作者: Itamar Kozlovski , Zahava Siegfried , Adi Amar-Schwartz , Rotem Karni
DOI: 10.1007/S00439-017-1803-X
关键词:
摘要: Tumor cells alter their metabolism by a wide array of mechanisms to promote growth and proliferation. Dysregulated expression and/or somatic mutations key components the glycolytic pathway/TCA cycle as well other metabolic pathways allow tumor improve ability survive harsh conditions such hypoxia presence reactive oxygen species, obtain nutrients increase lipids, protein, nucleic acids biogenesis. Approximately 95% human protein encoding genes undergo alternative splicing (AS), regulated process gene that greatly diversifies proteome creating multiple proteins from single gene. In recent years, growing body evidence suggests unbalanced AS, formation certain pro-tumorigenic isoforms reduction anti-tumorigenic isoforms, is implicated in variety cancers. It becoming increasingly clear cancer-associated AS contributes increased proliferation, partially due effects on reprogramming. Here, we summarize known roles regulating cancer metabolism. We present supporting idea many types cancer, acts molecular switch alters drive tumorigenesis. propose elucidation misregulated its downstream emphasizes need for new therapeutic approaches aiming modulate machinery selectively target cells.