Nuclear β-catenin localization is not sufficient for canonical Wnt signaling activation in human melanoma cell lines

Куликова, К. В.; Posvyatenko, Alexandra V.; Гнучев, Н. В.; Georgiev, G. P.; Kibardin, Alexey; Larin, Sergey

doi:10.1134/s0026893311050098

Cited by 5 publications

(2 citation statements)

References 21 publications

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“…Typically, melanoma metastasis is associated withthe activation of signaling pathways that are essential for embryogenesis [25]. In recent years, some molecular pathways have been reported tobe involved in many cancers.…”

Section: Discussionmentioning

confidence: 99%

The Role of PI3K and Wntsignaling Pathways and CSC Markers in Melanoma (B16F10) Therapy

sajedianfard

et al. 2021

Preprint

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Background Metformin has been the subject of recent studies aimed at the treatment of melanoma cancer. In this study, the anti-cancer effects of metformin, an antidiabetic drug, was investigated in-vitrousing the B16F10 melanoma cell line. Methods Melanoma cells were treated for 24 h with various concentrations of metformin, alone or incombination withdacarbazine. The effects of these two treatment agents on cell viability were evaluated by MTT assay. In addition, stemness and the activation of specific signaling pathways were evaluated by FACS and immunoblotting. Results Metformin induced β-catenin phosphorylation and decreasedmTOR and PARP expressions. Also, a normal dose of metformin was found toreducethe phosphorylation levels of4E-BP1, AKT, and S6rp.In this study, we evaluated the potential of metformin as a therapeutic agent against CSCs in the adjuvant setting. Conclusion Our data indicate that some transcriptional regulators and proteins in the above-mentioned pathwayswere associated with cancer progression and inhibited by adjuvant chemotherapy with metformin.Metformin significantly inhibited cell growth and proliferation pathways, including Wnt and PI3K/AKT/mTOR. These findings show the potential of metformin in cancer treatment.

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Section: Discussionmentioning

confidence: 99%

The Role of PI3K and Wntsignaling Pathways and CSC Markers in Melanoma (B16F10) Therapy

sajedianfard

et al. 2021

Preprint

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“…The role of "noncanonical" Wnt ligands in tumorigenesis is best understood for melanoma. In this case, expression of the Wnt5a "noncanonical" ligand is associated with a highly aggressive tumor phenotype [18][19][20], which may result, in particular, from Wnt5a functional activ ity [21]. Genetic changes that affect Wnt signaling and lead to uncontrollable activation of the canonical Wnt signaling pathway are detectable in the majority of colon cancer cases [22,23].…”

Section: Introductionmentioning

confidence: 94%

Functional properties of a new Wnt11 isoform expressed in colon carcinoma cell line HT29

et al. 2012

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Colon carcinoma is a common type of neoplastic transformation. The mechanisms of its estab lishment and progression have been studied for several decades. Aberrant activation of canonical Wnt signal ing is frequently observed in colon carcinoma cells. Moreover, expression of "noncanonical" Wnt ligands is also detected in this type of cancer. However, the role of noncanonical Wnt signaling in carcinogenesis and colorectal cancer (CRC) progression is still unclear. To study the characteristics of noncanonical Wnt signal ing activation in CRC, expression of "noncanonical" ligand hWnt11 was examined in HT29 human colon carcinoma cells. For the first time it was shown that alternative splicing accompanies hWnt11 expression in CRC. A new hWnt11 isoform (hWnt11sp3) was identified. Unlike hWnt11, the isoform is not secreted and lacks the ability to inhibit canonical Wnt signaling. Different functional properties of the ligand hWnt11 and its isoform may reflect a special role of alternative splicing in carcinogenesis and tumor progression, since aberrant activity of canonical Wnt signaling is observed in many tumor cells. The existence of several Wnt iso forms and the difference in their functional properties should be taken into account when investigating the role of Wnt ligands.

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Roads to melanoma: Key pathways and emerging players in melanoma progression and oncogenic signaling

Paluncic

Kovačević

Jansson

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

163

168

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Melanoma has markedly increased worldwide during the past several decades in the Caucasian population and is responsible for 80% of skin cancer deaths. Considering that metastatic melanoma is almost completely resistant to most current therapies and is linked with a poor patient prognosis, it is crucial to further investigate potential molecular targets. Major cell-autonomous drivers in the pathogenesis of this disease include the classical MAPK (i.e., RAS-RAF-MEK-ERK), WNT, and PI3K signaling pathways. These pathways play a major role in defining the progression of melanoma, and some have been the subject of recent pharmacological strategies to treat this belligerent disease. This review describes the latest advances in the understanding of melanoma progression and the major molecular pathways involved. In addition, we discuss the roles of emerging molecular players that are involved in melanoma pathogenesis, including the functional role of the melanoma tumor antigen, p97/MFI2 (melanotransferrin).

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Nuclear β-catenin localization is not sufficient for canonical Wnt signaling activation in human melanoma cell lines

Cited by 5 publications

References 21 publications

The Role of PI3K and Wntsignaling Pathways and CSC Markers in Melanoma (B16F10) Therapy

The Role of PI3K and Wntsignaling Pathways and CSC Markers in Melanoma (B16F10) Therapy

Functional properties of a new Wnt11 isoform expressed in colon carcinoma cell line HT29

Roads to melanoma: Key pathways and emerging players in melanoma progression and oncogenic signaling

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