AHNAK Nucleoprotein 2 Performs a Promoting Role in the Proliferation and Migration of Uveal Melanoma Cells
AHNAK nucleoprotein 2 (AHNAK2) is supposed to participate in calcium signaling and cytoarchitecture by directly interacting with some proteins. Recently, it was identified as a novel candidate oncogene in human tumors. The author's present study aimed to investigate the expression and biologica...
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Veröffentlicht in: | Cancer biotherapy & radiopharmaceuticals 2019-12, Vol.34 (10), p.626-633 |
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Zusammenfassung: | AHNAK nucleoprotein 2 (AHNAK2) is supposed to participate in calcium signaling and cytoarchitecture by directly interacting with some proteins. Recently, it was identified as a novel candidate oncogene in human tumors. The author's present study aimed to investigate the expression and biological function of AHNAK2 in uveal melanoma (UM). Based on microarray data of 63 UM patients that were downloaded from Gene Expression Omnibus database, the authors found that AHNAK2 expression is higher in UM primary tumor tissues from patients who developed metastases after enucleation than that in UM primary tumor tissues from patients without metastasis after enucleation. On the basis of the data obtained from The Cancer Genome Atlas database, they found that high AHNAK2 expression is closely associated with shorter overall survival time in UM patients. From quantitative reverse transcription polymerase chain reaction analyses, they revealed that the mRNA expression level of AHNAK2 was significantly upregulated in M17 and SP6.5 cell lines compared with that in D78. Functionally, knockdown of AHNAK2 using small interfering RNA in M17 and SP6.5 cells dramatically suppressed cell proliferation, migratory and invasive abilities, as well as inhibited the activation of phosphatidylinositol 3-kinase (PI3K) signaling pathway. Taken together, their results illustrated that AHNAK2 was upregulated in UM and plays a promoting role in the proliferation and migration of UM cells possibly via regulating PI3K signaling pathway. |
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ISSN: | 1084-9785 1557-8852 |
DOI: | 10.1089/cbr.2019.2778 |