxic concentrations. SKH-1 mice which were fed with diets containing GLSF (1.25%), GLS (0.99%) or the fruiting body (GLF) (0.26%) were exposed to chronic low-dose ultraviolet (UV) radiation to assess their effects on skin carcinogenesis. GLSF, but not GLS or GLF, reduced skin tumor incidence and multiplicity. In non-tumor skin tissues of mice, GLSF attenuated UV-induced epidermal thickening, expression of Ki-67, COX-2 and NF-κB, while in tumor tissues, GLSF increased expression of CD8 and Granzyme B. To examine the effects of GLSF on UV-induced immunosuppression, mice which were fed with GLSF were evaluated for the contact hypersensitivity (CHS) response to dinitrofluorobenzene (DNFB). GLSF significantly reversed UV-mediated suppression of DNFB-induced CHS by increasing CD8+ and decreasing CD4+ and FoxP3+ T-cells in mouse ears. Therefore, GLSF prevents skin cancer probably via attenuating UV-induced immunosuppression.</pubmed_abstract><journal>PloS one</journal><pagination>e0265615</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8936451</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The medicinal mushroom Ganoderma lucidum attenuates UV-induced skin carcinogenesis and immunosuppression.</pubmed_title><pmcid>PMC8936451</pmcid><pubmed_authors>Shahid A</pubmed_authors><pubmed_authors>Huang Y</pubmed_authors><pubmed_authors>Liu M</pubmed_authors><pubmed_authors>Parsa C</pubmed_authors><pubmed_authors>Huang M</pubmed_authors><pubmed_authors>Orlando R</pubmed_authors><pubmed_authors>Shamim MA</pubmed_authors></additional><is_claimable>false</is_claimable><name>The medicinal mushroom Ganoderma lucidum attenuates UV-induced skin carcinogenesis and immunosuppression.</name><description>The medicinal mushroom Ganoderma lucidum is traditionally used for treating multiple diseases, including cancer. This study examined skin cancer preventive activity of a commercial product containing spore and fruiting body in 30:8 ratio (GLSF). Extracts of GLSF and spore component (GLS) were prepared using artificial gastrointestinal juice and examined on JB6 cells. GLSF and GLS dose-dependently inhibited epidermal growth factor-induced JB6 transformation at non-toxic concentrations. SKH-1 mice which were fed with diets containing GLSF (1.25%), GLS (0.99%) or the fruiting body (GLF) (0.26%) were exposed to chronic low-dose ultraviolet (UV) radiation to assess their effects on skin carcinogenesis. GLSF, but not GLS or GLF, reduced skin tumor incidence and multiplicity. In non-tumor skin tissues of mice, GLSF attenuated UV-induced epidermal thickening, expression of Ki-67, COX-2 and NF-κB, while in tumor tissues, GLSF increased expression of CD8 and Granzyme B. To examine the effects of GLSF on UV-induced immunosuppression, mice which were fed with GLSF were evaluated for the contact hypersensitivity (CHS) response to dinitrofluorobenzene (DNFB). GLSF significantly reversed UV-mediated suppression of DNFB-induced CHS by increasing CD8+ and decreasing CD4+ and FoxP3+ T-cells in mouse ears. Therefore, GLSF prevents skin cancer probably via attenuating UV-induced immunosuppression.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-04T14:50:28.645Z</modification><creation>2025-04-04T14:50:28.645Z</creation></dates><accession>S-EPMC8936451</accession><cross_references><pubmed>35312729</pubmed><doi>10.1371/journal.pone.0265615</doi></cross_references></HashMap>