You may have access to the free features available through My Research. You can save searches, save documents, create alerts and more. Please log in through your library or institution to check if you have access.
If you log in through your library or institution you might have access to this article in multiple languages.
Styles include MLA, APA, Chicago and many more. This feature may be available for free if you log in through your library or institution.
You may have access to it for free by logging in through your library or institution.
You may have access to different export options including Google Drive and Microsoft OneDrive and citation management tools like RefWorks and EasyBib. Try logging in through your library or institution to get access to these tools.
As a highly malignant gastrointestinal tumor, pancreatic cancer is highly invasive and metastatic, which leads to the low overall survival rate of patients with pancreatic cancer. Studies have shown that long non-coding RNA (lncRNA) is involved in the development, progression, invasion, and metastasis of pancreatic cancer through epigenetic, transcriptional or post-transcriptional regulation. Dysregulated expression of lncRNA is observed in pancreatic cancer and induces epithelial mesenchymal transition (EMT) through specific regulatory mechanisms, thereby causing the changes in the biological behavior of tumor cells. This article reviews the mechanisms of lncRNA in promoting EMT, regulating tumor biological function as competing endogenous RNA, and affecting the development, invasion, and metastasis of pancreatic cancer via multiple pathways by regulating the ferroptosis, autophagy, and exosome of tumor cells, in order to provide a theoretical basis and new targets for the early diagnosis and treatment of pancreatic cancer.
