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RNA-seq analysis of gene regulations by the combination treatment of crizotinib plus cisplatin in established MCA205 tumors

ABSTRACT: RNA-seq analysis of gene regulations by the combination treatment of crizotinib plus cisplatin in established MCA205 tumors

PROVIDER: PRJNA524098 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8618120_1.fastq.gz	Fastqsanger.gz
	SRR8618120_2.fastq.gz	Fastqsanger.gz
	SRR8618113_1.fastq.gz	Fastqsanger.gz
	SRR8618113_2.fastq.gz	Fastqsanger.gz
	SRR8618114_1.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of gene regulations by the combination treatment of crizotinib plus cisplatin in established MCA205 tumors

Project description:Immunogenic cell death (ICD) converts dying cancer cells into a therapeutic vaccine and stimulates antitumor immune responses. Here we unravel the results of an unbiased screen identifying high-dose (10 µM) crizotinib as an ICD-inducing tyrosine kinase inhibitor that has exceptional antineoplastic activity when combined with non-ICD inducing chemotherapeutics like cisplatin. The combination of cisplatin and high-dose crizotinib induces ICD in non-small cell lung carcinoma (NSCLC) cells and effectively controls the growth of distinct (transplantable, carcinogen- or oncogene induced) orthotopic NSCLC models. These anticancer effects are linked to increased T lymphocyte infiltration and are abolished by T cell depletion or interferon-g neutralization. Crizotinib plus cisplatin leads to an increase in the expression of PD-1 and PD-L1 in tumors, coupled to a strong sensitization of NSCLC to immunotherapy with PD-1 antibodies. Hence, a sequential combination treatment consisting in conventional chemotherapy together with crizotinib, followed by immune checkpoint blockade may be active against NSCLC.

2019-02-25 | GSE126988 | GEO

Gene expression profiles of an ALK-fusion driven cell line and its derivatives resistant to crizotinib alone or resistant to crizotinib plus afatinib

Project description:Despite the initial benefit of the tyrosine kinase inhibitors targeting ALK gene fusions in non-small cell lung cancer, resistance to ALK inhibitors is almost inevitable. To determine the acquired resistance mechanism to ALK inhibition, we generated crizotinib-resistant ALK lines by chronically treating H3122 cells (driven by EML4-ALK) with an ALK inhibitor, crizotinib for approximately 3 months. RNA-seq and differential expression analyses were performed to determine the transcriptional changes of H3122-CR cells in comparison to parental H3122 cells. Because we demonstrated EGFR could mediate the early adaptive resistance to crizotinib, we further explored the mechanism that contributes to the resistance to the combination of crizotinib and afatinib. H3122-CAR (crizotinib and afatinib-resistant) cells were generated by treating them with a combination of crizotinib and afatinib for approximately 6 months and then profiled by RNA-seq to determine the associated transcriptional reprogramming.

2023-07-31 | GSE239666 | GEO

Gene expression profiles of an ALK-fusion driven cell line and its derivatives resistant to crizotinib alone or resistant to crizotinib plus afatinib

Project description:Gene expression profiles of an ALK-fusion driven cell line and its derivatives resistant to crizotinib alone or resistant to crizotinib plus afatinib

| PRJNA1000507 | ENA

Crizotinib v. DMSO in SW480 cells

Project description:SW480 cells were treated with 2uM crizotinib for 72h (versus DMSO)

2017-04-25 | GSE93124 | GEO

The effect of crizotinib in A549 lung cancer cell

Project description:TGFb and/or crizotinib were treated on A549 cell line to understand molecular mechanisms of action of crizotinib in TGF signaling pathway in lung cancer through gene expression profile data.

