<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang LH</submitter><funding>NIAAA NIH HHS</funding><pagination>36486</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5098232</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>6</volume><pubmed_abstract>SL4, a chalcone-based compound, has been shown to retard tumor invasion and angiogenesis by suppressing HIF1 activity and to induce apoptosis by promoting ROS release. Here, we report that SL4 is able to inhibit the proliferation of different types of breast cancer cell in vitro and in vivo by inducing G&lt;sub>2&lt;/sub>/M cell cycle arrest. Our results showed that SL4 exhibited strong anti-proliferative activity in several human breast cancer cell lines, with IC&lt;sub>50&lt;/sub> values lower than 1.3 μM. Further studies indicated that SL4 induced G&lt;sub>2&lt;/sub>/M arrest in these cell lines. Mechanistically, SL4 reduces the expression of cyclin A2 and cdc25C and decreases the activity of the cdc2/cyclin B1 complex. Notably, SL4 treatment resulted in an obvious increase in p21 mRNA and protein levels</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Anti-tumor activity of SL4 against breast cancer cells: induction of G&lt;sub>2&lt;/sub>/M arrest through modulation of the MAPK-dependent p21 signaling pathway.</pubmed_title><pmcid>PMC5098232</pmcid><funding_grant_id>R21 AA020305</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Yang JY</pubmed_authors><pubmed_authors>Cui LJ</pubmed_authors><pubmed_authors>Zhang JY</pubmed_authors><pubmed_authors>Jiang XR</pubmed_authors><pubmed_authors>Guo W</pubmed_authors><pubmed_authors>Wang LH</pubmed_authors><pubmed_authors>Wu CF</pubmed_authors><pubmed_authors>Chen GL</pubmed_authors><pubmed_authors>Li HH</pubmed_authors><pubmed_authors>Li M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Anti-tumor activity of SL4 against breast cancer cells: induction of G&lt;sub>2&lt;/sub>/M arrest through modulation of the MAPK-dependent p21 signaling pathway.</name><description>SL4, a chalcone-based compound, has been shown to retard tumor invasion and angiogenesis by suppressing HIF1 activity and to induce apoptosis by promoting ROS release. Here, we report that SL4 is able to inhibit the proliferation of different types of breast cancer cell in vitro and in vivo by inducing G&lt;sub>2&lt;/sub>/M cell cycle arrest. Our results showed that SL4 exhibited strong anti-proliferative activity in several human breast cancer cell lines, with IC&lt;sub>50&lt;/sub> values lower than 1.3 μM. Further studies indicated that SL4 induced G&lt;sub>2&lt;/sub>/M arrest in these cell lines. Mechanistically, SL4 reduces the expression of cyclin A2 and cdc25C and decreases the activity of the cdc2/cyclin B1 complex. Notably, SL4 treatment resulted in an obvious increase in p21 mRNA and protein levels</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Nov</publication><modification>2025-06-01T12:19:32.881Z</modification><creation>2019-03-27T02:28:24Z</creation></dates><accession>S-EPMC5098232</accession><cross_references><pubmed>27819344</pubmed><doi>10.1038/srep36486</doi></cross_references></HashMap>