Novel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancer
The pathogenesis of pancreatic cancer involves substantial metabolic reprogramming, resulting in abnormal proliferation of tumor cells. This tumorigenic reprogramming is often driven by genetic mutations, such as activating mutations of the KRAS oncogene and inactivating or delet...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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China Science Publishing & Media Ltd.
2023-04-01
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| Series: | Acta Biochimica et Biophysica Sinica |
| Subjects: | |
| Online Access: | https://www.sciengine.com/doi/10.3724/abbs.2023045 |
| _version_ | 1797635884730810368 |
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| author | Guo Duancheng Ye Longyun Wu Weiding Yu Xianjun Jin Kaizhou |
| author_facet | Guo Duancheng Ye Longyun Wu Weiding Yu Xianjun Jin Kaizhou |
| author_sort | Guo Duancheng |
| collection | DOAJ |
| description | The pathogenesis of pancreatic cancer involves substantial metabolic reprogramming, resulting in abnormal proliferation of tumor cells. This tumorigenic reprogramming is often driven by genetic mutations, such as activating mutations of the KRAS oncogene and inactivating or deletions of the tumor suppressor genes SMAD4, CDKN2A, and TP53, which play a critical role in the initiation and development of pancreatic cancer. As a normal cell gradually develops into a cancer cell, a series of signature characteristics are acquired: activation of signaling pathways that sustain proliferation; an ability to resist growth inhibitory signals and evade apoptosis; and an ability to generate new blood vessels and invade and metastasize. In addition to these features, recent research has revealed that metabolic reprogramming and immune escape are two other novel characteristics of tumor cells. The effect of the interactions between tumor and immune cells on metabolic reprogramming is a key factor determining the antitumor immunotherapy response. Lipid metabolism reprogramming, a feature of many malignancies, not only plays a role in maintaining tumor cell proliferation but also alters the tumor microenvironment by inducing the release of metabolites that in turn affect the metabolism of normal immune cells, ultimately leading to the attenuation of the antitumor immune response and resistance to immunotherapy. Pancreatic cancer has been found to have substantial lipid metabolism reprogramming, but the mechanisms remain elusive. Therefore, this review focuses on the mechanisms regulating lipid metabolism reprogramming in pancreatic cancer cells to provide new therapeutic targets and aid the development of new therapeutic strategies for pancreatic cancer. |
| first_indexed | 2024-03-11T12:26:28Z |
| format | Article |
| id | doaj.art-31f1afbfffd045af973b24681c922a0c |
| institution | Directory Open Access Journal |
| issn | 1672-9145 |
| language | English |
| last_indexed | 2024-03-11T12:26:28Z |
| publishDate | 2023-04-01 |
| publisher | China Science Publishing & Media Ltd. |
| record_format | Article |
| series | Acta Biochimica et Biophysica Sinica |
| spelling | doaj.art-31f1afbfffd045af973b24681c922a0c2023-11-06T08:40:11ZengChina Science Publishing & Media Ltd.Acta Biochimica et Biophysica Sinica1672-91452023-04-015592393710.3724/abbs.202304520d259ccNovel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancerGuo Duancheng0Ye Longyun1Wu Weiding2Yu Xianjun3Jin Kaizhou4["Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China","Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China","Shanghai Pancreatic Cancer Institute, Shanghai 200032, China","Pancreatic Cancer Institute, Fudan University, Shanghai 200032, China"]["Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China","Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China","Shanghai Pancreatic Cancer Institute, Shanghai 200032, China","Pancreatic Cancer Institute, Fudan University, Shanghai 200032, China"]["Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China","Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China","Shanghai Pancreatic Cancer Institute, Shanghai 200032, China","Pancreatic Cancer Institute, Fudan University, Shanghai 200032, China"]["Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China","Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China","Shanghai Pancreatic Cancer Institute, Shanghai 200032, China","Pancreatic Cancer Institute, Fudan University, Shanghai 200032, China"]["Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China","Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China","Shanghai Pancreatic Cancer Institute, Shanghai 200032, China","Pancreatic Cancer Institute, Fudan University, Shanghai 200032, China"]The pathogenesis of pancreatic cancer involves substantial metabolic reprogramming, resulting in abnormal proliferation of tumor cells. This tumorigenic reprogramming is often driven by genetic mutations, such as activating mutations of the KRAS oncogene and inactivating or deletions of the tumor suppressor genes SMAD4, CDKN2A, and TP53, which play a critical role in the initiation and development of pancreatic cancer. As a normal cell gradually develops into a cancer cell, a series of signature characteristics are acquired: activation of signaling pathways that sustain proliferation; an ability to resist growth inhibitory signals and evade apoptosis; and an ability to generate new blood vessels and invade and metastasize. In addition to these features, recent research has revealed that metabolic reprogramming and immune escape are two other novel characteristics of tumor cells. The effect of the interactions between tumor and immune cells on metabolic reprogramming is a key factor determining the antitumor immunotherapy response. Lipid metabolism reprogramming, a feature of many malignancies, not only plays a role in maintaining tumor cell proliferation but also alters the tumor microenvironment by inducing the release of metabolites that in turn affect the metabolism of normal immune cells, ultimately leading to the attenuation of the antitumor immune response and resistance to immunotherapy. Pancreatic cancer has been found to have substantial lipid metabolism reprogramming, but the mechanisms remain elusive. Therefore, this review focuses on the mechanisms regulating lipid metabolism reprogramming in pancreatic cancer cells to provide new therapeutic targets and aid the development of new therapeutic strategies for pancreatic cancer. https://www.sciengine.com/doi/10.3724/abbs.2023045pancreatic cancerlipid metabolism reprogrammingtumor microenvironmentimmune escapedrug resistance |
| spellingShingle | Guo Duancheng Ye Longyun Wu Weiding Yu Xianjun Jin Kaizhou Novel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancer Acta Biochimica et Biophysica Sinica pancreatic cancer lipid metabolism reprogramming tumor microenvironment immune escape drug resistance |
| title | Novel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancer |
| title_full | Novel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancer |
| title_fullStr | Novel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancer |
| title_full_unstemmed | Novel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancer |
| title_short | Novel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancer |
| title_sort | novel strategy for oncogenic alteration induced lipid metabolism reprogramming in pancreatic cancer |
| topic | pancreatic cancer lipid metabolism reprogramming tumor microenvironment immune escape drug resistance |
| url | https://www.sciengine.com/doi/10.3724/abbs.2023045 |
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