Molecular Cell from Zhejiang University published a paper explaining the tumor immune mechanism of NF2 and its mutants

2021 Nian 8 Yue 27 days, hospital Xu Pinglong Laboratory in Molecular Cell on online published a report entitled entitled "Mutant Induced Phase Separation of NF2 imprisons at TheCGAS-STING Machinery to abrogate antitumor Immunity" work describes the nucleic acid immune recognition signals cGAS-STING-IRF3 induces disease-related tumor suppressor protein NF2 to form cell aggregates through liquid phase separation, which regulates signal scale and tumor immunity
.

Nucleic innate immune recognition ( InnateNucleic AcidsSensing ) of the host cell resistant to microbial invasion exogenous essential, while playing an important role in tumor immunity and anti-tumor immune surveillance process .
Based on this, understanding the " biological connection between tumor suppressor and nucleic acid recognition " is of great significance for re-understanding tumor immunity, but there are few studies so far .
Neurofibroma protein 2 (NF2/Merlin) is a classic tumor suppressor.
It is located on the cell membrane , cell junctions and cytoskeleton, and mediates the signal transmission between cells .
Mutation and deletion of NF2 gene is the main cause of type II neurofibromas, and it also frequently appears in various malignant tumors, including mesothelioma and melanin.
Tumors, breast cancer and colorectal cancer and so on
.
Previous academic theories believed that the main mechanism of tumorigenesis caused by NF2 mutation or deletion is the abnormal regulation of cell proliferation signal pathways , such as Hippo-YAP signal , Ras- Erk MAPK signal and PI3K-AKT signal .
However , the role of NF2 in immune regulation and whether NF2 pathogenic mutations can regulate tumor immunity have not been explored .

Xu early laboratory phase study found, NF2 by influencing YAP activity of cells positive regulation of natural immune responses

Therefore, this work reveals for the first time that nucleic acid recognition can induce protein liquid- liquid separation ( LLPS ) to form membraneless organelles by activating IRF 3 .
Also identified classic tumor suppressor NF2 mutation results in the immunological mechanisms of tumorigenesis and of NF 2 important tumor immune function, and proposed a new class of immunomodulatory native mode .
These new discoveries are important advances in the biological functions of innate immunity, tumor immunity and tumor suppressor factors , and also provide new theoretical and experimental basis for the treatment of NF2- related tumors .

N F2 of molecular mechanisms and mutants identified by natural regulatory nucleic acid

Postdoctoral fellow Meng Fansen (currently a postdoctoral fellow in the James Martin Laboratory of Baylor College of Medicine) has left the laboratory.
Dr.
Yu Zhengyang, Dr.
Zhang Dan and Wenzhou University professor Chen Shasha are the co-first authors of the paper.

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