Two controls of cell proliferation underlie cancer relapse

Abstract

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.

Emerging Role of E2F Family in Cancer Stem Cells

“…Tumor initiation, development, metastasis, recurrence and acquisition of therapeutic resistance in numerous different human cancers has been attributed to the properties of CSCs, which include proliferation potential, self-renewal capacity, differentiation potential, high metastatic capacity, and drug resistance ( 20 , 53 ). Compared with normal stem cells, CSCs, with their abnormal expression of cell cycle-related regulatory factors and dysregulation of negative feedback mechanisms, are often able to proliferate extensively, potentially indefinitely ( 54 , 55 ).…”

MicroRNA-2355-5p Promotes the Proliferation of Head and Neck Squamous Cell Carcinoma via Suppressing NISCH Expression

“…Tumor cells with uncontrolled proliferation provide them with growth advantages, and consequently produce tumor recurrence after treatment. ese cells are always characterized by derangements in the cell cycle regulation [5,6]. Hence, it is essential to dissect the molecular disorders during the cell cycle regulation of HNSC cells, which might contribute to providing novel therapeutic targets for HNSC treatment.…”