Pathway landscapes and epigenetic regulation in breast cancer and melanoma cell lines

Baroudi, Mariama El; Sala, Dario La; Cinti, Caterina; Capobianco, Enrico

doi:10.1186/1742-4682-11-s1-s8

Cited by 9 publications

(4 citation statements)

References 77 publications

(78 reference statements)

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“…MiR-27 promotes human malignant melanoma cell metastasis by inducing the epithelial-to-mesenchymal transition [23,24]. NRP1 enhances signaling in three major pathways that have been linked to EMT, i.e., TGF-β, Hh and HGF/cMet [25][26][27][28][29][30]. In the previous study, over-expressed NRP1 promoted EMT and si-NRP1 restrained EMT was found in malignant melanoma, whereas the forced expression of miR-365 inhibited EMT.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-365 inhibits growth, invasion and metastasis of malignant melanoma by targeting NRP1 expression

Bai,

Zhang,

et al. 2015

CBM

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Section: Discussionmentioning

confidence: 99%

MicroRNA-365 inhibits growth, invasion and metastasis of malignant melanoma by targeting NRP1 expression

Bai,

Zhang,

et al. 2015

CBM

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“… 15 , 40 – 42 Among the candidate tumor related new biomarkers, MrgprF, a MAS related GPR family member, was revealed to be downregulated in CM due to the hypermethylation in its promoter region, which could be reversed by 5-Azacytidine treatment, a well-known anti-cancer drug. 43 , 44 Consistently, 5-Azacytidine has previously been shown to behave as an anti-neoplastic agent for B16 melanoma. 45 , 46…”

Section: Discussionmentioning

confidence: 76%

MrgprF acts as a tumor suppressor in cutaneous melanoma by restraining PI3K/Akt signaling

Shen

Han

et al. 2022

Sig Transduct Target Ther

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The incidence of cutaneous melanoma (CM) has been increasing annually worldwide. In this study, we identify that MrgprF, a MAS related GPR family member, is decreased in cutaneous melanoma tissues and cell lines due to hypermethylation of its promoter region, and show that patients with CM expressing high levels of MrgprF exhibit an improved clinical outcome. We demonstrate that MrgprF forced expression inhibits tumor cell proliferation, migration, xenograft tumor growth, and metastasis. On the contrary, MrgprF knockdown promotes tumor cell proliferation and transformation of immortalized human keratinocyte-HaCaT cells, supporting the inhibitory role of MrgprF during tumor progression. Mechanistic studies reveal that MrgprF reduces the phosphoinositol‑3‑kinase (PI3K) complex formation between p101 and p110γ subunits, the critical step for phosphatidylinositol-(3, 4)-P2 (PIP2) conversion to phosphatidylinositol-(3, 4, 5)-P3 (PIP3), and then reduces the activation of PI3K/Akt signaling. This effect can be reversed by Akt specific agonist SC79. In addition, AMG 706, a previously documented inhibitor for endothelial cell proliferation, is identified as a potential agonist for MrgprF, and can impede tumor growth both in vitro and in vivo. Taken together, our findings suggest that MrgprF, a novel tumor suppressor in cutaneous melanoma, may be useful as a therapeutic target in the future.

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“…At low doses, DNA synthesis is continued, while DNA–DNMT1 adduct bonds are being degraded and repaired, resulting in systematically hypomethylated DNA [41,42]. Studies show that DAC has effects on melanoma via decreasing cell growth and invasion [43] as well as alerting gene expression, includes tumor suppressor genes [44].…”

Section: Introductionmentioning

confidence: 99%

Effect of Sulforaphane and 5-Aza-2’-Deoxycytidine on Melanoma Cell Growth

Chiang

Koss

et al. 2019

Medicines

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Background: UV exposure-induced oxidative stress is implicated as a driving mechanism for melanoma. Increased oxidative stress results in DNA damage and epigenetic dysregulation. Accordingly, we explored whether a low dose of the antioxidant sulforaphane (SFN) in combination with the epigenetic drug 5-aza-2’-deoxycytidine (DAC) could slow melanoma cell growth. SFN is a natural bioactivated product of the cruciferous family, while DAC is a DNA methyltransferase inhibitor. Methods: Melanoma cell growth characteristics, gene transcription profiles, and histone epigenetic modifications were measured after single and combination treatments with SFN and DAC. Results: We detected melanoma cell growth inhibition and specific changes in gene expression profiles upon combinational treatments with SFN and DAC, while no significant alterations in histone epigenetic modifications were observed. Dysregulated gene transcription of a key immunoregulator cytokine—C-C motif ligand 5 (CCL-5)—was validated. Conclusions: These results indicate a potential combinatorial effect of a dietary antioxidant and an FDA-approved epigenetic drug in controlling melanoma cell growth.

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Pathway landscapes and epigenetic regulation in breast cancer and melanoma cell lines

Cited by 9 publications

References 77 publications

MicroRNA-365 inhibits growth, invasion and metastasis of malignant melanoma by targeting NRP1 expression

MicroRNA-365 inhibits growth, invasion and metastasis of malignant melanoma by targeting NRP1 expression

MrgprF acts as a tumor suppressor in cutaneous melanoma by restraining PI3K/Akt signaling

Effect of Sulforaphane and 5-Aza-2’-Deoxycytidine on Melanoma Cell Growth

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