Aurora B Is Regulated by the Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase (MAPK/ERK) Signaling Pathway and Is a Valuable Potential Target in Melanoma Cells

Abstract

Background: BRAFV600E melanoma cells develop resistance to vemurafenib. The BRAF/ERK axis controls melanoma cell proliferation. Aurora B is a key actor of mitosis. Results: The BRAF/ERK axis regulates Aurora B. Vemurafenib-resistant melanoma cells are sensitive to Aurora B inhibition. Conclusion: Aurora B is a valuable target in melanoma cells. Significance: Our findings provide insights into Aurora B regulation and on new druggable targets to overcome vemurafenib resistance.

Expression of Aurora-B and FOXM1 predict poor survival in patients with nasopharyngeal carcinoma

“…The basic biology of Aur-B functions are associated with genomic instability and aneuploidy, and overexpression of the Aur-B contributes to the pathogenesis of various tumors. The Aur-B has been reported to be associated with a variety of cancers, including melanoma [10], head and neck cancer [11], hepatocellular carcinoma [12], and non-small cell lung cancer [13]. However, to the best of our knowledge, the frequency of overexpression of Aur-B protein and its association with clinicopathologic features and prognosis of NPC have not been reported.…”

“…Compared with the relative full understanding of the prognostic value of Aurora A in head and neck cancers, including NPC, few studies of the prognostic role of Aur-B in nificant prognostic factor (p = 0.025); for LR-FFS, no significant prognostic factors were found; for D-FFS and Aur-B expression was a marginally significant prognostic factor (p = 0.056). When FOXM1 expression was analyzed, the Cox regression analyses (age, sex, T and N stage of tumor, FOXM1 expression as covariables) ( Bone et al [10] confirmed that Aur-B is highly expressed in metastatic melanoma cells, and the BRAF/ERK axis controls Aur-B expression at the transcriptional level, likely through the transcription factor FOXM1. FOXM1 is a member of the Fox transcription factor family, and regulates a number of cell cycle key factors involved in the transition from the G1 to S phase, G2 to M phase progression, and the transition to mitosis.…”

“…However, to the best of our knowledge, the frequency of overexpression of Aur-B protein and its association with clinicopathologic features and prognosis of NPC have not been reported. In addition, a study by Bonet et al [10] showed that the BRAF/ERK axis controls Aur-B expression at the transcriptional level, likely through the transcription factor forkhead box M1 (FOXM1). Therefore, in the present study, we investigated the expression of Aur-B and FOXM1 in an NPC tissue microarray.…”

Gene expression analysis in the lung of the rasH2 transgenic mouse at week 4 prior to induction of malignant tumor formation by urethane and N-methylolacrylamide

“…It has been demonstrated that activation of Aurk B induced aneuploidy and tumor formation (Ricke et al, 2011), and a selective inhibitor of Aurk B activity has been shown to be effective against cancers such as myeloma (Evans et al, 2008), hepatocellular carcinoma (Aihara et al, 2010) and breast cancer (Gully et al, 2010). Aurk B expression has also been reported to be positively regulated by the Ras/Raf/mitogen-activated protein kinase kinase (MEK)/ extracellular signal-regulated kinase (ERK) pathway at the transcriptional level (Bonet et al, 2012). The rasH2 Tg mice are known to show an elevation of total ras protein levels (Saitoh et al, 1990).…”

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“…In recent years Aurora kinases have been emerged as an important drug targets in several pharmaceutical companies and research industries since it plays a major role in regulating mitosis and cytokinesis 7 . Mitosis is a vital process for the regeneration of tissues and the genomic, development of an individual, and functional integrity of a cell 8 .…”