LncRNA LZTS1-AS1 induces proliferation, metastasis and inhibits autophagy of pancreatic cancer cells through the miR-532 /TWIST1 signaling pathway
Abstract The 5 year survival rate after diagnosis of pancreatic cancer (PANC) is less than 5%, and it is one of the malignant tumors with the worst prognosis. Identification of novel oncogenes involved in the occurrence of pancreatic cancer is of great significance to improve the overall survival of...
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BMC
2023-07-01
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Series: | Cancer Cell International |
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Online Access: | https://doi.org/10.1186/s12935-023-02979-7 |
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author | Hui Wu Anshu Li Qichang Zheng Jingyang Gu Wei Zhou |
author_facet | Hui Wu Anshu Li Qichang Zheng Jingyang Gu Wei Zhou |
author_sort | Hui Wu |
collection | DOAJ |
description | Abstract The 5 year survival rate after diagnosis of pancreatic cancer (PANC) is less than 5%, and it is one of the malignant tumors with the worst prognosis. Identification of novel oncogenes involved in the occurrence of pancreatic cancer is of great significance to improve the overall survival of PANC patients. Our previous study found that miR-532 is a key factor in PANC occurrence and development, and this study further explored its mechanism. We found that the expression of lncRNA LZTS1-AS1 was elevated in PANC tumor tissues and cells, and correlated with poor prognosis. In vitro experiments confirmed that LZTS1-AS1 could promote proliferation, oncogenicity, migration, and invasion of PANC cells, and inhibit apoptosis and autophagy. However, miR-532 had the completely opposite effect, and inhibition of miR-532 counteracted the effect of LZTS1-AS1 on PANC cells. Dual luciferase gene reporter assay and RNA immunoprecipitation assay confirmed the targeting relationship between LZTS1-AS1 and miR-532, and their expression levels were negatively correlated in PANC tissues. Overexpression of TWIST1 could counteract the effect of miR-532 in PANC cells, and the expression levels of both were negatively changed in PANC tissues and cells. Our results suggest that lncRNA LZTS1-AS1 acts as an oncogene to promote the metastasis of PANC and inhibit autophagy, and its mechanism may be to regulate TWIST1 through sponge miR-532. This study provides novel biomarkers and therapeutic targets for PANC. |
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issn | 1475-2867 |
language | English |
last_indexed | 2024-03-13T00:39:47Z |
publishDate | 2023-07-01 |
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spelling | doaj.art-89a385f0818846dc988691e326eb4cdf2023-07-09T11:25:39ZengBMCCancer Cell International1475-28672023-07-0123111410.1186/s12935-023-02979-7LncRNA LZTS1-AS1 induces proliferation, metastasis and inhibits autophagy of pancreatic cancer cells through the miR-532 /TWIST1 signaling pathwayHui Wu0Anshu Li1Qichang Zheng2Jingyang Gu3Wei Zhou4Research Center, Shanghai Healink Medical Information Consulting Co., LTDDepartment of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and TechnologyLiver Transplantation Center, Union Hospital, Tongji Medical College, Huazhong University of Science and TechnologyLiver Transplantation Center, Union Hospital, Tongji Medical College, Huazhong University of Science and TechnologyDepartment of Pancreatic Surgery, Wuhan No.1 HospitalAbstract The 5 year survival rate after diagnosis of pancreatic cancer (PANC) is less than 5%, and it is one of the malignant tumors with the worst prognosis. Identification of novel oncogenes involved in the occurrence of pancreatic cancer is of great significance to improve the overall survival of PANC patients. Our previous study found that miR-532 is a key factor in PANC occurrence and development, and this study further explored its mechanism. We found that the expression of lncRNA LZTS1-AS1 was elevated in PANC tumor tissues and cells, and correlated with poor prognosis. In vitro experiments confirmed that LZTS1-AS1 could promote proliferation, oncogenicity, migration, and invasion of PANC cells, and inhibit apoptosis and autophagy. However, miR-532 had the completely opposite effect, and inhibition of miR-532 counteracted the effect of LZTS1-AS1 on PANC cells. Dual luciferase gene reporter assay and RNA immunoprecipitation assay confirmed the targeting relationship between LZTS1-AS1 and miR-532, and their expression levels were negatively correlated in PANC tissues. Overexpression of TWIST1 could counteract the effect of miR-532 in PANC cells, and the expression levels of both were negatively changed in PANC tissues and cells. Our results suggest that lncRNA LZTS1-AS1 acts as an oncogene to promote the metastasis of PANC and inhibit autophagy, and its mechanism may be to regulate TWIST1 through sponge miR-532. This study provides novel biomarkers and therapeutic targets for PANC.https://doi.org/10.1186/s12935-023-02979-7AutophagylncRNA LZTS1-AS1miR-532Pancreatic cancer |
spellingShingle | Hui Wu Anshu Li Qichang Zheng Jingyang Gu Wei Zhou LncRNA LZTS1-AS1 induces proliferation, metastasis and inhibits autophagy of pancreatic cancer cells through the miR-532 /TWIST1 signaling pathway Cancer Cell International Autophagy lncRNA LZTS1-AS1 miR-532 Pancreatic cancer |
title | LncRNA LZTS1-AS1 induces proliferation, metastasis and inhibits autophagy of pancreatic cancer cells through the miR-532 /TWIST1 signaling pathway |
title_full | LncRNA LZTS1-AS1 induces proliferation, metastasis and inhibits autophagy of pancreatic cancer cells through the miR-532 /TWIST1 signaling pathway |
title_fullStr | LncRNA LZTS1-AS1 induces proliferation, metastasis and inhibits autophagy of pancreatic cancer cells through the miR-532 /TWIST1 signaling pathway |
title_full_unstemmed | LncRNA LZTS1-AS1 induces proliferation, metastasis and inhibits autophagy of pancreatic cancer cells through the miR-532 /TWIST1 signaling pathway |
title_short | LncRNA LZTS1-AS1 induces proliferation, metastasis and inhibits autophagy of pancreatic cancer cells through the miR-532 /TWIST1 signaling pathway |
title_sort | lncrna lzts1 as1 induces proliferation metastasis and inhibits autophagy of pancreatic cancer cells through the mir 532 twist1 signaling pathway |
topic | Autophagy lncRNA LZTS1-AS1 miR-532 Pancreatic cancer |
url | https://doi.org/10.1186/s12935-023-02979-7 |
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