{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Machado ART"],"funding":["São Paulo Research Foundation","Coordination for the Improvement of Higher Education Personnel","CNPq","National Council for Scientific and Technological Development"],"pagination":["2582"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9788602"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(12)"],"pubmed_abstract":["Hepatocellular carcinoma is the seventh most common type of cancer in the world, with limited treatment options. A promising strategy to treat cancer is to associate chemotherapeutics and plant bioactive compounds. Here, we examined whether diallyl disulfide (DADS; 50-200 μM) and sorafenib (SORA; 8 μM), either alone or in combination, were toxic to hepatocellular carcinoma cells (HepG2) in vitro. We assessed whether DADS and/or SORA induced cell death (LIVE/DEAD assay and autophagy) and cell cycle changes (flow cytometry), altered expression of key genes and proteins (RT-qPCR and Western blot), and modulated tumorigenesis signatures, such as proliferation (clonogenic assay), migration (wound healing), and invasion (inserts). The DADS + SORA combination elicited autophagic cell death by upregulating LC3 and NRF2 expression and downregulating <i>FOS</i> and <i>TNF</i> expression; induced the accumulation of cells in the G1 phase which thereby upregulated the <i>CHEK2</i> expression; and inhibited invasion by downregulating the <i>MMP2</i> expression. Predictive analysis indicated the participation of the MAPK pathway in the reported results. The DADS + SORA combination suppressed both cell invasion and clonogenic survival, which indicated that it dampened tumor growth, proliferation, invasion, and metastatic potential. Therefore, the DADS + SORA combination is a promising therapy to develop new clinical protocols."],"journal":["Pharmaceutics"],"pubmed_title":["Diallyl Disulfide Induces Chemosensitization to Sorafenib, Autophagy, and Cell Cycle Arrest and Inhibits Invasion in Hepatocellular Carcinoma."],"pmcid":["PMC9788602"],"funding_grant_id":["001","#2017/24576-0","#302479/2019-8","#168759/2018-7","#2019/08348-2"],"pubmed_authors":["Antunes LMG","Tuttis K","Aissa AF","Machado ART","Santos PWDS"],"additional_accession":[]},"is_claimable":false,"name":"Diallyl Disulfide Induces Chemosensitization to Sorafenib, Autophagy, and Cell Cycle Arrest and Inhibits Invasion in Hepatocellular Carcinoma.","description":"Hepatocellular carcinoma is the seventh most common type of cancer in the world, with limited treatment options. A promising strategy to treat cancer is to associate chemotherapeutics and plant bioactive compounds. Here, we examined whether diallyl disulfide (DADS; 50-200 μM) and sorafenib (SORA; 8 μM), either alone or in combination, were toxic to hepatocellular carcinoma cells (HepG2) in vitro. We assessed whether DADS and/or SORA induced cell death (LIVE/DEAD assay and autophagy) and cell cycle changes (flow cytometry), altered expression of key genes and proteins (RT-qPCR and Western blot), and modulated tumorigenesis signatures, such as proliferation (clonogenic assay), migration (wound healing), and invasion (inserts). The DADS + SORA combination elicited autophagic cell death by upregulating LC3 and NRF2 expression and downregulating <i>FOS</i> and <i>TNF</i> expression; induced the accumulation of cells in the G1 phase which thereby upregulated the <i>CHEK2</i> expression; and inhibited invasion by downregulating the <i>MMP2</i> expression. Predictive analysis indicated the participation of the MAPK pathway in the reported results. The DADS + SORA combination suppressed both cell invasion and clonogenic survival, which indicated that it dampened tumor growth, proliferation, invasion, and metastatic potential. Therefore, the DADS + SORA combination is a promising therapy to develop new clinical protocols.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Nov","modification":"2025-04-04T07:59:30.211Z","creation":"2025-04-04T07:59:30.211Z"},"accession":"S-EPMC9788602","cross_references":{"pubmed":["36559076"],"doi":["10.3390/pharmaceutics14122582"]}}