Autophagy inhibition and reactive oxygen species elimination by acetyl-CoA acetyltransferase 1 through fused in sarcoma protein to promote prostate cancer
Abstract Background Prostate cancer is a major health issue affecting the male population worldwide, and its etiology remains relatively unknown. As presented on the Gene Expression Profiling Interactive Analysis database, acetyl-CoA acetyltransferase 1 (ACAT1) acts as a prostate cancer-promoting fa...
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| Format: | Article |
| Language: | English |
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BMC
2022-12-01
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| Series: | BMC Cancer |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12885-022-10426-5 |
| _version_ | 1798004941034356736 |
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| author | Jingqian Guan Xizi Jiang Yaoxing Guo Wenhui Zhao Ji Li Yizhuo Li Ming Cheng Lin Fu Yue Zhao Qingchang Li |
| author_facet | Jingqian Guan Xizi Jiang Yaoxing Guo Wenhui Zhao Ji Li Yizhuo Li Ming Cheng Lin Fu Yue Zhao Qingchang Li |
| author_sort | Jingqian Guan |
| collection | DOAJ |
| description | Abstract Background Prostate cancer is a major health issue affecting the male population worldwide, and its etiology remains relatively unknown. As presented on the Gene Expression Profiling Interactive Analysis database, acetyl-CoA acetyltransferase 1 (ACAT1) acts as a prostate cancer-promoting factor. ACAT1 expression in prostate cancer tissues is considerably higher than that in normal tissues, leading to a poor prognosis in patients with prostate cancer. Here, we aimed to study the role of the ACAT1-fused in sarcoma (FUS) complex in prostate cancer and identify new targets for the diagnosis and treatment of the disease. Methods We conducted immunohistochemical analysis of 57 clinical samples and in vitro and in vivo experiments using a mouse model and plasmid constructs to determine the expression of ACAT1 in prostate cancer. Results The relationship between the expression of ACAT1 and the Gleason score was significant. The expression of ACAT1 was higher in tissues with a Gleason score of > 7 than in tissues with a Gleason score of ≤7 (P = 0.0011). In addition, we revealed that ACAT1 can interact with the FUS protein. Conclusions In prostate cancer, ACAT1 promotes the expression of P62 and Nrf2 through FUS and affects reactive oxygen species scavenging. These effects are due to the inhibition of autophagy by ACAT1. That is, ACAT1 promotes prostate cancer by inhibiting autophagy and eliminating active oxygen species. The expression of ACAT1 is related to prostate cancer. Studying the underlying mechanism may provide a new perspective on the treatment of prostate cancer. |
| first_indexed | 2024-04-11T12:31:34Z |
| format | Article |
| id | doaj.art-ac449d02b7754283844851d4d434765e |
| institution | Directory Open Access Journal |
| issn | 1471-2407 |
| language | English |
| last_indexed | 2024-04-11T12:31:34Z |
| publishDate | 2022-12-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Cancer |
| spelling | doaj.art-ac449d02b7754283844851d4d434765e2022-12-22T04:23:44ZengBMCBMC Cancer1471-24072022-12-0122111310.1186/s12885-022-10426-5Autophagy inhibition and reactive oxygen species elimination by acetyl-CoA acetyltransferase 1 through fused in sarcoma protein to promote prostate cancerJingqian Guan0Xizi Jiang1Yaoxing Guo2Wenhui Zhao3Ji Li4Yizhuo Li5Ming Cheng6Lin Fu7Yue Zhao8Qingchang Li9Department of Pathology, College of Basic Medical Sciences, China Medical UniversityDepartment of Pathology, The First Hospital of China Medical UniversityDepartment of Pathology, College of Basic Medical Sciences, China Medical UniversityDepartment of Pathology, College of Basic Medical Sciences, China Medical UniversityDepartment of Pathology, College of Basic Medical Sciences, China Medical UniversityDepartment of Pathology, College of Basic Medical Sciences, China Medical UniversityDepartment of Pathology, College of Basic Medical Sciences, China Medical UniversityDepartment of Pathology, College of Basic Medical Sciences, China Medical UniversityDepartment of Pathology, College of Basic Medical Sciences, China Medical UniversityDepartment of Pathology, College of Basic Medical Sciences, China Medical UniversityAbstract Background Prostate cancer is a major health issue affecting the male population worldwide, and its etiology remains relatively unknown. As presented on the Gene Expression Profiling Interactive Analysis database, acetyl-CoA acetyltransferase 1 (ACAT1) acts as a prostate cancer-promoting factor. ACAT1 expression in prostate cancer tissues is considerably higher than that in normal tissues, leading to a poor prognosis in patients with prostate cancer. Here, we aimed to study the role of the ACAT1-fused in sarcoma (FUS) complex in prostate cancer and identify new targets for the diagnosis and treatment of the disease. Methods We conducted immunohistochemical analysis of 57 clinical samples and in vitro and in vivo experiments using a mouse model and plasmid constructs to determine the expression of ACAT1 in prostate cancer. Results The relationship between the expression of ACAT1 and the Gleason score was significant. The expression of ACAT1 was higher in tissues with a Gleason score of > 7 than in tissues with a Gleason score of ≤7 (P = 0.0011). In addition, we revealed that ACAT1 can interact with the FUS protein. Conclusions In prostate cancer, ACAT1 promotes the expression of P62 and Nrf2 through FUS and affects reactive oxygen species scavenging. These effects are due to the inhibition of autophagy by ACAT1. That is, ACAT1 promotes prostate cancer by inhibiting autophagy and eliminating active oxygen species. The expression of ACAT1 is related to prostate cancer. Studying the underlying mechanism may provide a new perspective on the treatment of prostate cancer.https://doi.org/10.1186/s12885-022-10426-5AutophagyReactive oxygen speciesACAT1FUSProstate cancer |
| spellingShingle | Jingqian Guan Xizi Jiang Yaoxing Guo Wenhui Zhao Ji Li Yizhuo Li Ming Cheng Lin Fu Yue Zhao Qingchang Li Autophagy inhibition and reactive oxygen species elimination by acetyl-CoA acetyltransferase 1 through fused in sarcoma protein to promote prostate cancer BMC Cancer Autophagy Reactive oxygen species ACAT1 FUS Prostate cancer |
| title | Autophagy inhibition and reactive oxygen species elimination by acetyl-CoA acetyltransferase 1 through fused in sarcoma protein to promote prostate cancer |
| title_full | Autophagy inhibition and reactive oxygen species elimination by acetyl-CoA acetyltransferase 1 through fused in sarcoma protein to promote prostate cancer |
| title_fullStr | Autophagy inhibition and reactive oxygen species elimination by acetyl-CoA acetyltransferase 1 through fused in sarcoma protein to promote prostate cancer |
| title_full_unstemmed | Autophagy inhibition and reactive oxygen species elimination by acetyl-CoA acetyltransferase 1 through fused in sarcoma protein to promote prostate cancer |
| title_short | Autophagy inhibition and reactive oxygen species elimination by acetyl-CoA acetyltransferase 1 through fused in sarcoma protein to promote prostate cancer |
| title_sort | autophagy inhibition and reactive oxygen species elimination by acetyl coa acetyltransferase 1 through fused in sarcoma protein to promote prostate cancer |
| topic | Autophagy Reactive oxygen species ACAT1 FUS Prostate cancer |
| url | https://doi.org/10.1186/s12885-022-10426-5 |
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