title: Application of hRad9 in lung cancer treatment as a molecular marker and a molecular target.
abstract: DNA damage sensor proteins work as upstream components of the DNA damage checkpoint signaling pathways that are essential for cell cycle control and the induction of apoptosis. hRad9 is a member of a family of proteins that act as DNA damage sensors and plays an important role as an upstream regulator of checkpoint signaling. We clarified the significant accumulation of hRad9 in the nuclei of tumor cells in surgically-resected non-small-cell lung cancer (NSCLC) specimens and found the capacity to produce a functional hRad9 protein was intact in lung cancer cells. This finding suggested that hRad9 was a vital component in the pathways that lead to the survival and progression of NSCLC and suggested that hRad9 was a good candidate for a molecular target to control lung cancer cell growth. RNA interference targeting hRad9 was performed to examine this hypothesis. The impairment of the DNA damage checkpoint signaling pathway induced cancer cell death. hRad9 might be a novel molecular target for lung cancer treatment.
authors.affiliation: Division of Thoracic Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Maniwa
authors.affiliation: Division of Thoracic Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Wataru
authors.initials: W
authors.lastname: Nishio
authors.affiliation: Division of Thoracic Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Yoshimura
keywords: Cell cycle checkpoint; Chk1; DNA damage; hRad9; non-small-cell lung cancer