RSK1 and RSK2 as therapeutic targets: an up-to-date snapshot of emerging data.

Introduction: The four members of the p90 ribosomal S6 kinase (RSK) family are serine/threonine protein kinases, which are phosphorylated and activated by ERK1/2. RSK1/2/3 are further phosphorylated by PDK1. Receiving inputs from two major signaling pathways places RSK as a key signaling node in numerous pathologies.

Chronic High-Salt Diet Activates Tumor-Initiating Stem Cells Leading to Breast Cancer Proliferation.

Several chronic inflammatory diseases have been linked to high-salt (HS) diets. Chronic inflammation is an established causative hallmark of cancer. However, a direct role of HS diets in tumorigenesis is yet to be defined.

Therapeutic targeting of p90 ribosomal S6 kinase.

The Serine/Threonine protein kinase family, p90 ribosomal S6 kinases (RSK) are downstream effectors of extracellular signal regulated kinase 1/2 (ERK1/2) and are activated in response to tyrosine kinase receptor or G-protein coupled receptor signaling. RSK contains two distinct kinase domains, an N-terminal kinase (NTKD) and a C-terminal kinase (CTKD). The sole function of the CTKD is to aid in the activation of the NTKD, which is responsible for substrate phosphorylation.

Identifying the effectiveness of 3D culture systems to recapitulate breast tumor tissue in situ.

Purpose: Breast cancer heterogeneity contributes to chemotherapy resistance and decreased patient survival. To improve patient outcomes it is essential to develop a technology that is able to rapidly select the most efficacious therapy that targets the diverse phenotypes present within the tumor. Breast cancer organoid technologies are proposed as an attractive approach for evaluating drug responses prior to patient therapy.

ERK1/2-RSK2 Signaling in Regulation of ERα-Mediated Responses.

Signaling via extracellular regulated kinase 1/2 (ERK1/2) and p90 ribosomal S6 kinase (RSK), a downstream effector, mediates numerous processes. For example, ERK1/2-RSK signaling is essential for estrogen homeostasis in the mammary gland and uterus to maintain physiological responsiveness. This review will focus on the coordination of ERK1/2-RSK2 and estrogen signaling through estrogen receptor alpha (ERα).