title: Inhibition of ADP-ribosylation factor-like 6 interacting protein 1 suppresses proliferation and reduces tumor cell invasion in CaSki human cervical cancer cells.
abstract: ADP-ribosylation factor-like 6 interacting protein 1 (ARL6IP1) is an apoptotic regulator. To investigate the role of ARL6IP1 in human cervical cancer progression, we designed and used short hairpin RNA (shRNA) to inhibit ARL6IP1 expression in CaSki cells and validated its effect on cell proliferation and invasion. Changes in gene expression were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) or western blot. Down-regulation of ARL6IP1 expression by infection with ARL6IP1-specific RNAi-expressing vector inhibited CaSki cell proliferation and colony formation. In addition, down-regulation of ARL6IP1 expression arrested CaSki cell cycling at the G0/G1 phase and mitigated CaSki cell migration, determined by wound healing assays. ARL6IP1 was involved in cervical cancer cell growth, cell cycle progression, and invasion through regulation of gene expression, such as Caspase-3, Caspase-9, p53, TAp63, NF-κB, MAPK, Bcl-2, and Bcl-xL, suggesting that ARL6IP1 could have important implications in cervical cancer biology. Our findings illustrate the biological significance of ARL6IP1 in cervical cancer progression, and provide novel evidence that ARL6IP1 may serve as a therapeutic target in the prevention of human cervical cancer.
authors.affiliation: Cancer Research Institute, Xiangya Medical School, Central South University, Changsha, Hunan Province, China.
authors.forename: Fengjie
authors.initials: F
authors.lastname: Guo
authors.forename: Yan
authors.initials: Y
authors.lastname: Liu
authors.forename: Yalin
authors.initials: Y
authors.lastname: Li
authors.forename: Guancheng
authors.initials: G
authors.lastname: Li
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000378:metabolism*; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D053453:Caspase 9 / Q000235:genetics / Q000378:metabolism; D002453:Cell Cycle; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D015536:Down-Regulation / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D009361:Neoplasm Invasiveness; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism; D002583:Uterine Cervical Neoplasms / Q000201:enzymology / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D051020:bcl-X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: C488848:ARL6IP1 protein, human; D048868:Adaptor Proteins, Signal Transducing; D008565:Membrane Proteins; D016328:NF-kappa B; D012333:RNA, Messenger; C115051:TP63 protein, human; D015534:Trans-Activators; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D051020:bcl-X Protein; D019950:Mitogen-Activated Protein Kinase 1; D053148:Caspase 3; D053453:Caspase 9