AXL‐Mediated Drug Resistance in ALK‐Rearranged NSCLC Enhanced by GAS6 From Macrophages and MMP11 Positive Fibroblasts Article Swipe
Takahiro Utsumi
,
Hayato Mizuta
,
Yosuke Seto
,
Ken Uchibori
,
Makoto Nishio
,
Isamu Okamoto
,
Ryohei Katayama
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1111/cas.70006
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1111/cas.70006
Anaplastic lymphoma kinase (ALK) rearranged non‐small cell lung cancer (NSCLC) shows marked tumor shrinkage by ALK‐tyrosine kinase inhibitors (TKIs). However, tumors almost inevitably relapse owing to the development of acquired resistance. Resistance mechanisms include secondary ALK mutations and the activation of bypass pathways, such as cMET, cKIT, or EGFR, though some remain unknown. In this study, we analyzed alectinib‐resistant patient samples and identified a significant increase in AXL expression in the tumor, and a high level of GAS6, the ligand for AXL, in the pleural effusion. AXL‐overexpressing H3122 ALK‐rearranged NSCLC cells exhibited partial resistance to alectinib, which was enhanced by GAS6 supplementation but could be overcome by the ALK/AXL inhibitor gilteritinib. Moreover, GAS6‐overexpressing NIH3T3 cells and AXL‐expressing H3122 cells were subcutaneously injected into the left and right sides of nude mice simultaneously, followed by alectinib treatment. The supply of GAS6 from NIH3T3 may have accelerated tumor relapse under alectinib treatment. However, even without GAS6‐overexpressing NIH3T3, AXL‐overexpressing H3122 tumor relapsed within 1 month possibly due to increased host mouse Gas6 expression. Single‐cell RNA sequencing revealed that specific cancer‐associated fibroblasts (CAFs) and a subset of tumor‐associated macrophages (TAMs) are the primary sources of Gas6 in the tumor microenvironment (TME). During alectinib treatment, TAMs increased their infiltration into the TME, whereas CAFs altered their expression patterns, substantially upregulating Mmp11. These findings suggest that AXL expression in resistant cancer cells, combined with increased Gas6 production in the TME, contributes to enhanced ALK‐TKI resistance.
Related Topics
Concepts
GAS6
Alectinib
Cancer research
Tumor microenvironment
Anaplastic lymphoma kinase
Lung cancer
Receptor tyrosine kinase
Cancer
Medicine
Pathology
Internal medicine
Malignant pleural effusion
Receptor
Tumor cells
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1111/cas.70006
- OA Status
- gold
- References
- 45
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4407124395
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W4407124395Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1111/cas.70006Digital Object Identifier
- Title
-
AXL‐Mediated Drug Resistance in ALK‐Rearranged NSCLC Enhanced by GAS6 From Macrophages and MMP11 Positive FibroblastsWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2025Year of publication
- Publication date
-
2025-02-04Full publication date if available
- Authors
-
Takahiro Utsumi, Hayato Mizuta, Yosuke Seto, Ken Uchibori, Makoto Nishio, Isamu Okamoto, Ryohei KatayamaList of authors in order
- Landing page
-
https://doi.org/10.1111/cas.70006Publisher landing page
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://doi.org/10.1111/cas.70006Direct OA link when available
- Concepts
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GAS6, Alectinib, Cancer research, Tumor microenvironment, Anaplastic lymphoma kinase, Lung cancer, Receptor tyrosine kinase, Cancer, Medicine, Pathology, Internal medicine, Malignant pleural effusion, Receptor, Tumor cellsTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- References (count)
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45Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.sides | 128 |
| abstract_inverted_index.their | 203, 211 |
| abstract_inverted_index.tumor | 13, 146, 158, 195 |
| abstract_inverted_index.under | 148 |
| abstract_inverted_index.which | 97 |
| abstract_inverted_index.(CAFs) | 179 |
| abstract_inverted_index.(TAMs) | 186 |
| abstract_inverted_index.(TME). | 197 |
| abstract_inverted_index.During | 198 |
| abstract_inverted_index.Mmp11. | 216 |
| abstract_inverted_index.NIH3T3 | 114, 142 |
| abstract_inverted_index.almost | 22 |
| abstract_inverted_index.bypass | 42 |
| abstract_inverted_index.cancer | 9, 225 |
| abstract_inverted_index.cells, | 226 |
| abstract_inverted_index.kinase | 3, 17 |
| abstract_inverted_index.ligand | 80 |
| abstract_inverted_index.marked | 12 |
| abstract_inverted_index.remain | 52 |
| abstract_inverted_index.study, | 56 |
