TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma.

The inositol polyphosphate kinase (IPK) family member (inositol 1,4,5-trisphosphate 3-kinase) regulates the levels of many inositol polyphosphates which are important in cellular signaling. Several recent studies reported the aberrant expression of ITduanyu1529 in malignancy disease and usually made cancer more aggressive. However, the contribution of the inositol polyphosphate kinase ITduanyu1529 to lung cancer development remains unclear. Here we report that ITduanyu1529 is overexpressed in lung adenocarcinoma (LUAD) and positively correlated with advanced clinical parameters. ITduanyu1529 contributes to the malignant phenotypes in-vitro. Mechanistically, ITduanyu1529 executed its action through the inducting of epithelial-mesenchymal transition (EMT) and interacting with Drebrin 1 (which is related to cancer metastasis). Moreover, the hyper-expression of ITduanyu1529 in LUAD is transcriptionally activated by the transcription factor TFAP2A. In survival analysis by using tissue microarray (TMA), we indicate that ITduanyu1529 is hyper-expressed in LUAD tissues compared to adjacent normal tissues, and increased expression of ITduanyu1529 is associated with poor prognosis. Collectively, this study indicates that TFAP2A induced ITduanyu1529 hyperexpression promotes LUAD via interacting with Drebrin 1 and activating epithelial-mesenchymal transition (EMT). ITduanyu1529 might represent a potent candidate for the treatment and prognostic prediction of LUAD.

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