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 small cell lung cancer chemosensitive H69 and corresponding chemoresistant H69AR

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 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE223949 | GEO | 2025/01/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression from H69M versus H69 SCLC cell lines

Project description:H69M cells derive from H69 small cell lung cancer cells subjected to prolonged treatment with HGF. Among the whole population of cells, a subset of more fibroblastic cells was isolated (H69M-mesenchymal). In this experiment we compared expression profiles of both cell lines Keywords: Expression Profiling by array We analyzed 3 arrays from each condition:H69 versus H69M SCLC cell lines

2013-12-31 | E-GEOD-45120 | biostudies-arrayexpress

Small cell lung cancer responds to inhibition of Jumonji enzyme in vitro and in vivo

Project description:Small-cell lung cancer (SCLC) arises from neuroendocrine cells within the lung. Along with deletion or loss of function Rb and TP53 mutations, which occur in almost all cases, subsets of SCLC are driven by specific transcription factors including ASCL1, NEUROD1, POU2F3, or YAP1. Various MYC family members provide further inter-tumor heterogeneity. Despite this heterogeneity in SCLC, current treatment for SCLC is subtype agnostic. Although most patients are initially responsive to first line etoposide and platin chemotherapy they soon develop resistance with no effective second line therapy. A recent large NCI screen showed that over 60 SCLC cell line models responded to 500+ investigational drugs in a manner highly correlated with etoposide responses, suggesting none of these drugs would provide benefit for SCLC therapy beyond current chemotherapy. By analyzing publicly available data of shRNA and CRISPR screens in addition to our own RNA-seq expression data we identified KDM4A as a potential candidate to target in SCLC. To underscore the potential of KDM4A as an anti-SCLC target, we tested chemotherapy drug and three JmjC KDM inhibitors across a panel of SCLC cell lines representing all the SCLC transcription factor subtypes and found that SCLC responses to JmjC KDM inhibitors do not correlate to their responses to chemotherapy. Furthermore, we found upon treatment with pan-JmjC KDM inhibitor, JIB-04, many genes in the ER stress signaling pathways are upregulated in SCLC lines, suggesting this is the mechanistic path leading to SCLC slower growth or death. Additionally, analysis found that JIB-04 resistant cells activate pro-survival pathways such as mTOR to perhaps overcome the effects of JIB-04 treatment. Furthermore, the loss of KDM4A in SCLC cell line led to slower proliferation and activity in the ER stress signaling pathway.

2024-10-10 | GSE208446 | GEO

RNA-seq of human SCLC cell lines NCI-H69 and COR-L303

Project description:Transcriptome wide expression profiling of human SCLC cell lines H69 and COR-L303 under steady state growth conditions using a paired-end RNA-seq protocol.

2019-07-09 | E-MTAB-7410 | biostudies-arrayexpress

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

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

| PRJNA929197 | ENA

Transcription profiling of human H69 xenograft tumors in mice following PDT treatment.

Project description:The response of tumors to PDT treatment is expected to provide information on effects of oxygen depletion, induced apoptosis, induction of an inflammatory response and induction of an ani-tumor immune response. Experiment Overall Design: NCI-H69 human SCLC xenografts were induced in SCID mice. Three pairs of xenograft tumors, PDT treated and untreated controls, were harvested four hours after PDT treatment. RNA was isolated and prepared for hybridization to human Affymetrix GeneChip arrays.

2008-06-16 | E-GEOD-8920 | biostudies-arrayexpress

Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma

Project description:Chemotherapy of retinoblastoma (RB), a malignant ocular childhood disease, is often limited by the development of resistances against commonly used drugs. We identified inositol polyphosphate 4-phosphatase type II (INPP4B) as a differentially regulated gene in etoposide resistant RB cell lines, potentially involved in the development of RB resistances. INPP4B is controversially discussed as a tumor suppressor and an oncogenic driver in various cancers, but its role in retinoblastoma in general and chemoresistant RB in particular is yet unknown. In the study presented, we investigated the expression of INPP4B in RB cell lines and patients and analyzed the effect of INPP4B overexpression on etoposide resistant RB cell growth in vitro and in vivo. INPP4B mRNA levels were significantly downregulated in RB cells lines compared to the healthy human retina, with even lower expression levels in etoposide resistant compared to the sensitive cell lines. Besides, a significant increase in INPP4B expression was observed in chemotherapy treated RB tumor patient samples compared to untreated tumors. INPP4B overexpression in etoposide resistant RB cells resulted in a significant reduction in cell viability with reduced growth, proliferation, anchorage-independent growth, and in ovo tumor formation. Caspase-3/7 mediated apoptosis was concomitantly increased, suggesting a tumor suppressive role of INPP4B in chemoresistant RB cells. No changes in AKT signalling were discernible, but p-SGK3 levels increased following INPP4B overexpression, indicating a potential regulation of SGK3 signalling in etoposide-resistant RB cells. RNAseq analysis of INPP4B overexpressing, etoposide resistant RB cell lines revealed differentially regulated genes involved in cancer progression, mirroring observed in vitro and in vivo effects of INPP4B overexpression and strengthening INPP4B`s importance for cell growth control and tumorigenicity.

2023-03-15 | GSE226408 | GEO

Gene expression from H69M versus H69 SCLC cell lines

2013-12-31 | GSE45120 | GEO

miRNA expression profile of SCLC cell lines vs. normal lung

Project description:Aim: To determine the miRNA expression profile of SCLC cell lines vs. normal lung tissue. Keywords: disease state analysis Total RNA isolated from SCLC cell lines H69, HTB-172, HTB-173 and HTB-184 were compared to a mixed RNA sample derived from 6 normal lung tissue samples (fresh surgical material), from 6 tumor-free patients. The same reference sample (normal lung) was used on all 4 microarrays.

2010-07-24 | E-GEOD-8824 | biostudies-arrayexpress

Inhibition of LSD1 with bomedemstat sensitizes small cell lung cancer to immune checkpoint blockade and T cell killing

Project description:The addition of immune checkpoint blockade (ICB) to platinum/etoposide chemotherapy changed the standard of care for small cell lung cancer (SCLC) treatment. However, ICB addition only modestly improved clinical outcomes, likely reflecting the high prevalence of an immunologically “cold” tumor microenvironment in SCLC, despite high mutational burden. Nevertheless, some patients clearly benefit from ICB and recent reports have associated clinical responses to ICB in SCLC with A) decreased neuroendocrine characteristics and B) activation of NOTCH signaling. We previously showed that inhibition of the LSD1 demethylase activates NOTCH and suppresses neuroendocrine features of SCLC, leading us to investigate whether LSD1 inhibition would enhance the response to PD1 inhibition in SCLC.

2022-08-17 | GSE208614 | GEO

Gene expression after TSA treatment in H69 cells

Project description:Objective of the study is to determine global changes in gene expression after HDAC inhibitor Trichostatin (TSA) treatment in H69 cell line

2021-05-26 | GSE161313 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data