ALKBH5 regulates anti–PD-1 therapy response by modulating lactate and suppressive immune cell accumulation in tumor microenvironment

Although immune checkpoint blockade (ICB) therapy has revolutionized cancer treatment, many patients do not respond or develop resistance to ICB. N⁶-methylation of adenosine (m⁶A) in RNA regulates many pathophysiological processes. Here, we show that deletion of the m⁶A demethylase Alkbh5 sensitized...

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Veröffentlicht in:	Proceedings of the National Academy of Sciences - PNAS 2020-08, Vol.117 (33), p.20159-20170
Hauptverfasser:	Li, Na, Kang, Yuqi, Wang, Lingling, Huff, Sarah, Tang, Rachel, Hui, Hui, Agrawal, Kriti, Gonzalez, Gwendolyn Michelle, Wang, Yinsheng, Patel, Sandip Pravin, Rana, Tariq M.
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenosine AlkB Homolog 5, RNA Demethylase - genetics AlkB Homolog 5, RNA Demethylase - metabolism Antibodies Biological Sciences Cancer Cancer immunotherapy Cancer Vaccines - immunology Cytokines - genetics Cytokines - metabolism Gene Deletion Gene expression Gene Expression Regulation, Neoplastic Humans Immune checkpoint Immune system Immunotherapy Lactates - metabolism Lactic acid Lymphocytes T Melanoma Melanoma - metabolism Melanoma - therapy Methylation Methyltransferases - genetics Methyltransferases - metabolism Monocarboxylic Acid Transporters - genetics Monocarboxylic Acid Transporters - metabolism Muscle Proteins - genetics Muscle Proteins - metabolism Mutation Myeloid-Derived Suppressor Cells - physiology N6-methyladenosine PD-1 protein Point mutation Programmed Cell Death 1 Receptor - immunology Ribonucleic acid RNA RNA Splice Sites RNA Splicing Splicing Suppressor cells Symporters - genetics Symporters - metabolism T-Lymphocytes, Regulatory - physiology Transcriptome Tumor cells Tumor Microenvironment Tumors Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism
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