NDLI: LncRNA MALAT1 regulates METTL3-mediated PD-L1 expression and immune infiltrates in pancreatic cancer

Content Provider	Directory of Open Access Journals (DOAJ)
Author	Zhengwei Song Xiaoguang Wang Fei Chen Qiuli Chen Wenjun Liu Xiaodan Yang Xun Zhu Xiaorong Liu Peter Wang
Abstract	Pancreatic cancer is the fourth leading cause of cancer death in the United States. The main methods of treating pancreatic cancer are surgery and chemotherapy, but the treatment efficacy is low with a poor prognosis. Immunotherapy represented by PD-1/PD-L1 has brought a milestone progress in the treatment of pancreatic cancer. However, the unique tumor microenvironment of pancreatic cancer presents challenges for immunotherapy. In addition, m6A is a common RNA modification and a potential molecular target in tumor therapy. The expression pattern of m6A in pancreatic cancer is still unclear. LncRNAs also play an essential role in pancreatic cancer development and treatment. In this study, we found that some m6A regulators were significantly elevated in pancreatic cancer and associated with the expression of PD-1/PD-L1. Moreover, we observed that METTL3 can increase the expression of PD-L1. Notably, METTL3 positively regulates the expression of lncRNA MALAT1 in pancreatic cancer cells. Strikingly, lncRNA MALAT1 increased the expression of PD-L1 in pancreatic cancer cells. This finding indicated that METTL3 regulated the expression of PD-L1 possibly via targeting lncRNA MALAT1 in pancreatic cancer cells. Lastly, MALAT1 governed the viability of pancreatic cancer cells. Taken together, lncRNA MALAT1 is involved in METTL3-mediated promotion of PD-L1 expression in pancreatic cancer.
e-ISSN	2234943X
DOI	10.3389/fonc.2022.1004212
Journal	Frontiers in Oncology
Volume Number	12
Language	English
Publisher	Frontiers Media S.A.
Publisher Date	2022-09-01
Publisher Place	Switzerland
Access Restriction	Open
Subject Keyword	Neoplasms. Tumors. Oncology. Including Cancer and Carcinogens Lncrna Malat1 Pd-l1 Mettl3 Tme Pancreatic Cancer
Content Type	Text
Resource Type	Article

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