LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis
Abstract Pancreatic cancer (PC) is a common malignant cancer characterized by high mortality and poor prognosis. LINC00690 was involved in the occurrence and progression of PC, but the underlying mechanisms require further investigation. The goal of this study was to figure out how LINC00960 mediate...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2022-12-01
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| Series: | Kaohsiung Journal of Medical Sciences |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/kjm2.12594 |
| _version_ | 1798006480480239616 |
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| author | Bin Zhou Jing‐Hao Lei Qiang Wang Teng‐Fei Qu Li‐Chao Cha Han‐Xiang Zhan Shang‐Long Liu Xiao Hu Chuan‐Dong Sun Jing‐Yu Cao Fa‐Bo Qiu Wei‐Dong Guo |
| author_facet | Bin Zhou Jing‐Hao Lei Qiang Wang Teng‐Fei Qu Li‐Chao Cha Han‐Xiang Zhan Shang‐Long Liu Xiao Hu Chuan‐Dong Sun Jing‐Yu Cao Fa‐Bo Qiu Wei‐Dong Guo |
| author_sort | Bin Zhou |
| collection | DOAJ |
| description | Abstract Pancreatic cancer (PC) is a common malignant cancer characterized by high mortality and poor prognosis. LINC00690 was involved in the occurrence and progression of PC, but the underlying mechanisms require further investigation. The goal of this study was to figure out how LINC00960 mediates glycolysis in PC. LINC00960, miR‐326‐3p, and Tuftelin 1 (TUFT1) expression levels were detected in PC cell lines. LINC00960 and TUFT1 expression levels were increased in PC cells when compared with normal pancreatic cells, whereas miR‐326‐3p expression levels were decreased. The expression levels of LINC00690 affected glycolysis in PC, and inhibition of LINC00960 inhibited tumor growth in vivo. LINC00690 targeted and suppressed the expression of miR‐326‐3p. MiR‐326‐3p bound to TUFT1, and miR‐326‐3p inhibited AKT–mTOR pathway activation via TUFT1. In conclusion, the depletion of LINC00960 repressed cell proliferation and glycolysis in PC by mediating the miR‐326‐3p/TUFT1/AKT–mTOR axis. Thus, we present a novel mechanism underlying the progression of PC that suggests LINC00960 is a potential therapeutic target for this cancer. |
| first_indexed | 2024-04-11T12:56:29Z |
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| id | doaj.art-d9b526984b6142ad9eaee0c1da6b841c |
| institution | Directory Open Access Journal |
| issn | 1607-551X 2410-8650 |
| language | English |
| last_indexed | 2024-04-11T12:56:29Z |
| publishDate | 2022-12-01 |
| publisher | Wiley |
| record_format | Article |
| series | Kaohsiung Journal of Medical Sciences |
| spelling | doaj.art-d9b526984b6142ad9eaee0c1da6b841c2022-12-22T04:23:04ZengWileyKaohsiung Journal of Medical Sciences1607-551X2410-86502022-12-0138121155116710.1002/kjm2.12594LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axisBin Zhou0Jing‐Hao Lei1Qiang Wang2Teng‐Fei Qu3Li‐Chao Cha4Han‐Xiang Zhan5Shang‐Long Liu6Xiao Hu7Chuan‐Dong Sun8Jing‐Yu Cao9Fa‐Bo Qiu10Wei‐Dong Guo11Department of Hepatobiliary and Pancreatic Surgery and Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaDepartment of Hepatobiliary and Pancreatic Surgery and Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaDepartment of Anesthesiology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing People's Republic of ChinaDepartment of Hepatobiliary and Pancreatic Surgery and Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaDepartment of Hepatobiliary and Pancreatic Surgery and Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaDepartment of General Surgery Qilu Hospital, Shandong University Jinan People's Republic of ChinaDepartment of General Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaDepartment of Hepatobiliary and Pancreatic Surgery and Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaDepartment of Hepatobiliary and Pancreatic Surgery and Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaDepartment of Hepatobiliary and Pancreatic Surgery and Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaDepartment of Hepatobiliary and Pancreatic Surgery and Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaDepartment of Hepatobiliary and Pancreatic Surgery and Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao People's Republic of ChinaAbstract Pancreatic cancer (PC) is a common malignant cancer characterized by high mortality and poor prognosis. LINC00690 was involved in the occurrence and progression of PC, but the underlying mechanisms require further investigation. The goal of this study was to figure out how LINC00960 mediates glycolysis in PC. LINC00960, miR‐326‐3p, and Tuftelin 1 (TUFT1) expression levels were detected in PC cell lines. LINC00960 and TUFT1 expression levels were increased in PC cells when compared with normal pancreatic cells, whereas miR‐326‐3p expression levels were decreased. The expression levels of LINC00690 affected glycolysis in PC, and inhibition of LINC00960 inhibited tumor growth in vivo. LINC00690 targeted and suppressed the expression of miR‐326‐3p. MiR‐326‐3p bound to TUFT1, and miR‐326‐3p inhibited AKT–mTOR pathway activation via TUFT1. In conclusion, the depletion of LINC00960 repressed cell proliferation and glycolysis in PC by mediating the miR‐326‐3p/TUFT1/AKT–mTOR axis. Thus, we present a novel mechanism underlying the progression of PC that suggests LINC00960 is a potential therapeutic target for this cancer.https://doi.org/10.1002/kjm2.12594glycolysisLINC00960miR‐326‐3ppancreatic cancerTUFT1 |
| spellingShingle | Bin Zhou Jing‐Hao Lei Qiang Wang Teng‐Fei Qu Li‐Chao Cha Han‐Xiang Zhan Shang‐Long Liu Xiao Hu Chuan‐Dong Sun Jing‐Yu Cao Fa‐Bo Qiu Wei‐Dong Guo LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis Kaohsiung Journal of Medical Sciences glycolysis LINC00960 miR‐326‐3p pancreatic cancer TUFT1 |
| title | LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis |
| title_full | LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis |
| title_fullStr | LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis |
| title_full_unstemmed | LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis |
| title_short | LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR‐326‐3p/TUFT1/AKT–mTOR axis |
| title_sort | linc00960 regulates cell proliferation and glycolysis in pancreatic cancer through the mir 326 3p tuft1 akt mtor axis |
| topic | glycolysis LINC00960 miR‐326‐3p pancreatic cancer TUFT1 |
| url | https://doi.org/10.1002/kjm2.12594 |
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