HIF2A mediates lineage transition to aggressive phenotype of cancer-associated fibroblasts in lung cancer brain metastasis

Brain metastasis is the most devasting form of lung cancer. Recent studies highlight significant differences in the tumor microenvironment (TME) between lung cancer brain metastasis (LCBM) and primary lung cancer, which contribute significantly to tumor progression and drug resistance. Cancer-associ...

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Published inOncoimmunology Vol. 13; no. 1; p. 2356942
Main Authors You, Muyuan, Fu, Minjie, Shen, Zhewei, Feng, Yuan, Zhang, Licheng, Zhu, Xianmin, Zhuang, Zhengping, Mao, Ying, Hua, Wei
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Abstract Brain metastasis is the most devasting form of lung cancer. Recent studies highlight significant differences in the tumor microenvironment (TME) between lung cancer brain metastasis (LCBM) and primary lung cancer, which contribute significantly to tumor progression and drug resistance. Cancer-associated fibroblasts (CAFs) are the major component of pro-tumor TME with high plasticity. However, the lineage composition and function of CAFs in LCBM remain elusive. By reanalyzing single-cell RNA sequencing (scRNA-seq) data (GSE131907) from lung cancer patients with different stages of metastasis comprising primary lesions and brain metastasis, we found that CAFs undergo distinctive lineage transition during LCBM under a hypoxic situation, which is directly driven by hypoxia-induced HIF-2α activation. Transited CAFs enhance angiogenesis through VEGF pathways, trigger metabolic reprogramming, and promote the growth of tumor cells. Bulk RNA sequencing data was utilized as validation cohorts. Multiplex immunohistochemistry (mIHC) assay was performed on four paired samples of brain metastasis and their primary lung cancer counterparts to validate the findings. Our study revealed a novel mechanism of lung cancer brain metastasis featuring HIF-2α-induced lineage transition and functional alteration of CAFs, which offers potential therapeutic targets.
AbstractList Brain metastasis is the most devasting form of lung cancer. Recent studies highlight significant differences in the tumor microenvironment (TME) between lung cancer brain metastasis (LCBM) and primary lung cancer, which contribute significantly to tumor progression and drug resistance. Cancer-associated fibroblasts (CAFs) are the major component of pro-tumor TME with high plasticity. However, the lineage composition and function of CAFs in LCBM remain elusive. By reanalyzing single-cell RNA sequencing (scRNA-seq) data (GSE131907) from lung cancer patients with different stages of metastasis comprising primary lesions and brain metastasis, we found that CAFs undergo distinctive lineage transition during LCBM under a hypoxic situation, which is directly driven by hypoxia-induced HIF-2α activation. Transited CAFs enhance angiogenesis through VEGF pathways, trigger metabolic reprogramming, and promote the growth of tumor cells. Bulk RNA sequencing data was utilized as validation cohorts. Multiplex immunohistochemistry (mIHC) assay was performed on four paired samples of brain metastasis and their primary lung cancer counterparts to validate the findings. Our study revealed a novel mechanism of lung cancer brain metastasis featuring HIF-2α-induced lineage transition and functional alteration of CAFs, which offers potential therapeutic targets.
ABSTRACTBrain metastasis is the most devasting form of lung cancer. Recent studies highlight significant differences in the tumor microenvironment (TME) between lung cancer brain metastasis (LCBM) and primary lung cancer, which contribute significantly to tumor progression and drug resistance. Cancer-associated fibroblasts (CAFs) are the major component of pro-tumor TME with high plasticity. However, the lineage composition and function of CAFs in LCBM remain elusive. By reanalyzing single-cell RNA sequencing (scRNA-seq) data (GSE131907) from lung cancer patients with different stages of metastasis comprising primary lesions and brain metastasis, we found that CAFs undergo distinctive lineage transition during LCBM under a hypoxic situation, which is directly driven by hypoxia-induced HIF-2α activation. Transited CAFs enhance angiogenesis through VEGF pathways, trigger metabolic reprogramming, and promote the growth of tumor cells. Bulk RNA sequencing data was utilized as validation cohorts. Multiplex immunohistochemistry (mIHC) assay was performed on four paired samples of brain metastasis and their primary lung cancer counterparts to validate the findings. Our study revealed a novel mechanism of lung cancer brain metastasis featuring HIF-2α-induced lineage transition and functional alteration of CAFs, which offers potential therapeutic targets.
