Integrative single-cell RNA-seq and spatial transcriptomics analyses reveal diverse apoptosis-related gene expression profiles in EGFR-mutated lung cancer

In EGFR -mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance. Despite the crucial role played by apoptosis-related genes in tumor cell survival, how their expression changes as resistance to EGFR-TKIs emerges re...

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Published in:Cell death & disease Vol. 15; no. 8; pp. 580 - 11
Main Authors: Izumi, Motohiro, Fujii, Masanori, Kobayashi, Ikei S., Ho, Vivian, Kashima, Yukie, Udagawa, Hibiki, Costa, Daniel B., Kobayashi, Susumu S.
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 09.08.2024
Springer Nature B.V
Nature Publishing Group
Subjects:
13/1
13/109
38/39
38/91
631/337/2019
631/67/1612/1350
Animals
Antibodies
Apoptosis
Apoptosis - drug effects
Apoptosis - genetics
Bcl-2 protein
Bcl-x protein
bcl-X Protein - genetics
bcl-X Protein - metabolism
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Cell Line, Tumor
Cell survival
Drug resistance
Drug Resistance, Neoplasm - genetics
Epidermal growth factor receptors
ErbB Receptors - genetics
ErbB Receptors - metabolism
Gene expression
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
Genetic analysis
Humans
Immunology
Kinases
Life Sciences
Lung cancer
Lung Neoplasms - drug therapy
Lung Neoplasms - genetics
Lung Neoplasms - metabolism
Lung Neoplasms - pathology
Mcl-1 protein
Mice
Mice, Transgenic
Mutation - genetics
Nucleotide sequence
Protein Kinase Inhibitors - pharmacology
RNA-Seq
Single-Cell Analysis
Single-Cell Gene Expression Analysis
Spatial heterogeneity
Transcriptome - genetics
Transcriptomics
Transgenic mice
Tumor cell lines
Tumor cells
Tumors
Tyrosine kinase inhibitors
ISSN:2041-4889, 2041-4889
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Abstract In EGFR -mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance. Despite the crucial role played by apoptosis-related genes in tumor cell survival, how their expression changes as resistance to EGFR-TKIs emerges remains unclear. Here, we conduct a comprehensive analysis of apoptosis-related genes, including BCL-2 and IAP family members, using single-cell RNA sequence ( scRNA-seq) and spatial transcriptomics (ST). scRNA-seq of EGFR -mutated lung cancer cell lines captures changes in apoptosis-related gene expression following EGFR-TKI treatment, most notably BCL2L1 upregulation. scRNA-seq of EGFR -mutated lung cancer patient samples also reveals high BCL2L1 expression, specifically in tumor cells, while MCL1 expression is lower in tumors compared to non-tumor cells. ST analysis of specimens from transgenic mice with EGFR-driven lung cancer indicates spatial heterogeneity of tumors and corroborates scRNA-seq findings. Genetic ablation and pharmacological inhibition of BCL2L1 /BCL-XL overcome or delay EGFR-TKI resistance. Overall, our findings indicate that BCL2L1 /BCL-XL expression is important for tumor cell survival as EGFR-TKI resistance emerges.
AbstractList In EGFR -mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance. Despite the crucial role played by apoptosis-related genes in tumor cell survival, how their expression changes as resistance to EGFR-TKIs emerges remains unclear. Here, we conduct a comprehensive analysis of apoptosis-related genes, including BCL-2 and IAP family members, using single-cell RNA sequence ( scRNA-seq) and spatial transcriptomics (ST). scRNA-seq of EGFR -mutated lung cancer cell lines captures changes in apoptosis-related gene expression following EGFR-TKI treatment, most notably BCL2L1 upregulation. scRNA-seq of EGFR -mutated lung cancer patient samples also reveals high BCL2L1 expression, specifically in tumor cells, while MCL1 expression is lower in tumors compared to non-tumor cells. ST analysis of specimens from transgenic mice with EGFR-driven lung cancer indicates spatial heterogeneity of tumors and corroborates scRNA-seq findings. Genetic ablation and pharmacological inhibition of BCL2L1 /BCL-XL overcome or delay EGFR-TKI resistance. Overall, our findings indicate that BCL2L1 /BCL-XL expression is important for tumor cell survival as EGFR-TKI resistance emerges.
In EGFR-mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance. Despite the crucial role played by apoptosis-related genes in tumor cell survival, how their expression changes as resistance to EGFR-TKIs emerges remains unclear. Here, we conduct a comprehensive analysis of apoptosis-related genes, including BCL-2 and IAP family members, using single-cell RNA sequence (scRNA-seq) and spatial transcriptomics (ST). scRNA-seq of EGFR-mutated lung cancer cell lines captures changes in apoptosis-related gene expression following EGFR-TKI treatment, most notably BCL2L1 upregulation. scRNA-seq of EGFR-mutated lung cancer patient samples also reveals high BCL2L1 expression, specifically in tumor cells, while MCL1 expression is lower in tumors compared to non-tumor cells. ST analysis of specimens from transgenic mice with EGFR-driven lung cancer indicates spatial heterogeneity of tumors and corroborates scRNA-seq findings. Genetic ablation and pharmacological inhibition of BCL2L1/BCL-XL overcome or delay EGFR-TKI resistance. Overall, our findings indicate that BCL2L1/BCL-XL expression is important for tumor cell survival as EGFR-TKI resistance emerges.
