Interaction between fortilin and transforming growth factor-beta stimulated clone-22 (TSC-22) prevents apoptosis via the destabilization of TSC-22.
Yeast two-hybrid screening was conducted using a human ovary cDNA library to search for a novel binding protein using transforming growth factor-beta stimulated clone-22 (TSC-22). The selected protein was fortilin, which has been characterized as a nuclear anti-apoptotic protein. Overexpression of fortilin in ovarian carcinoma cells reversed TSC-22-mediated apoptosis, and the inhibition of fortilin expression via small interfering RNA (siRNA) resulted in an increase in the apoptosis of ovarian carcinoma cells. Moreover, fortilin overexpression promoted the degradation of TSC-22. Thus, an interaction between fortilin and TSC-22 prevents apoptosis via the destabilization of TSC-22 in ovarian carcinoma cells.
Lee
Jeong Heon
JH
Department of Obstetrics and Gynecology, Chonbuk National University Medical School, Jeonju 561-712, Republic of Korea.
Rho
Seung Bae
SB
Park
Sang-Yoon
SY
Chun
Taehoon
T
D017209:Apoptosis / Q000502:physiology*; D001483:Base Sequence; D014408:Biomarkers, Tumor / Q000378:metabolism* / Q000502:physiology; D053148:Caspase 3 / Q000378:metabolism; D045744:Cell Line, Tumor; D017931:DNA Primers; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D010051:Ovarian Neoplasms / Q000473:pathology; D034741:RNA, Small Interfering; D012097:Repressor Proteins / Q000378:metabolism*; D000090324:Tumor Protein, Translationally-Controlled 1
D014408:Biomarkers, Tumor; D017931:DNA Primers; D034741:RNA, Small Interfering; D012097:Repressor Proteins; C099726:TSC22D1 protein, human; D000090324:Tumor Protein, Translationally-Controlled 1; D053148:Caspase 3