Brain metastasis is the most devasting form of lung cancer. Recent studies highlight significant differences in the tumor microenvironment (TME) between lung cancer brain metastasis (LCBM) and primary lung cancer, which contribute significantly to tumor progression and drug resistance. Cancer-associated fibroblasts (CAFs) are the major component of pro-tumor TME with high plasticity. However, the lineage composition and function of CAFs in LCBM remain elusive. By reanalyzing single-cell RNA sequencing (scRNA-seq) data (GSE131907) from lung cancer patients with different stages of metastasis comprising primary lesions and brain metastasis, we found that CAFs undergo distinctive lineage transition during LCBM under a hypoxic situation, which is directly driven by hypoxia-induced HIF-2α activation. Transited CAFs enhance angiogenesis through VEGF pathways, trigger metabolic reprogramming, and promote the growth of tumor cells. Bulk RNA sequencing data was utilized as validation cohorts. Multiplex immunohistochemistry (mIHC) assay was performed on four paired samples of brain metastasis and their primary lung cancer counterparts to validate the findings. Our study revealed a novel mechanism of lung cancer brain metastasis featuring HIF-2α-induced lineage transition and functional alteration of CAFs, which offers potential therapeutic targets.Brain metastasis is the most devasting form of lung cancer. Recent studies highlight significant differences in the tumor microenvironment (TME) between lung cancer brain metastasis (LCBM) and primary lung cancer, which contribute significantly to tumor progression and drug resistance. Cancer-associated fibroblasts (CAFs) are the major component of pro-tumor TME with high plasticity. However, the lineage composition and function of CAFs in LCBM remain elusive. By reanalyzing single-cell RNA sequencing (scRNA-seq) data (GSE131907) from lung cancer patients with different stages of metastasis comprising primary lesions and brain metastasis, we found that CAFs undergo distinctive lineage transition during LCBM under a hypoxic situation, which is directly driven by hypoxia-induced HIF-2α activation. Transited CAFs enhance angiogenesis through VEGF pathways, trigger metabolic reprogramming, and promote the growth of tumor cells. Bulk RNA sequencing data was utilized as validation cohorts. Multiplex immunohistochemistry (mIHC) assay was performed on four paired samples of brain metastasis and their primary lung cancer counterparts to validate the findings. Our study revealed a novel mechanism of lung cancer brain metastasis featuring HIF-2α-induced lineage transition and functional alteration of CAFs, which offers potential therapeutic targets.
Author Fu, Minjie
Mao, Ying
Zhu, Xianmin
Zhuang, Zhengping
Zhang, Licheng
Hua, Wei
Shen, Zhewei
You, Muyuan
Feng, Yuan
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Cites_doi 10.1038/nm.3394
10.1158/2159-8290.Cd-21-1714
10.1097/cej.0000000000000790
10.1016/j.ccell.2018.01.010
10.1038/s12276-019-0299-y
10.1073/pnas.2020490118
10.1038/s41421-021-00271-4
10.1016/j.cmet.2018.09.012
10.1056/NEJMoa1205119
10.1038/s41392-022-01080-1
10.1158/1078-0432.Ccr-20-0798
10.1016/j.jhep.2023.01.011
10.1093/neuonc/noaa028
10.1186/s13046-018-0996-8
10.1097/PPO.0b013e318172d6e1
10.1016/j.xinn.2021.100141
10.1186/s40425-018-0349-3
10.1038/s41467-022-30633-9
10.1038/kisup.2014.20
10.1038/s41591-019-0654-5
10.1038/s42003-024-06087-8
10.1038/s41467-022-29366-6
10.1126/science.ade2292
10.1186/s11658-022-00408-7
10.1056/NEJMoa2103425
10.1038/s41467-022-33365-y
10.1093/biostatistics/kxj037
10.1002/ijc.28848
10.1016/j.jcmgh.2020.09.003
10.1016/j.cell.2021.04.048
10.1038/s41596-020-0336-2
10.1073/pnas.0506580102
10.1038/s41467-022-34395-2
10.1016/j.lungcan.2014.07.020
10.1186/s12943-023-01876-x
10.1016/j.annonc.2023.10.090
10.1038/s41523-017-0008-8
10.1038/s41467-021-21246-9
10.1038/s41467-020-16164-1
10.1002/ctm2.1101
10.1186/s13059-014-0550-8
10.1016/j.phrs.2023.106851
10.1038/nmeth.4402
10.1038/s41592-019-0619-0
10.1016/j.celrep.2018.10.045
10.1007/978-1-0716-0301-7_7
10.1172/jci.insight.144368
10.1093/neuonc/noad017
10.6004/jnccn.2017.0050
10.18632/aging.102967
10.1001/jamaoncol.2021.4932
10.1038/s43018-021-00195-8
10.1016/j.immuni.2019.03.024
10.1038/nrc.2016.73
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Keywords lung cancer
tumor microenvironment
HIF
Brain metastasis
Cancer-Associated Fibroblasts
Language English
License 2024 The Author(s). Published with license by Taylor & Francis Group, LLC.
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References e_1_3_10_26_1
e_1_3_10_24_1
e_1_3_10_47_1
e_1_3_10_28_1
e_1_3_10_49_1
e_1_3_10_4_1
e_1_3_10_54_1
e_1_3_10_2_1
e_1_3_10_8_1
e_1_3_10_12_1
e_1_3_10_33_1
e_1_3_10_50_1
e_1_3_10_6_1
e_1_3_10_10_1
e_1_3_10_31_1
e_1_3_10_52_1
e_1_3_10_15_1
e_1_3_10_38_1
e_1_3_10_13_1
e_1_3_10_36_1
e_1_3_10_19_1
e_1_3_10_17_1
e_1_3_10_41_1
e_1_3_10_43_1
e_1_3_10_45_1
e_1_3_10_22_1
e_1_3_10_20_1
e_1_3_10_27_1
e_1_3_10_25_1
e_1_3_10_46_1
e_1_3_10_29_1
e_1_3_10_48_1
e_1_3_10_30_1
e_1_3_10_53_1
e_1_3_10_5_1
e_1_3_10_55_1
e_1_3_10_3_1
e_1_3_10_11_1
e_1_3_10_34_1
e_1_3_10_9_1
e_1_3_10_32_1
e_1_3_10_51_1
e_1_3_10_7_1
e_1_3_10_16_1
e_1_3_10_37_1
e_1_3_10_14_1
e_1_3_10_35_1
e_1_3_10_18_1
e_1_3_10_39_1
e_1_3_10_40_1
e_1_3_10_44_1
e_1_3_10_23_1
e_1_3_10_21_1
e_1_3_10_42_1
References_xml – ident: e_1_3_10_16_1
  doi: 10.1038/nm.3394
– ident: e_1_3_10_45_1
  doi: 10.1158/2159-8290.Cd-21-1714
– ident: e_1_3_10_5_1
  doi: 10.1097/cej.0000000000000790
– ident: e_1_3_10_38_1
  doi: 10.1016/j.ccell.2018.01.010
– ident: e_1_3_10_49_1
  doi: 10.1038/s12276-019-0299-y
– ident: e_1_3_10_36_1
  doi: 10.1073/pnas.2020490118
– ident: e_1_3_10_44_1
  doi: 10.1038/s41421-021-00271-4
– ident: e_1_3_10_43_1
  doi: 10.1016/j.cmet.2018.09.012
– ident: e_1_3_10_51_1
  doi: 10.1056/NEJMoa1205119
– ident: e_1_3_10_35_1
  doi: 10.1038/s41392-022-01080-1
– ident: e_1_3_10_8_1
  doi: 10.1158/1078-0432.Ccr-20-0798
– ident: e_1_3_10_39_1
  doi: 10.1016/j.jhep.2023.01.011
– ident: e_1_3_10_13_1
  doi: 10.1093/neuonc/noaa028
– ident: e_1_3_10_37_1
  doi: 10.1186/s13046-018-0996-8
– ident: e_1_3_10_4_1
  doi: 10.1097/PPO.0b013e318172d6e1
– ident: e_1_3_10_26_1
  doi: 10.1016/j.xinn.2021.100141
– ident: e_1_3_10_7_1
  doi: 10.1186/s40425-018-0349-3
– ident: e_1_3_10_34_1
  doi: 10.1038/s41467-022-30633-9
– ident: e_1_3_10_47_1
  doi: 10.1038/kisup.2014.20
– ident: e_1_3_10_22_1
  doi: 10.1038/s41591-019-0654-5
– ident: e_1_3_10_40_1
  doi: 10.1038/s42003-024-06087-8
– ident: e_1_3_10_42_1
  doi: 10.1038/s41467-022-29366-6
– ident: e_1_3_10_41_1
  doi: 10.1126/science.ade2292
– ident: e_1_3_10_48_1
  doi: 10.1186/s11658-022-00408-7
– ident: e_1_3_10_54_1
  doi: 10.1056/NEJMoa2103425
– ident: e_1_3_10_12_1
  doi: 10.1038/s41467-022-33365-y
– ident: e_1_3_10_23_1
  doi: 10.1093/biostatistics/kxj037
– ident: e_1_3_10_20_1
  doi: 10.1002/ijc.28848
– ident: e_1_3_10_46_1
  doi: 10.1016/j.jcmgh.2020.09.003
– ident: e_1_3_10_24_1
  doi: 10.1016/j.cell.2021.04.048
– ident: e_1_3_10_32_1
  doi: 10.1038/s41596-020-0336-2
– ident: e_1_3_10_27_1
  doi: 10.1073/pnas.0506580102
– ident: e_1_3_10_18_1
  doi: 10.1038/s41467-022-34395-2
– ident: e_1_3_10_3_1
  doi: 10.1016/j.lungcan.2014.07.020
– ident: e_1_3_10_19_1
