Epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer
Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Jing, Meng [verfasserIn] He, Xia [verfasserIn] Cai, Cheng Zhi [verfasserIn] Ma, Qi Zhi [verfasserIn] Li, Kai [verfasserIn] Zhang, Ben Xia [verfasserIn] Yin, Yuan [verfasserIn] Shi, Ming Song [verfasserIn] Wang, Yong Sheng [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
Non-small-cell lung cancer (NSCLC) |
|---|
| Übergeordnetes Werk: |
Enthalten in: Biochemical and biophysical research communications - Orlando, Fla. : Academic Press, 1959, 681, Seite 218-224 |
|---|---|
| Übergeordnetes Werk: |
volume:681 ; pages:218-224 |
| DOI / URN: |
10.1016/j.bbrc.2023.09.047 |
|---|
| Katalog-ID: |
ELV06505895X |
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| 520 | |a Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological subtype, they lose their dependence on the original oncogenic driver, resulting in therapeutic resistance. However, the molecular details associated with this transformation remain unclear. It has been difficult to define molecular mechanisms of neuroendocrine (NE) transformation in lung cancer due to a lack of pre- and post-transformation clinical samples. In this study, we established a NSCLC cell line with concurrent RB1/TP53 mutations and built corresponding patient-derived xenograft (PDX) models to investigate the mechanisms underlying transformation to SCLC. Studying these PDX models, we demonstrate that EGFR loss facilitates lineage plasticity of lung adenocarcinoma initiated by biallelic mutations of TP53 and RB1. Gene expression analysis of these EGFR knockout tumors revealed altered expression of neuroendocrine synapse-associated lineage genes. There is an increased expression of epigenetic reprogramming factors like Sox2 and gene associated with neural development like NTRK in these EGFR knockout tumors. These findings uncovered the role of EGFR in the acquisition of plasticity, which is the ability of a cell to substantially modify its identity and take on a new phenotype, and defined a novel landscape of potential drivers of NE transformation in lung cancer. | ||
| 650 | 4 | |a Non-small-cell lung cancer (NSCLC) | |
| 650 | 4 | |a Small cell line lung cancer (SCLC) | |
| 650 | 4 | |a EGFR | |
| 650 | 4 | |a Cell line | |
| 650 | 4 | |a SCLC transformation | |
| 650 | 4 | |a Lineage plasticity | |
| 700 | 1 | |a He, Xia |e verfasserin |0 (orcid)0009-0004-4282-8014 |4 aut | |
| 700 | 1 | |a Cai, Cheng Zhi |e verfasserin |4 aut | |
| 700 | 1 | |a Ma, Qi Zhi |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Kai |e verfasserin |0 (orcid)0009-0000-2832-4822 |4 aut | |
| 700 | 1 | |a Zhang, Ben Xia |e verfasserin |0 (orcid)0000-0002-0063-624X |4 aut | |
| 700 | 1 | |a Yin, Yuan |e verfasserin |0 (orcid)0000-0002-0467-8092 |4 aut | |
| 700 | 1 | |a Shi, Ming Song |e verfasserin |0 (orcid)0000-0002-8979-5844 |4 aut | |
| 700 | 1 | |a Wang, Yong Sheng |e verfasserin |0 (orcid)0000-0001-7450-0006 |4 aut | |
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10.1016/j.bbrc.2023.09.047 doi (DE-627)ELV06505895X (ELSEVIER)S0006-291X(23)01083-5 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 35.70 bkl 42.12 bkl Jing, Meng verfasserin (orcid)0009-0006-8891-2654 aut Epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological subtype, they lose their dependence on the original oncogenic driver, resulting in therapeutic resistance. However, the molecular details associated with this transformation remain unclear. It has been difficult to define molecular mechanisms of neuroendocrine (NE) transformation in lung cancer due to a lack of pre- and post-transformation clinical samples. In this study, we established a NSCLC cell line with concurrent RB1/TP53 mutations and built corresponding patient-derived xenograft (PDX) models to investigate the mechanisms underlying transformation to SCLC. Studying these PDX models, we demonstrate that EGFR loss facilitates lineage plasticity of lung adenocarcinoma initiated by biallelic mutations of TP53 and RB1. Gene expression analysis of these EGFR knockout tumors revealed altered expression of neuroendocrine synapse-associated lineage genes. There is an increased expression of epigenetic reprogramming factors like Sox2 and gene associated with neural development like NTRK in these EGFR knockout tumors. These findings uncovered the role of EGFR in the acquisition of plasticity, which is the ability of a cell to substantially modify its identity and take on a new phenotype, and defined a novel landscape of potential drivers of NE transformation in lung cancer. Non-small-cell lung cancer (NSCLC) Small cell line lung cancer (SCLC) EGFR Cell line SCLC transformation Lineage plasticity He, Xia verfasserin (orcid)0009-0004-4282-8014 aut Cai, Cheng Zhi verfasserin aut Ma, Qi Zhi verfasserin aut Li, Kai verfasserin (orcid)0009-0000-2832-4822 aut Zhang, Ben Xia verfasserin (orcid)0000-0002-0063-624X aut Yin, Yuan verfasserin (orcid)0000-0002-0467-8092 aut Shi, Ming Song verfasserin (orcid)0000-0002-8979-5844 aut Wang, Yong Sheng verfasserin (orcid)0000-0001-7450-0006 aut Enthalten in Biochemical and biophysical research communications Orlando, Fla. : Academic Press, 1959 681, Seite 218-224 Online-Ressource (DE-627)254231691 (DE-600)1461396-7 (DE-576)103373039 0006-291X nnns volume:681 pages:218-224 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 35.70 Biochemie: Allgemeines VZ 42.12 Biophysik VZ AR 681 218-224 |
| spelling |
10.1016/j.bbrc.2023.09.047 doi (DE-627)ELV06505895X (ELSEVIER)S0006-291X(23)01083-5 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 35.70 bkl 42.12 bkl Jing, Meng verfasserin (orcid)0009-0006-8891-2654 aut Epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological subtype, they lose their dependence on the original oncogenic driver, resulting in therapeutic resistance. However, the molecular details associated with this transformation remain unclear. It has been difficult to define molecular mechanisms of neuroendocrine (NE) transformation in lung cancer due to a lack of pre- and post-transformation clinical samples. In this study, we established a NSCLC cell line with concurrent RB1/TP53 mutations and built corresponding patient-derived xenograft (PDX) models to investigate the mechanisms underlying transformation to SCLC. Studying these PDX models, we demonstrate that EGFR loss facilitates lineage plasticity of lung adenocarcinoma initiated by biallelic mutations of TP53 and RB1. Gene expression analysis of these EGFR knockout tumors revealed altered expression of neuroendocrine synapse-associated lineage genes. There is an increased expression of epigenetic reprogramming factors like Sox2 and gene associated with neural development like NTRK in these EGFR knockout tumors. These findings uncovered the role of EGFR in the acquisition of plasticity, which is the ability of a cell to substantially modify its identity and take on a new phenotype, and defined a novel landscape of potential drivers of NE transformation in lung cancer. Non-small-cell lung cancer (NSCLC) Small cell line lung cancer (SCLC) EGFR Cell line SCLC transformation Lineage plasticity He, Xia verfasserin (orcid)0009-0004-4282-8014 aut Cai, Cheng Zhi verfasserin aut Ma, Qi Zhi verfasserin aut Li, Kai verfasserin (orcid)0009-0000-2832-4822 aut Zhang, Ben Xia verfasserin (orcid)0000-0002-0063-624X aut Yin, Yuan verfasserin (orcid)0000-0002-0467-8092 aut Shi, Ming Song verfasserin (orcid)0000-0002-8979-5844 aut Wang, Yong Sheng verfasserin (orcid)0000-0001-7450-0006 aut Enthalten in Biochemical and biophysical research communications Orlando, Fla. : Academic Press, 1959 681, Seite 218-224 Online-Ressource (DE-627)254231691 (DE-600)1461396-7 (DE-576)103373039 0006-291X nnns volume:681 pages:218-224 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 35.70 Biochemie: Allgemeines VZ 42.12 Biophysik VZ AR 681 218-224 |
| allfields_unstemmed |
10.1016/j.bbrc.2023.09.047 doi (DE-627)ELV06505895X (ELSEVIER)S0006-291X(23)01083-5 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 35.70 bkl 42.12 bkl Jing, Meng verfasserin (orcid)0009-0006-8891-2654 aut Epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological subtype, they lose their dependence on the original oncogenic driver, resulting in therapeutic resistance. However, the molecular details associated with this transformation remain unclear. It has been difficult to define molecular mechanisms of neuroendocrine (NE) transformation in lung cancer due to a lack of pre- and post-transformation clinical samples. In this study, we