Data from Radiation-Induced Myofibroblasts Promote Tumor Growth via Mitochondrial ROS–Activated TGFβ Signaling Article Swipe
Tsutomu Shimura
,
Megumi Sasatani
,
Hidehiko Kawai
,
Kenji Kamiya
,
Junya Kobayashi
,
Kenshi Komatsu
,
Naoki Kunugita
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1541-7786.c.6541323
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1541-7786.c.6541323
Fibroblasts are a key stromal cell in the tumor microenvironment (TME) and promote tumor growth via release of various growth factors. Stromal fibroblasts in cancer, called cancer-associated fibroblasts (CAF), are related to myofibroblasts, an activated form of fibroblast. While investigating the role of stroma fibroblasts on radiation-related carcinogenesis, it was observed following long-term fractionated radiation (FR) that the morphology of human diploid fibroblasts changed from smaller spindle shapes to larger flat shapes. These cells expressed smooth muscle actin (α-SMA) and platelet-derived growth factor receptors, markers of myofibroblasts and CAFs, respectively. Long-term FR induces progressive damage to the fibroblast nucleus and mitochondria via increases in mitochondrial reactive oxygen species (ROS) levels. Here, it is demonstrated that long-term FR-induced α-SMA–positive cells have decreased mitochondrial membrane potential and activated oxidative stress responses. Antioxidant N-acetyl cysteine suppressed radiation-induced mitochondrial damage and generation of myofibroblasts. These results indicate that mitochondrial ROS are associated with the acquisition of myofibroblasts after long-term FR. Mechanistically, mitochondrial ROS activated TGFβ signaling which in turn mediated the expression of α-SMA in radiation-induced myofibroblasts. Finally, in vivo tumor growth analysis in a human tumor xenograft model system revealed that long-term FR-induced myofibroblasts promote tumor growth by enhancing angiogenesis.Implications: Radiation affects malignant cancer cells directly and indirectly via molecular alterations in stromal fibroblasts such as activation of TGFβ and angiogenic signaling pathways. Mol Cancer Res; 16(11); 1676–86. ©2018 AACR.
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- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1158/1541-7786.c.6541323
- OA Status
- gold
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- OpenAlex ID
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https://openalex.org/W4362541890Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1158/1541-7786.c.6541323Digital Object Identifier
- Title
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Data from Radiation-Induced Myofibroblasts Promote Tumor Growth via Mitochondrial ROS–Activated TGFβ SignalingWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2023Year of publication
- Publication date
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2023-04-03Full publication date if available
- Authors
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Tsutomu Shimura, Megumi Sasatani, Hidehiko Kawai, Kenji Kamiya, Junya Kobayashi, Kenshi Komatsu, Naoki KunugitaList of authors in order
- Landing page
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https://doi.org/10.1158/1541-7786.c.6541323Publisher landing page
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://doi.org/10.1158/1541-7786.c.6541323Direct OA link when available
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Myofibroblast, Stromal cell, Cell biology, Tumor microenvironment, Transforming growth factor, Chemistry, Mitochondrion, Mitochondrial ROS, Fibroblast, Cancer research, Biology, Pathology, Fibrosis, In vitro, Biochemistry, Medicine, Tumor cellsTop concepts (fields/topics) attached by OpenAlex
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.xenograft | 183 |
| abstract_inverted_index.1676–86. | 224 |
| abstract_inverted_index.FR-induced | 116, 189 |
| abstract_inverted_index.activation | 213 |
| abstract_inverted_index.angiogenic | 217 |
| abstract_inverted_index.associated | 147 |
| abstract_inverted_index.expression | 167 |
| abstract_inverted_index.fibroblast | 97 |
| abstract_inverted_index.generation | 137 |
| abstract_inverted_index.indirectly | 204 |
| abstract_inverted_index.morphology | 58 |
| abstract_inverted_index.receptors, | 83 |
| abstract_inverted_index.responses. | 128 |
| abstract_inverted_index.suppressed | 132 |
| abstract_inverted_index.<i>in | 174 |
| abstract_inverted_index.Antioxidant | 129 |
| abstract_inverted_index.acquisition | 150 |
| abstract_inverted_index.alterations | 207 |
| abstract_inverted_index.fibroblast. | 37 |
| abstract_inverted_index.fibroblasts | 22, 27, 44, 62, 210 |
| abstract_inverted_index.progressive | 93 |
| abstract_inverted_index.<i>Mol | 220 |
| abstract_inverted_index.demonstrated | 113 |
| abstract_inverted_index.fractionated | 53 |
| abstract_inverted_index.mitochondria | 100 |
| abstract_inverted_index.investigating | 39 |
| abstract_inverted_index.mitochondrial | 104, 121, 134, 144, 157 |
| abstract_inverted_index.respectively. | 89 |
| abstract_inverted_index.myofibroblasts | 86, 152, 190 |
| abstract_inverted_index.vivo</i> | 175 |
| abstract_inverted_index.carcinogenesis, | 47 |
| abstract_inverted_index.myofibroblasts, | 32 |
| abstract_inverted_index.myofibroblasts. | 139, 172 |
| abstract_inverted_index.Mechanistically, | 156 |
| abstract_inverted_index.microenvironment | 9 |
| abstract_inverted_index.platelet-derived | 80 |
| abstract_inverted_index.cancer-associated | 26 |
| abstract_inverted_index.radiation-induced | 133, 171 |
| abstract_inverted_index.radiation-related | 46 |
| abstract_inverted_index.α-SMA–positive | 117 |
| abstract_inverted_index.AACR</i>.</p></div> | 226 |
| abstract_inverted_index.<div>Abstract<p>Fibroblasts | 0 |
| abstract_inverted_index.angiogenesis.</p><p><b>Implications:</b> | 196 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 7 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.5 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.12700349 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |