TGF-[beta] signaling in the tumor metabolic microenvironment and targeted therapies
Transforming growth factor-[beta] (TGF-[beta]) signaling has a paradoxical role in cancer progression, and it acts as a tumor suppressor in the early stages but a tumor promoter in the late stages of cancer. Once cancer cells are generated, TGF-[beta] signaling is responsible for the orchestration o...
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| Veröffentlicht in: | Journal of hematology and oncology 2022-09, Vol.15 (1) |
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| container_title | Journal of hematology and oncology |
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| creator | Shi, Xueke Yang, Jin Deng, Shuzhi Xu, Hongdan Wu, Deyang Zeng, Qingxiang Wang, Shimeng Hu, Tao Wu, Fanglong Zhou, Hongmei |
| description | Transforming growth factor-[beta] (TGF-[beta]) signaling has a paradoxical role in cancer progression, and it acts as a tumor suppressor in the early stages but a tumor promoter in the late stages of cancer. Once cancer cells are generated, TGF-[beta] signaling is responsible for the orchestration of the immunosuppressive tumor microenvironment (TME) and supports cancer growth, invasion, metastasis, recurrence, and therapy resistance. These progressive behaviors are driven by an "engine" of the metabolic reprogramming in cancer. Recent studies have revealed that TGF-[beta] signaling regulates cancer metabolic reprogramming and is a metabolic driver in the tumor metabolic microenvironment (TMME). Intriguingly, TGF-[beta] ligands act as an "endocrine" cytokine and influence host metabolism. Therefore, having insight into the role of TGF-[beta] signaling in the TMME is instrumental for acknowledging its wide range of effects and designing new cancer treatment strategies. Herein, we try to illustrate the concise definition of TMME based on the published literature. Then, we review the metabolic reprogramming in the TMME and elaborate on the contribution of TGF-[beta] to metabolic rewiring at the cellular (intracellular), tissular (intercellular), and organismal (cancer-host) levels. Furthermore, we propose three potential applications of targeting TGF-[beta]-dependent mechanism reprogramming, paving the way for TGF-[beta]-related antitumor therapy from the perspective of metabolism. Keywords: TGF-[beta] signaling, Tumor metabolic microenvironment, Cancer cell, Stromal cell, Host metabolism |
| doi_str_mv | 10.1186/s13045-022-01349-6 |
| format | Article |
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Once cancer cells are generated, TGF-[beta] signaling is responsible for the orchestration of the immunosuppressive tumor microenvironment (TME) and supports cancer growth, invasion, metastasis, recurrence, and therapy resistance. These progressive behaviors are driven by an "engine" of the metabolic reprogramming in cancer. Recent studies have revealed that TGF-[beta] signaling regulates cancer metabolic reprogramming and is a metabolic driver in the tumor metabolic microenvironment (TMME). Intriguingly, TGF-[beta] ligands act as an "endocrine" cytokine and influence host metabolism. Therefore, having insight into the role of TGF-[beta] signaling in the TMME is instrumental for acknowledging its wide range of effects and designing new cancer treatment strategies. Herein, we try to illustrate the concise definition of TMME based on the published literature. Then, we review the metabolic reprogramming in the TMME and elaborate on the contribution of TGF-[beta] to metabolic rewiring at the cellular (intracellular), tissular (intercellular), and organismal (cancer-host) levels. Furthermore, we propose three potential applications of targeting TGF-[beta]-dependent mechanism reprogramming, paving the way for TGF-[beta]-related antitumor therapy from the perspective of metabolism. 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Once cancer cells are generated, TGF-[beta] signaling is responsible for the orchestration of the immunosuppressive tumor microenvironment (TME) and supports cancer growth, invasion, metastasis, recurrence, and therapy resistance. These progressive behaviors are driven by an "engine" of the metabolic reprogramming in cancer. Recent studies have revealed that TGF-[beta] signaling regulates cancer metabolic reprogramming and is a metabolic driver in the tumor metabolic microenvironment (TMME). Intriguingly, TGF-[beta] ligands act as an "endocrine" cytokine and influence host metabolism. Therefore, having insight into the role of TGF-[beta] signaling in the TMME is instrumental for acknowledging its wide range of effects and designing new cancer treatment strategies. Herein, we try to illustrate the concise definition of TMME based on the published literature. Then, we review the metabolic reprogramming in the TMME and elaborate on the contribution of TGF-[beta] to metabolic rewiring at the cellular (intracellular), tissular (intercellular), and organismal (cancer-host) levels. Furthermore, we propose three potential applications of targeting TGF-[beta]-dependent mechanism reprogramming, paving the way for TGF-[beta]-related antitumor therapy from the perspective of metabolism. 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Once cancer cells are generated, TGF-[beta] signaling is responsible for the orchestration of the immunosuppressive tumor microenvironment (TME) and supports cancer growth, invasion, metastasis, recurrence, and therapy resistance. These progressive behaviors are driven by an "engine" of the metabolic reprogramming in cancer. Recent studies have revealed that TGF-[beta] signaling regulates cancer metabolic reprogramming and is a metabolic driver in the tumor metabolic microenvironment (TMME). Intriguingly, TGF-[beta] ligands act as an "endocrine" cytokine and influence host metabolism. Therefore, having insight into the role of TGF-[beta] signaling in the TMME is instrumental for acknowledging its wide range of effects and designing new cancer treatment strategies. Herein, we try to illustrate the concise definition of TMME based on the published literature. Then, we review the metabolic reprogramming in the TMME and elaborate on the contribution of TGF-[beta] to metabolic rewiring at the cellular (intracellular), tissular (intercellular), and organismal (cancer-host) levels. Furthermore, we propose three potential applications of targeting TGF-[beta]-dependent mechanism reprogramming, paving the way for TGF-[beta]-related antitumor therapy from the perspective of metabolism. Keywords: TGF-[beta] signaling, Tumor metabolic microenvironment, Cancer cell, Stromal cell, Host metabolism</abstract><pub>BioMed Central Ltd</pub><doi>10.1186/s13045-022-01349-6</doi></addata></record> |
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| source | DOAJ Directory of Open Access Journals; SpringerLink Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access; Springer Nature OA Free Journals |
| subjects | Bone morphogenetic proteins Cancer Development and progression Physiological aspects Transforming growth factors |
| title | TGF-[beta] signaling in the tumor metabolic microenvironment and targeted therapies |
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