<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>49(6)</volume><submitter>Zalyte E</submitter><pubmed_abstract>Pancreatic cancer is a highly metastatic and therapy‑resistant disease. In the present study, the prospects of a novel approach to kill pancreatic cancer cells were examined: Starvation combined with ferroptosis induction. Established pancreatic cancer cell lines (Miapaca2, Panc‑1, Su.86.86 and T3M4), as well as a unique cell line, Capan‑26, which was originally derived in the authors' laboratory, were used. Cells were deprived from growth factors, amino acids and pseudo‑starved using treatment with mTOR inhibitors; erastin was used to induce ferroptosis. Cell viability and lipid peroxidation measurements using flow cytometry revealed that the starved pancreatic cancer cells reacted differently to ferroptosis induction: The Panc‑1, Su.86.86 and T3M4 cells gained sensitivity, while the Miap</pubmed_abstract><journal>International journal of molecular medicine</journal><pagination>84</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9106375</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Starvation mediates pancreatic cancer cell sensitivity to ferroptosis via ERK1/2, JNK and changes in the cell mesenchymal state.</pubmed_title><pmcid>PMC9106375</pmcid><pubmed_authors>Cicenas J</pubmed_authors><pubmed_authors>Zalyte E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Starvation mediates pancreatic cancer cell sensitivity to ferroptosis via ERK1/2, JNK and changes in the cell mesenchymal state.</name><description>Pancreatic cancer is a highly metastatic and therapy‑resistant disease. In the present study, the prospects of a novel approach to kill pancreatic cancer cells were examined: Starvation combined with ferroptosis induction. Established pancreatic cancer cell lines (Miapaca2, Panc‑1, Su.86.86 and T3M4), as well as a unique cell line, Capan‑26, which was originally derived in the authors' laboratory, were used. Cells were deprived from growth factors, amino acids and pseudo‑starved using treatment with mTOR inhibitors; erastin was used to induce ferroptosis. Cell viability and lipid peroxidation measurements using flow cytometry revealed that the starved pancreatic cancer cells reacted differently to ferroptosis induction: The Panc‑1, Su.86.86 and T3M4 cells gained sensitivity, while the Miap</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2025-04-18T21:52:12.704Z</modification><creation>2025-04-07T09:41:55.602Z</creation></dates><accession>S-EPMC9106375</accession><cross_references><pubmed>35514314</pubmed><doi>10.3892/ijmm.2022.5140</doi></cross_references></HashMap>