established a NSCLC cell line with concurrent RB1/TP53 mutations and built corresponding patient-derived xenograft (PDX) models to investigate the mechanisms underlying transformation to SCLC. Studying these PDX models, we demonstrate that EGFR loss facilitates lineage plasticity of lung adenocarcinoma initiated by biallelic mutations of TP53 and RB1. Gene expression analysis of these EGFR knockout tumors revealed altered expression of neuroendocrine synapse-associated lineage genes. There is an increased expression of epigenetic reprogramming factors like Sox2 and gene associated with neural development like NTRK in these EGFR knockout tumors. These findings uncovered the role of EGFR in the acquisition of plasticity, which is the ability of a cell to substantially modify its identity and take on a new phenotype, and defined a novel landscape of potential drivers of NE transformation in lung cancer. Non-small-cell lung cancer (NSCLC) Small cell line lung cancer (SCLC) EGFR Cell line SCLC transformation Lineage plasticity He, Xia verfasserin (orcid)0009-0004-4282-8014 aut Cai, Cheng Zhi verfasserin aut Ma, Qi Zhi verfasserin aut Li, Kai verfasserin (orcid)0009-0000-2832-4822 aut Zhang, Ben Xia verfasserin (orcid)0000-0002-0063-624X aut Yin, Yuan verfasserin (orcid)0000-0002-0467-8092 aut Shi, Ming Song verfasserin (orcid)0000-0002-8979-5844 aut Wang, Yong Sheng verfasserin (orcid)0000-0001-7450-0006 aut Enthalten in Biochemical and biophysical research communications Orlando, Fla. : Academic Press, 1959 681, Seite 218-224 Online-Ressource (DE-627)254231691 (DE-600)1461396-7 (DE-576)103373039 0006-291X nnns volume:681 pages:218-224 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 35.70 Biochemie: Allgemeines VZ 42.12 Biophysik VZ AR 681 218-224 |
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10.1016/j.bbrc.2023.09.047 doi (DE-627)ELV06505895X (ELSEVIER)S0006-291X(23)01083-5 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 35.70 bkl 42.12 bkl Jing, Meng verfasserin (orcid)0009-0006-8891-2654 aut Epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological subtype, they lose their dependence on the original oncogenic driver, resulting in therapeutic resistance. However, the molecular details associated with this transformation remain unclear. It has been difficult to define molecular mechanisms of neuroendocrine (NE) transformation in lung cancer due to a lack of pre- and post-transformation clinical samples. In this study, we established a NSCLC cell line with concurrent RB1/TP53 mutations and built corresponding patient-derived xenograft (PDX) models to investigate the mechanisms underlying transformation to SCLC. Studying these PDX models, we demonstrate that EGFR loss facilitates lineage plasticity of lung adenocarcinoma initiated by biallelic mutations of TP53 and RB1. Gene expression analysis of these EGFR knockout tumors revealed altered expression of neuroendocrine synapse-associated lineage genes. There is an increased expression of epigenetic reprogramming factors like Sox2 and gene associated with neural development like NTRK in these EGFR knockout tumors. These findings uncovered the role of EGFR in the acquisition of plasticity, which is the ability of a cell to substantially modify its identity and take on a new phenotype, and defined a novel landscape of potential drivers of NE transformation in lung cancer. Non-small-cell lung cancer (NSCLC) Small cell line lung cancer (SCLC) EGFR Cell line SCLC transformation Lineage plasticity He, Xia verfasserin (orcid)0009-0004-4282-8014 aut Cai, Cheng Zhi verfasserin aut Ma, Qi Zhi verfasserin aut Li, Kai verfasserin (orcid)0009-0000-2832-4822 aut Zhang, Ben Xia verfasserin (orcid)0000-0002-0063-624X aut Yin, Yuan verfasserin (orcid)0000-0002-0467-8092 aut Shi, Ming Song verfasserin (orcid)0000-0002-8979-5844 aut Wang, Yong Sheng verfasserin (orcid)0000-0001-7450-0006 aut Enthalten in Biochemical and biophysical research communications Orlando, Fla. : Academic Press, 1959 681, Seite 218-224 Online-Ressource (DE-627)254231691 (DE-600)1461396-7 (DE-576)103373039 0006-291X nnns volume:681 pages:218-224 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 35.70 Biochemie: Allgemeines VZ 42.12 Biophysik VZ AR 681 218-224 |
