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EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma (eIF6_KD)

ABSTRACT: EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma (eIF6_KD)

PROVIDER: PRJNA1092618 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28473577_1.fastq.gz	Fastqsanger.gz
	SRR28473577_2.fastq.gz	Fastqsanger.gz
	SRR28473578_1.fastq.gz	Fastqsanger.gz
	SRR28473578_2.fastq.gz	Fastqsanger.gz
	SRR28473579_1.fastq.gz	Fastqsanger.gz

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EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma (eIF6_KD)

Project description:Drug-tolerant persister cells withstand treatments by adapting their identity through lineage-dependent plasticity during systemic anti-cancer therapies. This phenomenon is evident in small-cell lung carcinoma (SCLC), a lethal neuroendocrine cancer initially responsive (60-80%) to platinum-based chemotherapy but succumbing to resistance within 6 months in advanced stages. This resistance associates with the transdifferentiation of residual tumour cells into a non-neuroendocrine state, a process intricately tied to SCLC's chemotolerance, yet molecular mechanisms governing this lineage conversion remain completed understood. Here we use paired cytoplasmic RNA-seq and polysomal RNA-seq to compare gene expression between NE and non-NE SCLC cell lines on both transcriptional and translational level. We report that first-line chemotherapy induces translation initiation factor eIF6 in drug-tolerant persister-like cells in SCLC, correlating with the non-neuroendocrine state in SCLC. Intervening eIF6 inhibits non-neuroendocrine transdifferentiation, thus enhancing SCLC responsiveness to chemotherapy. This study sheds light on eIF6's potential therapeutic interventions to mitigate treatment resistance in SCLC.

2024-04-30 | GSE262596 | GEO

EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma (SCLC cell lines)

2024-04-30 | GSE262593 | GEO

EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma

Project description:EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma

| PRJNA1092614 | ENA

EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma (SCLC cell lines)

Project description:EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma (SCLC cell lines)

| PRJNA1092617 | ENA

EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-30 | GSE262597 | GEO

Gene expression profiling of drug-tolerant persister BT474 breast cancer cells derived from lapatinib treatment

Project description:Acquired drug resistance prevents targeted cancer therapy from achieving stable and complete responses. Emerging evidence implicates a key role for nonmutational mechanisms including changes in cell state during early stages of acquired drug resistance. Targeting nonmutational resistance may therefore present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. A variety of cancer cell lines harbor quiescent, reversibly drug-tolerant âpersisterâ cells which survive cytotoxic drugs including targeted therapies and chemotherapies. These persister cells survive drug through nonmutational mechanisms which are poorly understood. Specifically targeting persister cells is a promising strategy to prevent tumor relapse. We sought to identify therapeutically exploitable vulnerabilities in persister cells using the HER2-amplified breast cancer line BT474 as an experimental model. Similar to other persister cell models, upon treatment with the HER2 inhibitor lapatinib (2uM concentration) for nine or more days, the majority of BT474 cells die, revealing a small population of quiescent surviving persister cells. Removal of lapatinib allows the persister cells to regrow and to re-acquire sensitivity to lapatinib. Subsequent lapatinib treatment re-derives persister cells. The reversibility of persister cell drug resistance indicates a nonmutational resistance mechanism. Here we provide RNAseq gene expression profiling data generated from parental BT474 cells compared to BT474 persister cells generated from nine days of treatment with 2 uM lapatinib. These data can be used to identify genes and pathways which are upregulated in persister cells, revealing potential therapeutic targets. 3 biological replicates of BT474 persister cells, two biological replicates of BT474 parental cells

2016-07-28 | E-GEOD-84896 | biostudies-arrayexpress

Drug tolerant persister cells of EGFR-mutant cell line under kinase-inhibitor combination

Project description:Drug tolerant persister cells of EGFR-mutant PC9 cell lines surviving treatment with kinase inhibitor combination. Cells were treated with combination of erlotinib, osimertinib, trametinib and dasatinib and surviving cells were harvested for RNA extraction. 3' UTR RNA-seq profiles were compared to parental control cells and to outgrowing cells after treatment had been removed

2023-06-30 | E-MTAB-13045 | biostudies-arrayexpress

EIF6 conditions drug-tolerant persister-like transdifferentiation in small cell lung carcinoma

Project description:Quantitative high-coverage tandem-mass-tag (TMT) mass spectrometry in SCLC cells to assess the expression of proteins in monosomes (M, a single ribosome), light polysomes (LP, 2-4 ribosomes), and heavy polysomes (HP, ≥ 5 ribosomes).

2024-03-27 | PXD051035 |

Gene expression profiling of drug-tolerant persister BT474 breast cancer cells derived from lapatinib treatment

Project description:Acquired drug resistance prevents targeted cancer therapy from achieving stable and complete responses. Emerging evidence implicates a key role for nonmutational mechanisms including changes in cell state during early stages of acquired drug resistance. Targeting nonmutational resistance may therefore present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. A variety of cancer cell lines harbor quiescent, reversibly drug-tolerant “persister” cells which survive cytotoxic drugs including targeted therapies and chemotherapies. These persister cells survive drug through nonmutational mechanisms which are poorly understood. Specifically targeting persister cells is a promising strategy to prevent tumor relapse. We sought to identify therapeutically exploitable vulnerabilities in persister cells using the HER2-amplified breast cancer line BT474 as an experimental model. Similar to other persister cell models, upon treatment with the HER2 inhibitor lapatinib (2uM concentration) for nine or more days, the majority of BT474 cells die, revealing a small population of quiescent surviving persister cells. Removal of lapatinib allows the persister cells to regrow and to re-acquire sensitivity to lapatinib. Subsequent lapatinib treatment re-derives persister cells. The reversibility of persister cell drug resistance indicates a nonmutational resistance mechanism. Here we provide RNAseq gene expression profiling data generated from parental BT474 cells compared to BT474 persister cells generated from nine days of treatment with 2 uM lapatinib. These data can be used to identify genes and pathways which are upregulated in persister cells, revealing potential therapeutic targets.

2016-07-28 | GSE84896 | GEO

Fungicide-tolerant persister formation during cryptococcal pulmonary infection

Project description:Bacterial persisters, a subpopulation of genetically susceptible cells that are normally dormant and tolerant to bactericides, have been studied extensively because of their clinical importance. In comparison, much less is known about the determinants underlying fungicide-tolerant fungal persister formation in vivo. Here, we report that during mouse lung infection, Cryptococcus neoformans forms persisters that are highly tolerant to amphotericin B (AmB), the standard of care for treating cryptococcosis. By exploring stationary-phase indicator molecules and developing single-cell tracking strategies, we show that in the lung, AmB persisters are enriched in cryptococcal cells that abundantly produce stationary-phase molecules. The antioxidant ergothioneine plays a specific and key role in AmB persistence, which is conserved in phylogenetically distant fungi. Furthermore, the antidepressant sertraline shows potent activity specifically against cryptococcal AmB persisters. Our results provide evidence for and the determinant of AmB-tolerant persister formation in pulmonary cryptococcosis, which has potential clinical significance.

2024-01-08 | GSE233619 | GEO

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