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Two controls of cell proliferation underlie cancer relapse
Author(s) -
Pardee Arthur B.,
Li Chiang J.
Publication year - 2018
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26597
Subject(s) - cancer stem cell , stem cell , cancer research , cancer cell , biology , cancer , cell growth , differentiation therapy , microbiology and biotechnology , intracellular , cell culture , biochemistry , genetics , acute promyelocytic leukemia , retinoic acid
Much progress has been made in understanding the basis of cancer. Current therapies can effectively shrink tumors. But they frequently relapse, metastasize to other locations, and are lethal. Effective therapies are very much needed for preventing this relapse. Creation of a eukaryotic organism commences with one original stem cell, a fertilized egg, which multiplies and differentiates. Mutations of normal stem cells can produce cancer stem cells (CSC). These cells may resist chemotherapy, proliferate, and produce new tumors. Human chorionic gonadotrophin (hCG) is composed of two proteins (alpha and beta) that bind to the cell membrane and activate a number of intracellular pathways. hCG has been shown to activate the proliferation of cancer stem cells. Cyclin dependent regulation of the adult cells is created in normal differentiation and replaces the hCG regulation of stem cells. To selectively kill the cancer stem cells conventional cancer therapies could be followed with a therapy based on inactivating human chronic gonadotrophin (HCG). For example chemically modified prostaglandins like RU486 prevent binding of the unmodified steroid to hCG and inactivate hCG.