期刊
CANCER BIOLOGY & THERAPY
卷 23, 期 1, 页码 34-50出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384047.2021.2017223
关键词
C-myc; pancreatic cancer; BET inhibitor; chemoresistance; KRAS
类别
C-Myc overexpression in pancreatic cancer is associated with aggressive behavior of cancer cells and can regulate various cellular processes. Recent studies have shown that C-Myc can be targeted directly or indirectly, offering potential therapeutic strategies for pancreatic cancer.
C-Myc overexpression is a common finding in pancreatic cancer and predicts the aggressive behavior of cancer cells. It binds to the promoter of different genes, thereby regulating their transcription. C-Myc is downstream of KRAS and interacts with several oncogenic and proliferative pathways in pancreatic cancer. C-Myc enhances aerobic glycolysis in cancer cells and regulates glutamate biosynthesis from glutamine. It provides enough energy for cancer cells' metabolism and sufficient substrate for the synthesis of organic molecules. C-Myc overexpression is associated with chemoresistance, intra-tumor angiogenesis, epithelial-mesenchymal transition (EMT), and metastasis in pancreatic cancer. Despite its title, c-Myc is not undruggable and recent studies unveiled that it can be targeted, directly or indirectly. Small molecules that accelerate c-Myc ubiquitination and degradation have been effective in preclinical studies. Small molecules that hinder c-Myc-MAX heterodimerization or c-Myc/MAX/DNA complex formation can functionally inhibit c-Myc. In addition, c-Myc can be targeted through transcriptional, post-transcriptional, and translational modifications.
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