In EGFR-mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance. Despite the crucial role played by apoptosis-related genes in tumor cell survival, how their expression changes as resistance to EGFR-TKIs emerges remains unclear. Here, we conduct a comprehensive analysis of apoptosis-related genes, including BCL-2 and IAP family members, using single-cell RNA sequence (scRNA-seq) and spatial transcriptomics (ST). scRNA-seq of EGFR-mutated lung cancer cell lines captures changes in apoptosis-related gene expression following EGFR-TKI treatment, most notably BCL2L1 upregulation. scRNA-seq of EGFR-mutated lung cancer patient samples also reveals high BCL2L1 expression, specifically in tumor cells, while MCL1 expression is lower in tumors compared to non-tumor cells. ST analysis of specimens from transgenic mice with EGFR-driven lung cancer indicates spatial heterogeneity of tumors and corroborates scRNA-seq findings. Genetic ablation and pharmacological inhibition of BCL2L1/BCL-XL overcome or delay EGFR-TKI resistance. Overall, our findings indicate that BCL2L1/BCL-XL expression is important for tumor cell survival as EGFR-TKI resistance emerges.In EGFR-mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance. Despite the crucial role played by apoptosis-related genes in tumor cell survival, how their expression changes as resistance to EGFR-TKIs emerges remains unclear. Here, we conduct a comprehensive analysis of apoptosis-related genes, including BCL-2 and IAP family members, using single-cell RNA sequence (scRNA-seq) and spatial transcriptomics (ST). scRNA-seq of EGFR-mutated lung cancer cell lines captures changes in apoptosis-related gene expression following EGFR-TKI treatment, most notably BCL2L1 upregulation. scRNA-seq of EGFR-mutated lung cancer patient samples also reveals high BCL2L1 expression, specifically in tumor cells, while MCL1 expression is lower in tumors compared to non-tumor cells. ST analysis of specimens from transgenic mice with EGFR-driven lung cancer indicates spatial heterogeneity of tumors and corroborates scRNA-seq findings. Genetic ablation and pharmacological inhibition of BCL2L1/BCL-XL overcome or delay EGFR-TKI resistance. Overall, our findings indicate that BCL2L1/BCL-XL expression is important for tumor cell survival as EGFR-TKI resistance emerges.
Abstract In EGFR-mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance. Despite the crucial role played by apoptosis-related genes in tumor cell survival, how their expression changes as resistance to EGFR-TKIs emerges remains unclear. Here, we conduct a comprehensive analysis of apoptosis-related genes, including BCL-2 and IAP family members, using single-cell RNA sequence (scRNA-seq) and spatial transcriptomics (ST). scRNA-seq of EGFR-mutated lung cancer cell lines captures changes in apoptosis-related gene expression following EGFR-TKI treatment, most notably BCL2L1 upregulation. scRNA-seq of EGFR-mutated lung cancer patient samples also reveals high BCL2L1 expression, specifically in tumor cells, while MCL1 expression is lower in tumors compared to non-tumor cells. ST analysis of specimens from transgenic mice with EGFR-driven lung cancer indicates spatial heterogeneity of tumors and corroborates scRNA-seq findings. Genetic ablation and pharmacological inhibition of BCL2L1/BCL-XL overcome or delay EGFR-TKI resistance. Overall, our findings indicate that BCL2L1/BCL-XL expression is important for tumor cell survival as EGFR-TKI resistance emerges.
ArticleNumber 580
Author Ho, Vivian
Kashima, Yukie
Costa, Daniel B.
Udagawa, Hibiki
Fujii, Masanori
Kobayashi, Ikei S.
Izumi, Motohiro
Kobayashi, Susumu S.
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  email: skobbidmc@gmail.com
  organization: Department of Medicine, Division of Medical Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Division of Translational Genomics, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Department of Respiratory Medicine, Juntendo University Faculty of Medicine and Graduate School of Medicine
BackLink https://www.ncbi.nlm.nih.gov/pubmed/39122703$$D View this record in MEDLINE/PubMed
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SSID ssj0000330256
Score 2.4377115
Snippet In EGFR -mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance. Despite...
In EGFR-mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance. Despite...
Abstract In EGFR-mutated lung cancer, the duration of response to tyrosine kinase inhibitors (TKIs) is limited by the development of acquired drug resistance....
SourceID doaj
proquest
pubmed
crossref
springer
SourceType Open Website
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 580
SubjectTerms 13/1
13/109
38/39
38/91
631/337/2019
631/67/1612/1350
Animals
Antibodies
Apoptosis
Apoptosis - drug effects
Apoptosis - genetics
Bcl-2 protein
Bcl-x protein
bcl-X Protein - genetics
bcl-X Protein - metabolism
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Cell Line, Tumor
Cell survival
Drug resistance
Drug Resistance, Neoplasm - genetics
Epidermal growth factor receptors
ErbB Receptors - genetics
ErbB Receptors - metabolism
Gene expression
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
Genetic analysis
Humans
Immunology
Kinases
Life Sciences
Lung cancer
Lung Neoplasms - drug therapy
Lung Neoplasms - genetics
Lung Neoplasms - metabolism
Lung Neoplasms - pathology
Mcl-1 protein
Mice
Mice, Transgenic
Mutation - genetics
Nucleotide sequence
Protein Kinase Inhibitors - pharmacology
RNA-Seq
Single-Cell Analysis
Single-Cell Gene Expression Analysis
Spatial heterogeneity
Transcriptome - genetics
Transcriptomics
Transgenic mice
Tumor cell lines
Tumor cells
Tumors
Tyrosine kinase inhibitors
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Title Integrative single-cell RNA-seq and spatial transcriptomics analyses reveal diverse apoptosis-related gene expression profiles in EGFR-mutated lung cancer
URI https://link.springer.com/article/10.1038/s41419-024-06940-y
https://www.ncbi.nlm.nih.gov/pubmed/39122703
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