Increasing the Potential Targets and Molecularly Targeted Agent Combinations Against Cancer Cell ProliferationVictor M Valdespino1*, Victor E Valdespino-Castillo2 and Patricia M Valdespino-Castillo3
- *Corresponding Author:
- Victor M Valdespino
Heath Attention Department
Universidad Autónoma Metropolitana, México
E-mail: [email protected]
Received date: January 27, 2017; Accepted date: March 02, 2017; Published date: March 10, 2017
Citation: Valdespino VM, Valdespino-Castillo VE, Valdespino-Castillo PM (2017) Increasing the Potential Targets and Molecularly Targeted Agent Combinations Against Cancer Cell Proliferation. J Cell Signal 2:139.
Copyright: © 2017 Valdespino VM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
At least four main groups of intracellular signaling pathways or submodules concur in the cell division and proliferation module: those for the control of the cell cycle, those for the metabolism programming, those for cytoskeleton remodeling, and those for DNA replication and repair. Precise signaling pathways that control cell proliferation module require the joint functional collaboration of signaling pathways of cell growth, cell survival, cell differentiation, intracellular senescence and death programs, and appropriate interaction with angiogenesis, cell micro-environment regulation and immunologic system modules. Seeking out actionable aberrations in cancer cells may now selectively targeted by drug compounds to optimize treatment efficacy and minimize toxicity.
This critical review provides an overview of the use of the CDK4/6 inhibitors as the first cell cycle inhibitor that improve the outcomes of patients with HR+ breast cancer. Discusses the connection of different inhibitory agents to modify cell proliferation signaling pathways and sketches the potential use of other molecularly targeted agents in close relationship with proliferation signaling pathways carcinoma cells.