2022-09-27 | GSE189047 | GEO

Fasting potentiates the anticancer activity of Crizotinib

Project description:Background: Tyrosine kinase inhibitors (TKIs) are widely used for treating solid and hematologic malignancies. However, their efficacy is frequently short lived, warranting the search for safe potentiation strategies. Short courses of fasting were shown to sensitize cancer cells to chemo- and radiotherapy while increasing the resistance of healthy tissues to the same agents. The purpose of this study was to assess the potential of fasting to increase the efficacy of TKIs. Methods: starvation-mimicking culture conditions were studied for their ability to potentiate the effects of Epidermal Growth Factor Receptor (EGFR), Human Epidermal Growth Factor Receptor 2 (HER2), Anaplastic Lymphoma Kinase (ALK) and multitarget TKIs in terms of cancer cell growth, signaling cascades inhibition, and changes in gene expression profile in TKI-sensitive cancer cells. In vivo, the activity of crizotinib or regorafenib, weekly cycles of fasting, or their combination was compared in tumor xenografts models. Results: In vitro, starvation-mimicking culture conditions increased the ability of TKIs to block cancer cell growth and to inhibit the mitogen-activated protein kinase (MAPK) signaling pathway. At the gene expression profile level, starvation and crizotinib led to similar changes, but their combination strengthened Rb-, MYC-, and E2F-dependent transcription inhibition. In vivo, both TKIs and cycles of fasting slowed tumor growth, but, when combined, they were significantly more effective than either type of treatment alone. Conclusions: Cycles of fasting or of specifically designed fasting-mimicking diets should be evaluated in clinical studies as a means to potentiate the activity of TKIs in clinical use. RNA was collected from H3122 cells in 4 different conditions: serum, starvation, treated with Crizotinib, starvation and treated with Crizotinib. Each condition was run in quadruplicate

2016-07-03 | E-GEOD-62663 | biostudies-arrayexpress

Transcription profiling of ALK-rearranged cell lines resistent and sensitive to crizotinib

Project description:In this study we have analysed the transcription profile of ALK rearranged cell lines (COST, DEL, JB6, KARPAS, SR786, SUPM2, TS). The analysis was done on untreated cell lines and on the te same cell lines surviving to progressive increasing addition of crizotinib to the culture medium. Crizotinib concentration was progressively increased to reach a final concentration of 1 μM. The resulting pool of resistant cells (designated crizotinib-resistant (CR)) were maintained in RPMI with 10% FBS containing 0.5-1 μM crizotinib.

2022-12-31 | GSE173306 | GEO

Profiling non-small cell lung carcinoma cell line PC9 treated with etoposide, erlotinib and its combination with crizotinib

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. To be able to better understand the differences in response between individual cells, we performed treatment of PC9 cells grown in cell culture with etoposide, erlotinib and its combination with crizotinib, followed by Drop-seq. The addition of crizotinib was guided by our previous data that an erlotinib-resistant drug population may be sensitive to crizotinib. To better understand the common events in drug resistance, we compared the resistant cell populations arising from the treatment with etoposide and from the treatment with erlotinib. The results of our study will address emerging drug resistance that limits clinical usefulness of conventional and targeted strategies, particularly in NSCLC.

2020-12-19 | GSE149215 | GEO

Gene Expression in Cisplatin Resistance HeLa Cells

Project description:Cisplatin resistance is a problem in cancer treatment. Using DNA microarray, we detected differentially expressed genes in cisplatin-resistant cervix carcinoma HeLa cells compared to parental cells. Three cisplatin resistant cell lines were established by stepwise increasing cisplatin concentration. RNA from these resistant lines and its parental HeLa cells were labeled with Cy5 and Cy3. Equal amount of RNA from resistant cell line and HeLa were mixed and were hybridized to cDNA array. Signals were scanned and analyzed to find out the candidate genes involved in cisplatin resistant mechanism.

2010-05-06 | E-GEOD-15120 | biostudies-arrayexpress

Phase II Clinical Trial of Nab-Paclitaxel (NAB)Plus Cisplatin (PLA) Plus Gemcitabine (GEM) (NABPLAGEM) in Patients with Untreated Advanced Pancreatic Cancer.

Project description:Phase II Clinical Trial of Nab-Paclitaxel (NAB)Plus Cisplatin (PLA) Plus Gemcitabine (GEM) (NABPLAGEM) in Patients with Untreated Advanced Pancreatic Cancer.

| PRJNA977689 | ENA

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