| abstract_inverted_index.subset | 182 |
| abstract_inverted_index.supply | 138 |
| abstract_inverted_index.though | 50 |
| abstract_inverted_index.tumor, | 72 |
| abstract_inverted_index.tumors | 21 |
| abstract_inverted_index.within | 160 |
| abstract_inverted_index.(NSCLC) | 10 |
| abstract_inverted_index.(TKIs). | 19 |
| abstract_inverted_index.ALK/AXL | 109 |
| abstract_inverted_index.NIH3T3, | 155 |
| abstract_inverted_index.altered | 210 |
| abstract_inverted_index.include | 34 |
| abstract_inverted_index.partial | 93 |
| abstract_inverted_index.patient | 60 |
| abstract_inverted_index.pleural | 85 |
| abstract_inverted_index.primary | 189 |
| abstract_inverted_index.relapse | 24, 147 |
| abstract_inverted_index.samples | 61 |
| abstract_inverted_index.sources | 190 |
| abstract_inverted_index.suggest | 219 |
| abstract_inverted_index.whereas | 208 |
| abstract_inverted_index.without | 153 |
| abstract_inverted_index.ABSTRACT | 0 |
| abstract_inverted_index.However, | 20, 151 |
| abstract_inverted_index.acquired | 30 |
| abstract_inverted_index.analyzed | 58 |
| abstract_inverted_index.combined | 227 |
| abstract_inverted_index.enhanced | 99, 237 |
| abstract_inverted_index.findings | 218 |
| abstract_inverted_index.followed | 133 |
| abstract_inverted_index.increase | 66 |
| abstract_inverted_index.injected | 122 |
| abstract_inverted_index.lymphoma | 2 |
| abstract_inverted_index.overcome | 106 |
| abstract_inverted_index.possibly | 163 |
| abstract_inverted_index.relapsed | 159 |
| abstract_inverted_index.revealed | 174 |
| abstract_inverted_index.specific | 176 |
| abstract_inverted_index.unknown. | 53 |
| abstract_inverted_index.ALK‐TKI | 238 |
| abstract_inverted_index.Moreover, | 112 |
| abstract_inverted_index.alectinib | 135, 149, 199 |
| abstract_inverted_index.effusion. | 86 |
| abstract_inverted_index.exhibited | 92 |
| abstract_inverted_index.increased | 166, 202, 229 |
| abstract_inverted_index.inhibitor | 110 |
| abstract_inverted_index.mutations | 37 |
| abstract_inverted_index.pathways, | 43 |
| abstract_inverted_index.patterns, | 213 |
| abstract_inverted_index.resistant | 224 |
| abstract_inverted_index.secondary | 35 |
| abstract_inverted_index.shrinkage | 14 |
| abstract_inverted_index.Anaplastic | 1 |
| abstract_inverted_index.Resistance | 32 |
| abstract_inverted_index.activation | 40 |
| abstract_inverted_index.alectinib, | 96 |
| abstract_inverted_index.expression | 69, 212, 222 |
| abstract_inverted_index.identified | 63 |
| abstract_inverted_index.inevitably | 23 |
| abstract_inverted_index.inhibitors | 18 |
| abstract_inverted_index.mechanisms | 33 |
| abstract_inverted_index.production | 231 |
| abstract_inverted_index.rearranged | 5 |
| abstract_inverted_index.resistance | 94 |
| abstract_inverted_index.sequencing | 173 |
| abstract_inverted_index.treatment, | 200 |
| abstract_inverted_index.treatment. | 136, 150 |
| abstract_inverted_index.accelerated | 145 |
| abstract_inverted_index.contributes | 235 |
| abstract_inverted_index.development | 28 |
| abstract_inverted_index.expression. | 170 |
| abstract_inverted_index.fibroblasts | 178 |
| abstract_inverted_index.macrophages | 185 |
| abstract_inverted_index.non‐small | 6 |
| abstract_inverted_index.resistance. | 31, 239 |
| abstract_inverted_index.significant | 65 |
| abstract_inverted_index.infiltration | 204 |
| abstract_inverted_index.upregulating | 215 |
| abstract_inverted_index.Single‐cell | 171 |
| abstract_inverted_index.gilteritinib. | 111 |
| abstract_inverted_index.substantially | 214 |
| abstract_inverted_index.ALK‐tyrosine | 16 |
| abstract_inverted_index.subcutaneously | 121 |
| abstract_inverted_index.simultaneously, | 132 |
| abstract_inverted_index.supplementation | 102 |
| abstract_inverted_index.ALK‐rearranged | 89 |
| abstract_inverted_index.AXL‐expressing | 117 |
| abstract_inverted_index.microenvironment | 196 |
| abstract_inverted_index.tumor‐associated | 184 |
| abstract_inverted_index.cancer‐associated | 177 |
| abstract_inverted_index.AXL‐overexpressing | 87, 156 |
| abstract_inverted_index.GAS6‐overexpressing | 113, 154 |
| abstract_inverted_index.alectinib‐resistant | 59 |
| cited_by_percentile_year | |
| corresponding_author_ids | https://openalex.org/A5011207225 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 7 |
| corresponding_institution_ids | https://openalex.org/I74801974 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.8500000238418579 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.0382303 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |