Shifting perspectives from "oncogenic" to oncofetal proteins; how these factors drive placental development

• Published in: Reproductive biology and endocrinology Vol. 16; no. 1; pp. 101 - 12
• Main Authors: West, Rachel C, Bouma, Gerrit J, Winger, Quinton A
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 19-10-2018; BioMed Central; BMC
• Subjects: Angiogenesis; Antigens, Neoplasm - metabolism; Carcinogenesis; Cell Movement; Cell Proliferation; Female; Fetus; Genomic instability; Growth; Humans; Invasion; Migration; Oncogene Proteins - metabolism; Physiological aspects; Placenta; Placenta - cytology; Placenta - metabolism; Placentation; Pregnancy; Review; Trophoblasts - cytology; Trophoblasts - metabolism; United States; Cell proliferation; Angiogenesis; Placenta; Migration; Placental insufficiency; Invasion; Genomic instability
• ISSN: 1477-7827; 1477-7827
• DOI: 10.1186/s12958-018-0421-3

Early human placental development strongly resembles carcinogenesis in otherwise healthy tissues. The progenitor cells of the placenta, the cytotrophoblast, rapidly proliferate to produce a sufficient number of cells to form an organ that will contribute to fetal development as early as the first trimester. The cytotrophoblast cells begin to differentiate, some towards the fused cells of the syncytiotrophoblast and some towards the highly invasive and migratory extravillous trophoblast. Invasion and migration of extravillous trophoblast cells mimics tumor metastasis. One key difference between cancer progression and placental development is the tight regulation of these oncogenes and oncogenic processes. Often, tumor suppressors and oncogenes work synergistically to regulate cell proliferation, differentiation, and invasion in a restrained manner compared to the uncontrollable growth in cancer. This review will compare and contrast the mechanisms that drive both cancer progression and placental development. Specifically, this review will focus on the molecular mechanisms that promote cell proliferation, evasion of apoptosis, cell invasion, and angiogenesis.