title: Ganoderma lucidum (Reishi) inhibits cancer cell growth and expression of key molecules in inflammatory breast cancer.
abstract: Inflammatory breast cancer (IBC) is the most lethal and least understood form of advanced breast cancer. Its lethality originates from its nature of invading the lymphatic system and absence of a palpable tumor mass. Different from other metastatic breast cancer cells, IBC cells invade by forming tumor spheroids that retain E-cadherin-based cell-cell adhesions. Herein we describe the potential of the medicinal mushroom Ganoderma lucidum (Reishi) as an attractive candidate for anti-IBC therapy. Reishi contains biological compounds that are cytotoxic against cancer cells. We report the effects of Reishi on viability, apoptosis, invasion, and its mechanism of action in IBC cells (SUM-149). Results show that Reishi selectively inhibits cancer cell viability although it does not affect the viability of noncancerous mammary epithelial cells. Apoptosis induction is consistent with decreased cell viability. Reishi inhibits cell invasion and disrupts the cell spheroids that are characteristic of the IBC invasive pathology. Reishi decreases the expression of genes involved in cancer cell survival and proliferation (BCL-2, TERT, PDGFB), and invasion and metastasis (MMP-9), whereas it increases the expression of IL8. Reishi reduces BCL-2, BCL-XL, E-cadherin, eIF4G, p120-catenin, and c-Myc protein expression and gelatinase activity. These findings suggest that Reishi is an effective anti-IBC therapeutic.
authors: Department of Biochemistry, Universidad Central del Caribe, School of Medicine, Bayamón, Puerto Rico. mmmtz92@gmail.com
authors: Michelle M
authors: MM
authors: Martínez-Montemayor
authors: Raysa Rosario
authors: RR
authors: Acevedo
authors: Elisa
authors: E
authors: Otero-Franqui
authors: Luis A
authors: LA
authors: Cubano
authors: Suranganie F
authors: SF
authors: Dharmawardhane
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D015820:Cadherins / Q000378:metabolism; D051177:Catenins / Q000235:genetics / Q000378:metabolism; D045744:Cell Line, Tumor / Q000187:drug effects; D049109:Cell Proliferation; D002470:Cell Survival / Q000187:drug effects; D039603:Eukaryotic Initiation Factor-4G; D005260:Female; D005455:Fluorescent Antibody Technique; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D058922:Inflammatory Breast Neoplasms / Q000235:genetics* / Q000473:pathology*; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D020940:Reishi / Q000737:chemistry*; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism; D051020:bcl-X Protein / Q000235:genetics / Q000378:metabolism; D000095002:Delta Catenin
chemical_list: D000970:Antineoplastic Agents; C494811:BCL2L1 protein, human; D015820:Cadherins; D051177:Catenins; C113920:EIF4G1 protein, human; D039603:Eukaryotic Initiation Factor-4G; D016271:Proto-Oncogene Proteins c-myc; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; D000095002:Delta Catenin