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10.1016/j.bbrc.2023.09.047 doi (DE-627)ELV06505895X (ELSEVIER)S0006-291X(23)01083-5 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 35.70 bkl 42.12 bkl Jing, Meng verfasserin (orcid)0009-0006-8891-2654 aut Epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological subtype, they lose their dependence on the original oncogenic driver, resulting in therapeutic resistance. However, the molecular details associated with this transformation remain unclear. It has been difficult to define molecular mechanisms of neuroendocrine (NE) transformation in lung cancer due to a lack of pre- and post-transformation clinical samples. In this study, we established a NSCLC cell line with concurrent RB1/TP53 mutations and built corresponding patient-derived xenograft (PDX) models to investigate the mechanisms underlying transformation to SCLC. Studying these PDX models, we demonstrate that EGFR loss facilitates lineage plasticity of lung adenocarcinoma initiated by biallelic mutations of TP53 and RB1. Gene expression analysis of these EGFR knockout tumors revealed altered expression of neuroendocrine synapse-associated lineage genes. There is an increased expression of epigenetic reprogramming factors like Sox2 and gene associated with neural development like NTRK in these EGFR knockout tumors. These findings uncovered the role of EGFR in the acquisition of plasticity, which is the ability of a cell to substantially modify its identity and take on a new phenotype, and defined a novel landscape of potential drivers of NE transformation in lung cancer. Non-small-cell lung cancer (NSCLC) Small cell line lung cancer (SCLC) EGFR Cell line SCLC transformation Lineage plasticity He, Xia verfasserin (orcid)0009-0004-4282-8014 aut Cai, Cheng Zhi verfasserin aut Ma, Qi Zhi verfasserin aut Li, Kai verfasserin (orcid)0009-0000-2832-4822 aut Zhang, Ben Xia verfasserin (orcid)0000-0002-0063-624X aut Yin, Yuan verfasserin (orcid)0000-0002-0467-8092 aut Shi, Ming Song verfasserin (orcid)0000-0002-8979-5844 aut Wang, Yong Sheng verfasserin (orcid)0000-0001-7450-0006 aut Enthalten in Biochemical and biophysical research communications Orlando, Fla. : Academic Press, 1959 681, Seite 218-224 Online-Ressource (DE-627)254231691 (DE-600)1461396-7 (DE-576)103373039 0006-291X nnns volume:681 pages:218-224 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 35.70 Biochemie: Allgemeines VZ 42.12 Biophysik VZ AR 681 218-224 |
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Enthalten in Biochemical and biophysical research communications 681, Seite 218-224 volume:681 pages:218-224 |
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Non-small-cell lung cancer (NSCLC) Small cell line lung cancer (SCLC) EGFR Cell line SCLC transformation Lineage plasticity |
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Biochemical and biophysical research communications |
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Jing, Meng @@aut@@ He, Xia @@aut@@ Cai, Cheng Zhi @@aut@@ Ma, Qi Zhi @@aut@@ Li, Kai @@aut@@ Zhang, Ben Xia @@aut@@ Yin, Yuan @@aut@@ Shi, Ming Song @@aut@@ Wang, Yong Sheng @@aut@@ |
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2023-01-01T00:00:00Z |
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Jing, Meng |
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Jing, Meng ddc 570 fid BIODIV bkl 35.70 bkl 42.12 misc Non-small-cell lung cancer (NSCLC) misc Small cell line lung cancer (SCLC) misc EGFR misc Cell line misc SCLC transformation misc Lineage plasticity Epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer |
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570 VZ BIODIV DE-30 fid 35.70 bkl 42.12 bkl Epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer Non-small-cell lung cancer (NSCLC) Small cell line lung cancer (SCLC) EGFR Cell line SCLC transformation Lineage plasticity |
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epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer |
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Epidermal growth factor receptor regulates lineage plasticity driving transformation to small cell lung cancer |
