Identification by differential display of a protein phosphatase-2A regulatory subunit preferentially expressed in malignant melanoma cells

Francia, Guilio; Poulsom, Richard; Hanby, Andrew M.; Mitchell, Siobhán; Williams, Gillian; McKee, Peter; Hart, Ian R.

doi:10.1002/(sici)1097-0215(19990827)82:5<709::aid-ijc14>3.0.co;2-r

Cited by 50 publications

(52 citation statements)

References 19 publications

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“…In a study by Francia et al (26), the mRNA expression levels of AnxA6 were observed to be lower in murine B16F1O-metastatic melanoma cells than in syngeneic melan-A immortalized melanocyte cells. In addition, the protein levels of AnxA6 were markedly reduced in the B16F1O cells compared with the melan-A cells, and inversely correlated with melanoma progression (26). Immunohistochemical (IHC) analyses demonstrated that the expression of AnxA6 was reduced or eliminated following an increase in tumor malignancy (26).…”

Section: Role Of Anxa6 In Melanoma Progressionmentioning

confidence: 91%

“…It has been implicated as a potential marker for cervical cancer (CC) (25), and as a tumor suppressor in melanoma (26), epithelial carcinoma (23,(27)(28)(29), breast cancer (BC) (23,28), gastric cancer (GC) (30), prostate cancer (PCa) (31,32) and chronic myeloid leukemia (CML) (33). Furthermore, AnxA6 is considered to act as a promoting factor in the cellular adhesion, motility and invasiveness of BC (34,35), the progression of acute lymphoblastic leukemia (ALL) (36), the adhesion of lymphoma (37), and the secretory processes in myeloma cells (21).…”

Section: Introductionmentioning

confidence: 99%

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Role of annexin A6 in cancer

Liu

Guo

et al. 2015

Oncology Letters

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Abstract. Annexin A6 (AnxA6) is a member of a conserved superfamily of Ca 2+ -dependent membrane-binding annexin proteins. It participates in membrane and cytoskeleton organization, cholesterol homeostasis, membrane trafficking, cell adhesion and signal transduction. The expression levels of AnxA6 are closely associated with melanoma, cervical cancer, epithelial carcinoma, breast cancer, gastric cancer, prostate cancer, acute lymphoblastic leukemia, chronic myeloid leukemia, large-cell lymphoma and myeloma. AnxA6 exhibits dual functions in cancer, acting either as a tumor suppressor or promoter, depending on the type of cancer and the degree of malignancy. In several types of cancer, AnxA6 acts via Ras, Ras/MAPK and/or FAK/PI3K signaling pathways by mainly mediating PKCα, p120GAP, Bcr-Abl and YY1. In the present review, the roles of AnxA6 in different types of cancer are summarized.

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Section: Role Of Anxa6 In Melanoma Progressionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Role of annexin A6 in cancer

Liu

Guo

et al. 2015

Oncology Letters

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“…Alterations in the quaternary structure of PP2A also appears to have a crucial function in cells transformation and tumour development, as different B subunits have been found either aberrantly expressed in human cancers or displaced by the interaction of PR65/A with the SV40 small-t antigen, and by mutations of the PP2A A subunits (Janssens et al, 2005). For example, the B56g subunit is highly expressed in numerous human malignant melanoma cells compared to normal epidermal melanocytes (Francia et al, 1999). Importantly, B56g participates also in the regulation of the Wnt/ b-catenin signalling, a pathway important in the control of cell proliferation and self-renewal of the cancer stem cell.…”

Section: Protein Phosphatase 2a (Pp2a) a Phosphatase With Tumour Supmentioning

confidence: 99%

ReSETting PP2A tumour suppressor activity in blast crisis and imatinib-resistant chronic myelogenous leukaemia

