Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 20, Pages -Publisher
MDPI
DOI: 10.3390/ijms222010964
Keywords
PIK3C3; Vps34; autophagy; colorectal cancer; cancer
Funding
- Ministry of Science and Technology, Taiwan [NSC108-2320-B-006-050-MY3, 110-2314-B-006-083, 110-2320-B-006-026]
- National Cheng Kung University Hospital, Tainan, Taiwan [NCKUH-10704015, NCKUH-11008004]
- Higher Education Sprout Project, Ministry of Education
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PIK3C3, as a member of the PI3K family, plays a critical role in autophagy and tumor development. Inhibition of PIK3C3 can suppress autophagy and affect tumor cell proliferation, growth, and invasion. Discovery of pharmacological inhibitors targeting PIK3C3 may provide new strategies for improving treatment outcomes in PIK3C3-mediated diseases.
Phosphatidylinositol 3-kinase catalytic subunit type 3 (PIK3C3), the mammalian ortholog of yeast vesicular protein sorting 34 (Vps34), belongs to the phosphoinositide 3-kinase (PI3K) family. PIK3C3 can phosphorylate phosphatidylinositol (PtdIns) to generate phosphatidylinositol 3-phosphate (PI3P), a phospholipid central to autophagy. Inhibition of PIK3C3 successfully inhibits autophagy. Autophagy maintains cell survival when modifications occur in the cellular environment and helps tumor cells resist metabolic stress and cancer treatment. In addition, PIK3C3 could induce oncogenic transformation and enhance tumor cell proliferation, growth, and invasion through mechanisms independent of autophagy. This review addresses the structural and functional features, tissue distribution, and expression pattern of PIK3C3 in a variety of human tumors and highlights the underlying mechanisms involved in carcinogenesis. The implications in cancer biology, patient prognosis prediction, and cancer therapy are discussed. Altogether, the discovery of pharmacological inhibitors of PIK3C3 could reveal novel strategies for improving treatment outcomes for PIK3C3-mediated human diseases.
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