Using siRNA to uncover novel oncogenic signaling pathways.
Tumor invasion and metastasis are the primary causes of cancer patient mortality, underscoring the need for identification of novel genes and signaling pathways that mediate these prognosis-determining phenomena. To identify and characterize novel lung adenocarcinoma genes associated with lung cancer progression, we created a bioinformatics-based approach that focuses on human cell-cycle-regulated genes that have evolved only in higher organisms but not in lower eukaryotic cells. In siRNA experiments in lung cancer cells, FLJ10540 was identified as one of several novel targets involved in cell migration and invasion. Here, we demonstrate that PI3K inhibition affects FLJ10540-mediated cell migration and invasion and further, that FLJ10540 knockdown ablates AKT-Ser(473) phosphorylation. Taken together, these findings indicate that the FLJ10540/PI3K/AKT pathway may harbor new therapeutic targets for treating invasive lung adenocarcinoma.
Lai
Jin-Mei
JM
Department of Life Science, Fu-Jen Catholic University, Taipei, Taiwan.
Huang
Chi-Ying F
CY
Chen
Chang-Han
CH
D000230:Adenocarcinoma / Q000378:metabolism*; D000818:Animals; D018797:Cell Cycle Proteins / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008175:Lung Neoplasms / Q000378:metabolism*; D051379:Mice; D009687:Nuclear Proteins / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism*; D022661:RNA, Untranslated / Q000378:metabolism*; D015398:Signal Transduction
D018797:Cell Cycle Proteins; C505378:Cep55 protein, human; D009687:Nuclear Proteins; D034741:RNA, Small Interfering; D022661:RNA, Untranslated