Cancer cell viability and survival pathways

Cancer cell viability and survival pathways represent the integrated network of intracellular signaling cascades and regulatory mechanisms that enable malignant cells to bypass homeostatic growth controls and resist programmed cell death [1]. These pathways, most notably the PI3K/AKT/mTOR and MAPK/ERK cascades, are frequently hyperactivated in human cancers via somatic mutations, gene amplifications, or autocrine signaling loops [2, 4]. By maintaining the balance between pro-survival and pro-apoptotic signals, these pathways allow tumors to survive metabolic stress, hypoxia, and therapeutic challenges [3]. Although these pathways are the focus of intense drug development, the term itself describes a collective biological process rather than a discrete, druggable molecular entity [5]. Consequently, pharmacological strategies involve the use of small molecules or monoclonal antibodies to inhibit specific nodes—such as kinases or anti-apoptotic proteins—to restore the cell's natural inclination toward apoptosis [6]. Citations: [1] Hanahan D, Weinberg RA. Cell. 2011; [2] Sever R, Brugge JS. Cold Spring Harb Perspect Med. 2015; [3] Czabotar PE, et al. Nat Rev Mol Cell Biol. 2014; [4] Manning BD, Toker A. Cell. 2017; [5] Yuan TL, Cantley LC. Oncogene. 2008; [6] Braicu C, et al. Cancers (Basel). 2019.

Other names

Oncogenic survival signalingTumor cell viability pathwaysCell survival pathwaysAnti-apoptotic signaling networks

Inhibition of specific signaling nodes, such as kinases or anti-apoptotic proteins, within survival cascades to restore programmed cell death or induce growth arrest in malignant cells.