Na+/K+ ATPase activity promotes invasion of endocrine resistant breast cancer cells.

Background: The Na+/K+-ATPase (NKP) is an important ion transporter also involved in signal transduction. Its expression profile is altered in various tumours including that of the breast. We studied the effect of inhibiting NKP activity in non-tumorigenic breast cell line and in estrogen receptor positive and negative breast cancer cells.

Inhibitors of PI3K/ERK1/2/p38 MAPK Show Preferential Activity Against Endocrine-Resistant Breast Cancer Cells.

Current mainstream pharmacological options for the treatment of endocrine-resistant breast cancer have limitations in terms of their side effect profile and lack of discrimination between normal and cancer cells. In the current study, we assessed the responses of normal breast epithelial cells MCF10A, estrogen receptor-positive (ER+) MCF-7, and ER-silenced pII breast cancer cells to inhibitors (either individually or in combination) of downstream signaling molecules. The expression/activity of ERK1/2, p38 MAPK, and Akt was determined by Western blotting.

Antiproliferative activity of a series of 5‑(1H‑1,2,3‑triazolyl) methyl‑ and 5‑acetamidomethyl‑oxazolidinone derivatives.

In the face of increasing resistance to the existing antibiotics, oxazolidinones (exemplified by linezolid) have been developed as promising antibacterial agents, but may have other useful actions. In the present study, a series of 5‑(1H‑1,2,3‑triazoly) l‑methyl‑, 5‑acetamidomethyl‑morpholino and N‑substituted‑piperazino oxazolidinone derivatives were investigated to determine whether they are active against eukaryotic cells. An MTT assay, validated by cell counting, was used to assess the effect of nine oxazolidinone derivatives (concentrations 100 nM‑10 µM) on the proliferation of MCF7 human breast cancer cells.

Bleb formation is induced by alkaline but not acidic pH in estrogen receptor silenced breast cancer cells.

De novo and acquired resistance to endocrine-based therapies in breast cancer occurs in parallel with epithelial to mesenchymal transition (EMT), which is associated with enhanced proliferative and metastatic potential, and poor clinical outcome. We have established several endocrine insensitive breast cancer lines by shRNA-induced depletion of estrogen receptor (ER) by transfection of MCF7 cells. All of these exhibit EMT.

Extracellular alkaline pH leads to increased metastatic potential of estrogen receptor silenced endocrine resistant breast cancer cells.

Introduction: Endocrine resistance in breast cancer is associated with enhanced metastatic potential and poor clinical outcome, presenting a significant therapeutic challenge. We have established several endocrine insensitive breast cancer lines by shRNA induced depletion of estrogen receptor (ER) by transfection of MCF-7 cells which all exhibit enhanced expression profile of mesenchymal markers with reduction of epithelial markers, indicating an epithelial to mesenchymal transition. In this study we describe their behaviour in response to change in extracellular pH, an important factor controlling cell motility and metastasis.

Assessment of tracer 99mTc(V)-DMSA uptake as a measure of tumor cell proliferation in vitro.

Purpose: To examine whether (99m)Tc(V)-DMSA could be used as a non-invasive measure of cancer cell proliferation.

Methods: Human breast cancer MCF-7, MDA-MB-231 and pII, and prostate cancer PC-3 cell lines were grown to 30, 50 and 100% confluency and pulsed with (99m)Tc(V)-DMSA in media for 60 min at 37°C. DNA synthesis was analysed by quantification of the S phase using flow cytometry, [methyl-(3)H]thymidine incorporation and expression of proliferation markers PCNA and Ki-67 using realtime PCR.

Differential effect of growth factors on invasion and proliferation of endocrine resistant breast cancer cells.

We have established several breast cancer cell lines that exhibit a permanent ER-depleted phenotype, induced by shRNA transfection of MCF-7 cells, which afford a useful model for studying acquired endocrine resistance. Previously we showed that MDA-231 as well as ER-silenced cells could invade through simulated extracellular matrix components. However, the contribution of individual serum components responsible for cell invasion was not determined.