  doi: 10.1186/s12943-023-01876-x
– ident: e_1_3_10_55_1
  doi: 10.1016/j.annonc.2023.10.090
– ident: e_1_3_10_21_1
  doi: 10.1038/s41523-017-0008-8
– ident: e_1_3_10_30_1
  doi: 10.1038/s41467-021-21246-9
– ident: e_1_3_10_9_1
  doi: 10.1038/s41467-020-16164-1
– ident: e_1_3_10_17_1
  doi: 10.1002/ctm2.1101
– ident: e_1_3_10_25_1
  doi: 10.1186/s13059-014-0550-8
– ident: e_1_3_10_50_1
  doi: 10.1016/j.phrs.2023.106851
– ident: e_1_3_10_31_1
  doi: 10.1038/nmeth.4402
– ident: e_1_3_10_29_1
  doi: 10.1038/s41592-019-0619-0
– ident: e_1_3_10_33_1
  doi: 10.1016/j.celrep.2018.10.045
– ident: e_1_3_10_28_1
  doi: 10.1007/978-1-0716-0301-7_7
– ident: e_1_3_10_52_1
  doi: 10.1172/jci.insight.144368
– ident: e_1_3_10_10_1
  doi: 10.1093/neuonc/noad017
– ident: e_1_3_10_6_1
  doi: 10.6004/jnccn.2017.0050
– ident: e_1_3_10_53_1
  doi: 10.18632/aging.102967
– ident: e_1_3_10_2_1
  doi: 10.1001/jamaoncol.2021.4932
– ident: e_1_3_10_14_1
  doi: 10.1038/s43018-021-00195-8
– ident: e_1_3_10_11_1
  doi: 10.1016/j.immuni.2019.03.024
– ident: e_1_3_10_15_1
  doi: 10.1038/nrc.2016.73
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Snippet Brain metastasis is the most devasting form of lung cancer. Recent studies highlight significant differences in the tumor microenvironment (TME) between lung...
ABSTRACTBrain metastasis is the most devasting form of lung cancer. Recent studies highlight significant differences in the tumor microenvironment (TME)...
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SubjectTerms Animals
Basic Helix-Loop-Helix Transcription Factors - genetics
Basic Helix-Loop-Helix Transcription Factors - metabolism
Brain metastasis
Brain Neoplasms - genetics
Brain Neoplasms - metabolism
Brain Neoplasms - pathology
Brain Neoplasms - secondary
Cancer-Associated Fibroblasts
Cancer-Associated Fibroblasts - metabolism
Cancer-Associated Fibroblasts - pathology
Cell Line, Tumor
Cell Lineage
Gene Expression Regulation, Neoplastic
HIF
Humans
lung cancer
Lung Neoplasms - genetics
Lung Neoplasms - metabolism
Lung Neoplasms - pathology
Lung Neoplasms - secondary
Mice
Neovascularization, Pathologic - genetics
Neovascularization, Pathologic - metabolism
Neovascularization, Pathologic - pathology
Original Research
Phenotype
Single-Cell Analysis
Tumor Microenvironment
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Title HIF2A mediates lineage transition to aggressive phenotype of cancer-associated fibroblasts in lung cancer brain metastasis
URI https://www.ncbi.nlm.nih.gov/pubmed/38778816
https://www.proquest.com/docview/3059256549
https://pubmed.ncbi.nlm.nih.gov/PMC11110709
https://doaj.org/article/1aabdee1ffb34512ae1b102ab1503aee
Volume 13
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