<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(17)</volume><submitter>Hasanpourghadi M</submitter><pubmed_abstract>Microtubule Targeting Agents (MTAs) induce cell death through mitotic arrest, preferentially affecting rapidly dividing cancer cells over slowly proliferating normal cells. Previously, we showed that Methyl 2-(-5-fluoro-2-hydroxyphenyl)-1H-benzo[d]imidazole-5-carboxylate (MBIC) acts as a potential MTA. In this study, we demonstrated that MBIC exhibits greater toxicity towards non-aggressive breast cancer cell-line, MCF-7 (IC50 = 0.73 ± 0.0 μM) compared to normal fibroblast cell-line, L-cells (IC50 = 59.6 ± 2.5 μM). The IC50 of MBIC against the aggressive breast cancer cell-line, MDA-MB-231 was 20.4 ± 0.2 μM. We hypothesized that the relatively high resistance of MDA-MB-231 cells to MBIC is associated with p53 mutation. We investigated p53 and three of its downstream proteins: survivin, cyc</pubmed_abstract><journal>Oncotarget</journal><pagination>28840-28853</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5438696</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Mechanisms of the anti-tumor activity of Methyl 2-(-5-fluoro-2-hydroxyphenyl)-1 H-benzo[d]imidazole-5-carboxylate against breast cancer in vitro and in vivo.</pubmed_title><pmcid>PMC5438696</pmcid><pubmed_authors>Pandurangan AK</pubmed_authors><pubmed_authors>Karthikeyan C</pubmed_authors><pubmed_authors>Mustafa MR</pubmed_authors><pubmed_authors>Hasanpourghadi M</pubmed_authors><pubmed_authors>Trivedi P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mechanisms of the anti-tumor activity of Methyl 2-(-5-fluoro-2-hydroxyphenyl)-1 H-benzo[d]imidazole-5-carboxylate against breast cancer in vitro and in vivo.</name><description>Microtubule Targeting Agents (MTAs) induce cell death through mitotic arrest, preferentially affecting rapidly dividing cancer cells over slowly proliferating normal cells. Previously, we showed that Methyl 2-(-5-fluoro-2-hydroxyphenyl)-1H-benzo[d]imidazole-5-carboxylate (MBIC) acts as a potential MTA. In this study, we demonstrated that MBIC exhibits greater toxicity towards non-aggressive breast cancer cell-line, MCF-7 (IC50 = 0.73 ± 0.0 μM) compared to normal fibroblast cell-line, L-cells (IC50 = 59.6 ± 2.5 μM). The IC50 of MBIC against the aggressive breast cancer cell-line, MDA-MB-231 was 20.4 ± 0.2 μM. We hypothesized that the relatively high resistance of MDA-MB-231 cells to MBIC is associated with p53 mutation. We investigated p53 and three of its downstream proteins: survivin, cyc</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Apr</publication><modification>2025-04-26T11:08:37.703Z</modification><creation>2019-03-27T02:45:31Z</creation></dates><accession>S-EPMC5438696</accession><cross_references><pubmed>28392503</pubmed><doi>10.18632/oncotarget.16263</doi></cross_references></HashMap>