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Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological subtype, they lose their dependence on the original oncogenic driver, resulting in therapeutic resistance. However, the molecular details associated with this transformation remain unclear. It has been difficult to define molecular mechanisms of neuroendocrine (NE) transformation in lung cancer due to a lack of pre- and post-transformation clinical samples. In this study, we established a NSCLC cell line with concurrent RB1/TP53 mutations and built corresponding patient-derived xenograft (PDX) models to investigate the mechanisms underlying transformation to SCLC. Studying these PDX models, we demonstrate that EGFR loss facilitates lineage plasticity of lung adenocarcinoma initiated by biallelic mutations of TP53 and RB1. Gene expression analysis of these EGFR knockout tumors revealed altered expression of neuroendocrine synapse-associated lineage genes. There is an increased expression of epigenetic reprogramming factors like Sox2 and gene associated with neural development like NTRK in these EGFR knockout tumors. These findings uncovered the role of EGFR in the acquisition of plasticity, which is the ability of a cell to substantially modify its identity and take on a new phenotype, and defined a novel landscape of potential drivers of NE transformation in lung cancer. |
| abstractGer |
Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological subtype, they lose their dependence on the original oncogenic driver, resulting in therapeutic resistance. However, the molecular details associated with this transformation remain unclear. It has been difficult to define molecular mechanisms of neuroendocrine (NE) transformation in lung cancer due to a lack of pre- and post-transformation clinical samples. In this study, we established a NSCLC cell line with concurrent RB1/TP53 mutations and built corresponding patient-derived xenograft (PDX) models to investigate the mechanisms underlying transformation to SCLC. Studying these PDX models, we demonstrate that EGFR loss facilitates lineage plasticity of lung adenocarcinoma initiated by biallelic mutations of TP53 and RB1. Gene expression analysis of these EGFR knockout tumors revealed altered expression of neuroendocrine synapse-associated lineage genes. There is an increased expression of epigenetic reprogramming factors like Sox2 and gene associated with neural development like NTRK in these EGFR knockout tumors. These findings uncovered the role of EGFR in the acquisition of plasticity, which is the ability of a cell to substantially modify its identity and take on a new phenotype, and defined a novel landscape of potential drivers of NE transformation in lung cancer. |
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Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) is clinically and genetically heterogeneous, with concurrent RB1/TP53 mutations, indicating an increased risk of transformation into small cell lung cancer (SCLC). When tumor cells convert into a different histological subtype, they lose their dependence on the original oncogenic driver, resulting in therapeutic resistance. However, the molecular details associated with this transformation remain unclear. It has been difficult to define molecular mechanisms of neuroendocrine (NE) transformation in lung cancer due to a lack of pre- and post-transformation clinical samples. In this study, we established a NSCLC cell line with concurrent RB1/TP53 mutations and built corresponding patient-derived xenograft (PDX) models to investigate the mechanisms underlying transformation to SCLC. Studying these PDX models, we demonstrate that EGFR loss facilitates lineage plasticity of lung adenocarcinoma initiated by biallelic mutations of TP53 and RB1. Gene expression analysis of these EGFR knockout tumors revealed altered expression of neuroendocrine synapse-associated lineage genes. There is an increased expression of epigenetic reprogramming factors like Sox2 and gene associated with neural development like NTRK in these EGFR knockout tumors. These findings uncovered the role of EGFR in the acquisition of plasticity, which is the ability of a cell to substantially modify its identity and take on a new phenotype, and defined a novel landscape of potential drivers of NE transformation in lung cancer. |
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| score |
7.402011 |