mTOR intersects antibody-inducing signals from TACI in marginal zone B cells.

Mechanistic target of rapamycin (mTOR) enhances immunity in addition to orchestrating metabolism. Here we show that mTOR coordinates immunometabolic reconfiguration of marginal zone (MZ) B cells, a pre-activated lymphocyte subset that mounts antibody responses to T-cell-independent antigens through a Toll-like receptor (TLR)-amplified pathway involving transmembrane activator and CAML interactor (TACI). This receptor interacts with mTOR via the TLR adapter MyD88.

Androgen-induced cell migration: role of androgen receptor/filamin A association.

Background: Androgen receptor (AR) controls male morphogenesis, gametogenesis and prostate growth as well as development of prostate cancer. These findings support a role for AR in cell migration and invasiveness. However, the molecular mechanism involved in AR-mediated cell migration still remains elusive.

Hormone-dependent nuclear export of estradiol receptor and DNA synthesis in breast cancer cells.

In breast cancer cells, cytoplasmic localization of the estradiol receptor alpha (ERalpha) regulates estradiol-dependent S phase entry. We identified a nuclear export sequence (NES) in ERalpha and show that its export is dependent on both estradiol-mediated phosphatidylinositol-3-kinase (PI3K)/AKT activation and chromosome region maintenance 1 (CRM1). A Tat peptide containing the ERalpha NES disrupts ERalpha-CRM1 interaction and prevents nuclear export of ERalpha- and estradiol-induced DNA synthesis.

Integrating signals between cAMP and MAPK pathways in breast cancer.

Breast cancer is one of the most common malignancies in Western society. Localized breast cancer, before it spreads, can be cured by surgery. However, the high mortality rate associated with breast cancer is due to a propensity of the tumor to metastasize when the primary tumor is small or undetectable.

Crosstalk between EGFR and extranuclear steroid receptors.

Epidermal growth factor (EGF) stimulates DNA synthesis and cytoskeletal rearrangement in human breast cancer (MCF-7) and human prostate cancer (LNCaP) cells. Both effects are inhibited by estrogen (ICI 182,780) and androgen (Casodex) antagonists. This supports the view that crosstalk exists between EGF and estradiol (ER) and androgen (AR) receptors and suggests that these receptors are directly involved in the EGF action.

Steroid receptor regulation of epidermal growth factor signaling through Src in breast and prostate cancer cells: steroid antagonist action.

Under conditions of short-term hormone deprivation, epidermal growth factor (EGF) induces DNA synthesis, cytoskeletal changes, and Src activation in MCF-7 and LNCaP cells. These effects are drastically inhibited by pure estradiol or androgen antagonists, implicating a role of the steroid receptors in these findings. Interestingly, EGF triggers rapid association of Src with androgen receptor (AR) and estradiol receptor alpha (ERalpha) in MCF-7 cells or ERbeta in LNCaP cells.