Perrotti

Neviani

2006

Br J Cancer

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The deregulated kinase activity of p210-BCR/ABL oncoproteins, hallmark of chronic myelogenous leukaemia (CML), induces and sustains the leukaemic phenotype, and contributes to disease progression. Imatinib mesylate, a BCR/ABL kinase inhibitor, is effective in most of chronic phase CML patients. However, a significant percentage of CML patients develop resistance to imatinib and/or still progresses to blast crisis, a disease stage that is often refractory to imatinib therapy. Furthermore, there is compelling evidence indicating that the CML leukaemia stem cell is also resistant to imatinib. Thus, there is still a need for new drugs that, if combined with imatinib, will decrease the rate of relapse, fully overcome imatinib resistance and prevent blastic transformation of CML. We recently reported that the activity of the tumour suppressor protein phosphatase 2A (PP2A) is markedly inhibited in blast crisis CML patient cells and that molecular or pharmacologic re-activation of PP2A phosphatase led to growth suppression, enhanced apoptosis, impaired clonogenic potential and decreased in vivo leukaemogenesis of imatinib-sensitive and -resistant (T315I included) CML-BC patient cells and/or BCR/ABL þ myeloid progenitor cell lines. Thus, the combination of PP2A phosphatase-activating and BCR/ABL kinase-inhibiting drugs may represent a powerful therapeutic strategy for blast crisis CML patients.

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“…25 In contrast, ANXA6 has tumor suppressive activity in squamous cell carcinoma, 26 and a decrease in ANXA6 and ANXA7 proteins is associated with malignant phenotype and the metastatic potential of melanoma. 27,28 Moreover, ANXA4 plays a role in chemoresistance. 29 Hence, there are at least two categories of ANXs implicated in tumor progression and tumor suppression, and different ANXs play important and complex roles in cancer.…”

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confidence: 99%

Down-Regulation of Annexin A10 in Hepatocellular Carcinoma Is Associated with Vascular Invasion, Early Recurrence, and Poor Prognosis in Synergy with p53 Mutation

Liu¹,

Lin²,

Peng³

et al. 2002

The American Journal of Pathology

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Annexins (ANXs) are a large group of calcium-binding proteins participating in diverse important biological processes. ANXA10 is the least expressed new member of unknown function. We showed that ANXA10 mRNA was expressed in adult liver and hepatocellular carcinoma (HCC), but not in multiple adult and fetal tissues, cholangiocarcinoma, and several other common carcinomas. Of 182 unifocal primary HCCs, ANXA10 mRNA was dramatically reduced in 121 (66%), and the down-regulation correlated with p53 mutation (P ‫؍‬ 0.024), early intrahepatic tumor recurrence (P ‫؍‬ 0.0007), and lower 4-year survival (P ‫؍‬ 0.0014). Down-regulation of ANXA10 was twofold more frequent in large than small HCCs (P ‫؍‬ 0.0012), in grade II to III than grade I HCC (P < 0.00001), and in stage IIIA to IV than stage I to II HCC (P < 0.00001). Moreover, ANXA10 down-regulation and p53 mutation acted synergistically toward high-grade (P < 0.00001), high-stage HCC (P < 0.00001), and poorer prognosis (P ‫؍‬ 0.0025). Our results indicate that the expression of the tissue-and tumor-restricted ANXA10 is a marker of liver cell differentiation and growth arrest, and its down-regulation associated with malignant phenotype of hepatocytes, vascular invasion, and progression of HCC, leading to poor prognosis. Thus, ANXA10 might serve as a new potential target of gene therapy for HCC.

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Identification by differential display of a protein phosphatase-2A regulatory subunit preferentially expressed in malignant melanoma cells

Cited by 50 publications

References 19 publications

Role of annexin A6 in cancer

Role of annexin A6 in cancer

ReSETting PP2A tumour suppressor activity in blast crisis and imatinib-resistant chronic myelogenous leukaemia

Down-Regulation of Annexin A10 in Hepatocellular Carcinoma Is Associated with Vascular Invasion, Early Recurrence, and Poor Prognosis in Synergy with p53 Mutation

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