<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(1)</volume><submitter>Omar A</submitter><pubmed_abstract>We screened some phytochemicals for cytotoxic activity to human cancer cells and identified Soyasapogenol-A (Snol-A) as a potent candidate anti-cancer compound. Interestingly, Soyasapogenin-I (Snin-I) was ineffective. Viability assays endorsed toxicity of Snol-A to a wide variety of cancer cells. Of note, wild type p53 deficient cancer cells (SKOV-3 and Saos-2) also showed potent growth inhibitory effect. Molecular analyses demonstrated that it targets CARF yielding transcriptional upregulation of p21&lt;sup>WAF1&lt;/sup> (an inhibitor of cyclin-dependent kinases) and downregulation of its effector proteins, CDK2, CDK-4, Cyclin A and Cyclin D1. Targeting of CARF by Snol-A also caused (i) downregulation of pATR-Chk1 signaling leading to caspase-mediated apoptosis and (ii) inactivation of β-cateni</pubmed_abstract><journal>Scientific reports</journal><pagination>6323</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7156697</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Soyasapogenol-A targets CARF and results in suppression of tumor growth and metastasis in p53 compromised cancer cells.</pubmed_title><pmcid>PMC7156697</pmcid><pubmed_authors>Putri J</pubmed_authors><pubmed_authors>Wadhwa R</pubmed_authors><pubmed_authors>Elwakeel A</pubmed_authors><pubmed_authors>Kaul SC</pubmed_authors><pubmed_authors>Omar A</pubmed_authors><pubmed_authors>Kalra RS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Soyasapogenol-A targets CARF and results in suppression of tumor growth and metastasis in p53 compromised cancer cells.</name><description>We screened some phytochemicals for cytotoxic activity to human cancer cells and identified Soyasapogenol-A (Snol-A) as a potent candidate anti-cancer compound. Interestingly, Soyasapogenin-I (Snin-I) was ineffective. Viability assays endorsed toxicity of Snol-A to a wide variety of cancer cells. Of note, wild type p53 deficient cancer cells (SKOV-3 and Saos-2) also showed potent growth inhibitory effect. Molecular analyses demonstrated that it targets CARF yielding transcriptional upregulation of p21&lt;sup>WAF1&lt;/sup> (an inhibitor of cyclin-dependent kinases) and downregulation of its effector proteins, CDK2, CDK-4, Cyclin A and Cyclin D1. Targeting of CARF by Snol-A also caused (i) downregulation of pATR-Chk1 signaling leading to caspase-mediated apoptosis and (ii) inactivation of β-cateni</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Apr</publication><modification>2025-05-29T21:15:26.094Z</modification><creation>2025-05-29T21:15:26.094Z</creation></dates><accession>S-EPMC7156697</accession><cross_references><pubmed>32286347</pubmed><doi>10.1038/s41598-020-62953-5</doi></cross_references></HashMap>