<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>43(11)</volume><submitter>Wang WD</submitter><pubmed_abstract>The forkhead box M1 (FoxM1) protein, a transcription factor, plays critical roles in regulating tumor growth and drug resistance, while cellular FLICE-inhibitory protein (c-FLIP), an anti-apoptotic regulator, is involved in the ubiquitin-proteasome pathway. In this study, we investigated the effects of c-FLIP on the expression and ubiquitination levels of FoxM1 along with drug susceptibility in non-small-cell lung cancer (NSCLC) cells. We first showed that the expression levels of FoxM1 and c-FLIP were increased and positively correlated (R&lt;sup>2&lt;/sup> = 0.1106, P &lt; 0.0001) in 90 NSCLC samples. The survival data from prognostic analysis demonstrated that high expression of c-FLIP and/or FoxM1 was related to poor prognosis in NSCLC patients and that the combination of FoxM1 and c-FLIP could</pubmed_abstract><journal>Acta pharmacologica Sinica</journal><pagination>2956-2966</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9622852</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>c-FLIP promotes drug resistance in non-small-cell lung cancer cells via upregulating FoxM1 expression.</pubmed_title><pmcid>PMC9622852</pmcid><pubmed_authors>Ni J</pubmed_authors><pubmed_authors>Chen SZ</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Wang AM</pubmed_authors><pubmed_authors>Shang Y</pubmed_authors><pubmed_authors>Li GJ</pubmed_authors><pubmed_authors>Su L</pubmed_authors><pubmed_authors>Wang WD</pubmed_authors></additional><is_claimable>false</is_claimable><name>c-FLIP promotes drug resistance in non-small-cell lung cancer cells via upregulating FoxM1 expression.</name><description>The forkhead box M1 (FoxM1) protein, a transcription factor, plays critical roles in regulating tumor growth and drug resistance, while cellular FLICE-inhibitory protein (c-FLIP), an anti-apoptotic regulator, is involved in the ubiquitin-proteasome pathway. In this study, we investigated the effects of c-FLIP on the expression and ubiquitination levels of FoxM1 along with drug susceptibility in non-small-cell lung cancer (NSCLC) cells. We first showed that the expression levels of FoxM1 and c-FLIP were increased and positively correlated (R&lt;sup>2&lt;/sup> = 0.1106, P &lt; 0.0001) in 90 NSCLC samples. The survival data from prognostic analysis demonstrated that high expression of c-FLIP and/or FoxM1 was related to poor prognosis in NSCLC patients and that the combination of FoxM1 and c-FLIP could</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-05-29T21:44:19.8Z</modification><creation>2025-05-29T21:44:19.8Z</creation></dates><accession>S-EPMC9622852</accession><cross_references><pubmed>35422085</pubmed><doi>10.1038/s41401-022-00905-7</doi></cross_references></HashMap>