Sulforaphane inhibits growth of phenotypically different breast cancer cells.

Purpose: Cancer development and resistance to chemotherapy correlates with aberrant activity of mitogenic pathways. In breast cancers, pro-survival PI3K-Akt-mTOR-S6K1 [corrected] signaling pathway is often hyperactive due to overexpression of genes coding for growth factors or estrogen receptors, constitutive activation of PI3K or Akt and loss of PTEN, a negative regulator of the pathway. Since epidemiologic as well as rodent tumor studies indicate that sulforaphane (SFN), a constituent of many edible cruciferous vegetables, might be a potent inhibitor of mammary carcinogenesis, we analyzed the response of four breast cancer cell lines representing different abnormalities in ErbB2/ER-PI3K-Akt-mTOR-S6K1[corrected] signaling pathway to this compound.

Sulforaphane, a cruciferous vegetable-derived isothiocyanate, inhibits protein synthesis in human prostate cancer cells.

Sulforaphane (SFN) is a compound derived from cruciferous plants. Its anticancer properties have been demonstrated both, in cancer cell lines as well as tumors in animal models. It has been shown that SFN inhibits cell proliferation, induces apoptosis, autophagy, and sensitizes cancer cells to therapies.

Persistence of bacteriophage T4 in a starved Escherichia coli culture: evidence for the presence of phage subpopulations.

Bacteriophage T4 is able to adjust its development to the growth parameters of the host cell. Here, we present evidence for the production of two different subpopulations of phage particles, which differ in their ability to infect starved Escherichia coli cells. The ability of phage T4 to produce a fraction of virions unable to infect starved cells is linked to the functions of genes rI and rIII, as well as rIIA.

A role for accessory genes rI.-1 and rI.1 in the regulation of lysis inhibition by bacteriophage T4.

Lysis inhibition (LIN) is a known feature of the T-even family of bacteriophages. Despite its historical role in the development of modern molecular genetics, many aspects of this phenomenon remain mostly unexplained. The key element of LIN is an interaction between two phage-encoded proteins, the T holin and the RI antiholin.