myricetin and Colonic-Neoplasms

myricetin has been researched along with Colonic-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for myricetin and Colonic-Neoplasms

Article	Year
Biological evaluation and docking studies of recently identified inhibitors of phosphoinositide-3-kinases. Bioorganic & medicinal chemistry letters, 2012, Jan-15, Volume: 22, Issue:2 The alpha isoform of the phosphatidylinositol-3-kinases (PI3Kα) is often mutated, amplified and overexpressed in human tumors. In an effort to develop new inhibitors targeting this enzyme, we carried out a pharmacophore model study based on six PI3Kα-selective compounds. The pharmacophore searching identified three structurally novel inhibitors of PI3Kα and its H1047R mutant. Our biological studies show that two of our hit molecules suppressed the formation of pAKT, a downstream effector of PI3Kα, and induced apoptosis in the HCT116 colon cancer cell line. QPLD-based docking showed that residues Asp933, Glu849, Val851, and Gln859 appeared to be key binding residues for active inhibitors. Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Colonic Neoplasms; Dose-Response Relationship, Drug; Drug Screening Assays, Antitumor; Humans; Models, Molecular; Molecular Structure; Phosphatidylinositol 3-Kinases; Phosphoinositide-3 Kinase Inhibitors; Protein Kinase Inhibitors; Stereoisomerism; Structure-Activity Relationship	2012

Article

Year

Biological evaluation and docking studies of recently identified inhibitors of phosphoinositide-3-kinases.

Bioorganic & medicinal chemistry letters, 2012, Jan-15, Volume: 22, Issue:2

The alpha isoform of the phosphatidylinositol-3-kinases (PI3Kα) is often mutated, amplified and overexpressed in human tumors. In an effort to develop new inhibitors targeting this enzyme, we carried out a pharmacophore model study based on six PI3Kα-selective compounds. The pharmacophore searching identified three structurally novel inhibitors of PI3Kα and its H1047R mutant. Our biological studies show that two of our hit molecules suppressed the formation of pAKT, a downstream effector of PI3Kα, and induced apoptosis in the HCT116 colon cancer cell line. QPLD-based docking showed that residues Asp933, Glu849, Val851, and Gln859 appeared to be key binding residues for active inhibitors.

Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Colonic Neoplasms; Dose-Response Relationship, Drug; Drug Screening Assays, Antitumor; Humans; Models, Molecular; Molecular Structure; Phosphatidylinositol 3-Kinases; Phosphoinositide-3 Kinase Inhibitors; Protein Kinase Inhibitors; Stereoisomerism; Structure-Activity Relationship

2012