Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

High-throughput sequencing of chemosensitive small cell lung cancer cell lines H82 and DMS114, and their corresponding chemoresistant counterparts

ABSTRACT: Small cell lung cancer (SCLC) is the most aggressive subtype of lung cancer. Although most patients are initially sensitive to first-line chemotherapy with combined cisplatin and etoposide, chemotherapy drug resistance easily develops and quickly leads to tumor progression. Therefore, understanding the mechanisms of chemotherapy drug resistance and how to reverse it is key to improving the prognosis of patients with SCLC. The parental SCLC cell lines H82 and DMS114, along with their corresponding cisplatin-induced resistant counterparts (H82DDP and DMS114DDP), were used to explore the mechanisms of chemoresistance in SCLC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE313099 | GEO | 2026/06/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

High throughput sequencing of small cell lung cancer chemosensitive H69 and corresponding chemoresistant H69AR

Project description:Small cell lung cancer (SCLC) is the most aggressive subtype of lung cancer. Although most patients are initially sensitive to first-line chemotherapy with combined cisplatin and etoposide, chemotherapy drugs resistance easily develops and quickly leads to tumor progression. Therefore, understanding mechanisms of chemotherapy drugs resistance and how to reverse it is key to improving the prognosis of patients with SCLC. The parental SCLC cell lines H69 and corresponding doxorubicin-induced multidrug resistant variant (H69AR) were used to explore the mechanism of chemoresistance in SCLC.

2025-01-28 | GSE223949 | GEO

High-throughput sequencing of chemosensitive small cell lung cancer cell lines H82 and DMS114, and their corresponding chemoresistant counterparts

Project description:High-throughput sequencing of chemosensitive small cell lung cancer cell lines H82 and DMS114, and their corresponding chemoresistant counterparts

| PRJNA1378256 | ENA

ATAC-seq of lung cancer cell lines with doxycycline KRAS G12V and drug treatments

Project description:We modelled the effects of KRAS activation on three SCLC cell lines H2107, H82, H524 and investigated the effects of KRAS induction and various drug treatments on motif and chromatin accessibility profiles.

2021-08-17 | GSE160204 | GEO

Expression data from chemoresistant human non-small cell lung cancer

Project description:Chemoresistance induced by cisplatin application hinders the clinical outcomes of chemotherapy and needs resolving, hence we sought to find its modulating role in tumorogenesis or drug resistance between human lung adenocarcinoma cancer cell line A549 and its chemoresistant cell line A549/DDP.

2020-11-18 | GSE154243 | GEO

Laccaria bicolor S238N-H82

Project description:Laccaria bicolor S238N-H82 genome sequencing

| PRJNA547225 | ENA

Tumor heterogeneity underlies differential cisplatin sensitivity in mouse models of small cell lung cancer

Project description:SCLC is the most aggressive subtype of lung cancer characterized by a remarkable response to chemotherapy followed by development of resistance. Mechanisms of initial sensitivity and of subsequent resistance are not understood. Here we highlight a broad tumor heterogeneity in mouse models of SCLC, which includes a CDH1 high primary cisplatin-resistant peripheral neuroendocrine lesion with unique metabolic and structural profile. Cisplatin treatment preferentially eliminates CDH1 negative secondary tumor leaving behind CDH1 high primary lesions, thus revealing a striking differential response. We profile global protein and messenger RNA levels in vehicle and cisplatin treated lung tumor populations and find a marked reduction in proliferation and a pronounced metabolic shift following cisplatin-treatment. Our proteo-transcriptomic analysis gives insight into gene expression alterations that characterize cisplatin resistance and uncovers potential novel targets to overcome resistance of distinct populations. SCLC tumors in the mouse show heterogeneity which appears, as might be the case in humans, to be one of the underlying mechanisms of differential sensitivity to cisplatin.

2019-11-12 | PXD010680 | Pride

Differential Gene Expression between Chemoresistant and Chemosensitive T24 Human Bladder Cancer Cells

Project description:This project employed proteomics to analyze protein expression profiles between chemoresistant and chemosensitive variants of the human bladder cancer T24 cell line. The objective was to identify key differentially expressed proteins and their associated signaling pathways involved in chemotherapy resistance. The findings aim to provide new insights and potential therapeutic targets for overcoming chemoresistance in bladder cancer.

2026-02-09 | PXD069140 | Pride

Gene expression in H82R cells

Project description:H82R cells was derived from H82 P4 tumors and was resistant to etoposide plus cisplatin

2021-12-01 | GSE160240 | GEO

An in vivo screening platform using PDX models reveals KEAP1, USP22 and other drivers of chemoresistance in small cell lung cancer

Project description:Small cell lung cancer (SCLC) is characterized by exquisite chemosensitivity followed by rapid emergence of chemoresistance. To identify genetic events that drive resistance to cisplatin-etoposide chemotherapy, we conducted cDNA overexpression and CRISPR knockout screens in an in vivo platform centered on chemosensitive patient derived xenograft (PDX) models of SCLC. cDNA overexpression screens revealed MYC, MYCN and MYCL as drivers of tumor cell growth through chemotherapy. CRISPR knockout screens identified the KEAP1/NRF2 pathway and members of the SAGA (Spt-Ada-Gcn5 acetyltransferase) complex, including the deubiquitylase USP22. We demonstrated that knockout of either KEAP1 or USP22 switches chemosensitive PDX models to become chemoresistant, with our data supporting distinct molecular consequences, including suppression of DNA damage signaling upon USP22 deletion. Data from the IMpower133 clinical trial revealed that a substantial proportion of SCLC patients exhibit KEAP1/NFE2L2 genetic alterations, with activation of an NRF2 transcriptional signature associated with reduced SCLC patient survival with chemotherapy.

2026-04-20 | PXD048813 | Pride

Laccaria bicolor S238N-H82

Project description:Laccaria bicolor S238N-H82 WGS sequencing, assembly, and annotation

| PRJNA19043 | ENA