GAIP-Interacting Protein, C-Terminus Is Involved in the Induction of Zinc-Finger Protein 143 in Response to Insulin-like Growth Factor-1 in Colon Cancer Cells

Abstract

Previously, we reported that the expression of zinc-finger protein 143 (ZNF143) was induced by insulin-like growth factor-1 (IGF-1) via reactive oxygen species (ROS)- and phosphatidylinositide-3-kinase (PI3-kinase)-linked pathways in colon cancer cells. Here, we investigated whether GAIP-interacting protein, C-terminus (GIPC), a binding partner of IGF-1R, is involved in ZNF143 expression through IGF-1 and IGF-1R signaling in colon cancer cells. The knockdown of GIPC in colon cancer cells reduced ZNF143 expression in response to IGF-1. IGF-1 signaling through its receptor, leading to the phosphorylation and activation of the PI3-kinase-Akt pathway and mitogenactivated protein kinases (MAPKs) was unaffected by the knockdown of GIPC, indicating the independence of the GIPC-linked pathway from PI3-kinase- and MAPK-linked signaling in IGF-1-induced ZNF143 expression. In accordance with previous results in breast cancer cells (Choi et al., 2010), the knockdown of GIPC reduced ROS production in response to IGF-1 in colon cancer cells. Furthermore, the knockdown of GIPC reduced the expression of Rad51, which is regulated by ZNF143, in response to IGF-1 in colon cancer cells. Taken together, these data suggest that GIPC is involved in IGF-1 signaling leading to ZNF143 expression through the regulation of ROS production, which may play a role for colon cancer tumorigenesis.

A role of zinc‐finger protein 143 for cancer cell migration and invasion through ZEB1 and E‐cadherin in colon cancer cells

“…We reported recently that ZNF143 is induced in response to IGF‐1 in HCT116 colon cancer cells . IGF‐1 is a homodimeric polypeptide growth factor that is known to play essential roles in a variety of cellular processes such as cell survival and proliferation by binding and stimulating its type I receptor (IGF‐1R) to initiate a cascade of intracellular tyrosine phosphorylation events .…”

“…We reported previously that ZNF143 is an inducible gene in response to IGF‐1 in colon cancer and non‐small cell lung cancer cells which are responsive to IGF‐1 in terms of cell proliferation . However, ZNF143 might not be involved in cancer cell proliferation.…”

“…To achieve the stable lentivirus‐mediated expression of shRNA specific for the gene encoding ZNF143 in HCT116 cells, cells were grown for 24 h, incubated with 5 µg/mL polybrene for 1 h, and then infected with the lentiviral vector (approximately 1 molar ratio of infection) as described previously . After 48 h, the medium was replaced and the cells were grown for 1 d. The control cell lines (HCT116 sh‐control) and cell lines stably expressing ZNF143 shRNA (HCT116 sh‐ZNF143) were selected in 10 µg/mL puromycin dihydrochloride for 2 wk and maintained in growth medium containing 1 µg/mL puromycin dihydrochloride.…”

“…ZNF143 is involved in cell survival and apoptosis by regulating SepSecS expression , the key enzyme responsible for selenocysteine transfer RNA synthesis, and transaldoase expression . We reported recently that ZNF143 is induced in response to insulin‐like growth factor‐1 (IGF‐1) in various cancer cells, implying that ZNF143 plays a role in cancer cell biology . Despite emerging evidence suggesting that ZNF143 acts as a transcription factor in a variety of cancer cells, whether ZNF143 is involved in regulating cancer cell motility remains unknown.…”

The GIPC1-Akt1 Pathway Is Required for the Specification of the Eye Field in Mouse Embryonic Stem Cells

“…Ectopic expression of IGF1R in dorsal positions of the amphibian embryo induced the formation of ectopic eyes and a dominant‐negative IGFR construct reduced the expression of eye field markers (e.g., Rax) . Additionally, GIPC1 has been shown to interact with IGF1R and in Xenopus , Kermit2/GIPC is required for IGF1‐induced ocular tissues in both embryos and animal caps . We therefore hypothesized that GIPC1 could also be interacting with IGF1R during eye field induction in mouse.…”