Evidences that<em> Annona cherimola</em> leaves extracts suppress the malignant melanoma cells growth and migration

2021 ◽  
Author(s):  
Jessica Ceramella ◽  
Chiara La Torre ◽  
Domenico Iacopetta ◽  
Alexia Barbarossa ◽  
Fabrizio Francomano ◽  
...  
Keyword(s):  
Malignant Melanoma ◽  
Melanoma Cells ◽  
Annona Cherimola ◽  
And Migration

scholarly journals Tumour Progression Stage-Dependent Secretion of YB-1 Stimulates Melanoma Cell Migration and Invasion

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2328 ◽  
Author(s):  
Corinna Kosnopfel ◽  
Tobias Sinnberg ◽  
Birgit Sauer ◽  
Heike Niessner ◽  
Alina Muenchow ◽  
...  
Keyword(s):  
Cell Migration ◽  
Malignant Melanoma ◽  
Melanoma Cell ◽  
Cell Biology ◽  
Secretory Pathway ◽  
Tumour Progression ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Melanoma Progression ◽  
And Migration

Secreted factors play an important role in intercellular communication. Therefore, they are not only indispensable for the regulation of various physiological processes but can also decisively advance the development and progression of tumours. In the context of inflammatory disease, Y-box binding protein 1 (YB-1) is actively secreted and the extracellular protein promotes cell proliferation and migration. In malignant melanoma, intracellular YB-1 expression increases during melanoma progression and represents an unfavourable prognostic marker. Here, we show active secretion of YB-1 from melanoma cells as opposed to benign cells of the skin. Intriguingly, YB-1 secretion correlates with the stage of melanoma progression and depends on a calcium- and ATP-dependent non-classical secretory pathway leading to the occurrence of YB-1 in the extracellular space as a free protein. Along with an elevated YB-1 secretion of melanoma cells in the metastatic growth phase, extracellular YB-1 exerts a stimulating effect on melanoma cell migration, invasion, and tumourigenicity. Collectively, these data suggest that secreted YB-1 plays a functional role in melanoma cell biology, stimulating metastasis, and may serve as a novel biomarker in malignant melanoma that reflects tumour aggressiveness.

RNAi-mediated human Nestin silence inhibits proliferation and migration of malignant melanoma cells by G1/S arrest via Akt-GSK3β-Rb pathway

2017 ◽  
Vol 37 (6) ◽  
pp. 895-903
Author(s):  
Xu-hui Yang ◽  
Tian Xia ◽  
Jie Zhang ◽  
Shao-fen Yang ◽  
Hui-xia Tang ◽  
...  
Keyword(s):  
Malignant Melanoma ◽  
Melanoma Cells ◽  
Rb Pathway ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Functional Implication of Netrin Expression in Malignant Melanoma

2009 ◽  
Vol 31 (6) ◽  
pp. 415-422
Author(s):  
Simone Kaufmann ◽  
Silke Kuphal ◽  
Thomas Schubert ◽  
Anja K. Bosserhoff
Keyword(s):  
Malignant Melanoma ◽  
Melanoma Cells ◽  
Transcriptional Level ◽  
Altered Expression ◽  
Invasion And Migration ◽  
Expression Of Genes ◽  
Functional Relevance ◽  
And Migration

Background: Malignant melanoma cells are known to have altered expression of genes supporting proliferation and invasion, however, the expression of molecules of the Netrin family of repellent factors has not been analyzed in melanomas until now.Results: Here, we show that Netrin-1 expression is strongly induced in melanoma cells compared to melanocytes in vivo and in vitro controlled at the transcriptional level via ETS-1. In addition, the expression of the netrin receptor UNC5B was induced and that of UNC5C was reduced in the tumor cells. In order to determine the functional relevance of Netrin-1 expression in malignant melanoma, Netrin expression in melanoma cells was reduced by siRNA attempts and primary human melanocytes were treated with recombinant Netrin-1. The cells showed no changes in proliferation or apoptosis, however, a strong reduction of migratory properties was observed in the melanoma cells after reduction of Netrin expression whereas melanocyte migration was strongly induced by treatment with Netrin.Conclusions: Our study suggests that Netrin-1 promotes melanoma cell invasion and migration and therefore has an important role in the progression of malignant melanoma.

scholarly journals P2X7 promotes metastatic spreading and triggers release of miRNA-containing exosomes and microvesicles from melanoma cells

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Anna Pegoraro ◽  
Elena De Marchi ◽  
Manuela Ferracin ◽  
Elisa Orioli ◽  
Michele Zanoni ◽  
...  
Keyword(s):  
Malignant Melanoma ◽  
Melanoma Cell ◽  
P2x7 Receptor ◽  
Metastatic Malignant Melanoma ◽  
Melanoma Cells ◽  
Vesicular Release ◽  
And Migration ◽  
Metastatic Spreading

AbstractTumor growth and metastatic spreading are heavily affected by the P2X7 receptor as well as microvesicles and exosomes release into the tumor microenvironment. P2X7 receptor stimulation is known to trigger vesicular release from immune and central nervous system cells. However, P2X7 role in microvesicles and exosomes delivery from tumor cells was never analyzed in depth. Here we show that P2X7 is overexpressed in patients affected by metastatic malignant melanoma and that its expression closely correlates with reduced overall survival. Antagonism of melanoma cell-expressed P2X7 receptor inhibited in vitro anchorage-independent growth and migration and in vivo dissemination and lung metastasis formation. P2X7 stimulation triggered the release of miRNA-containing microvesicles and exosomes from melanoma cells, profoundly altering the nature of their miRNA content, as well as their dimensions and quantity. Among the more than 200 miRNAs that we found up-or-down-modulated for each vesicular fraction tested, we identified three miRNAs, miR-495-3p, miR-376c-3p, and miR-6730-3p, that were enriched in both the exosome and microvesicle fraction in a P2X7-dependent fashion. Interestingly, upon transfection, these miRNAs promoted melanoma cell growth or migration, and their vesicular release was minimized by P2X7 antagonism. Our data unveil an exosome/microvesicle and miRNA-dependent mechanism for the pro-metastatic activity of the P2X7 receptor and highlight this receptor as a suitable prognostic biomarker and therapeutic target in malignant melanoma.

scholarly journals Bee Venom and Its Peptide Component Melittin Suppress Growth and Migration of Melanoma Cells via Inhibition of PI3K/AKT/mTOR and MAPK Pathways

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 929 ◽  
Author(s):  
Haet Lim ◽  
Seung Baek ◽  
Hye Jung
Keyword(s):  
Malignant Melanoma ◽  
Biological Activities ◽  
Clonogenic Survival ◽  
Inhibitory Effect ◽  
Melanoma Cells ◽  
Mapk Signaling ◽  
Bee Venom ◽  
Migration And Invasion ◽  
Amino Acid Residues ◽  
And Migration

Malignant melanoma is the deadliest form of skin cancer and highly chemoresistant. Melittin, an amphiphilic peptide containing 26 amino acid residues, is the major active ingredient from bee venom (BV). Although melittin is known to have several biological activities such as anti-inflammatory, antibacterial and anticancer effects, its antimelanoma effect and underlying molecular mechanism have not been fully elucidated. In the current study, we investigated the inhibitory effect and action mechanism of BV and melittin against various melanoma cells including B16F10, A375SM and SK-MEL-28. BV and melittin potently suppressed the growth, clonogenic survival, migration and invasion of melanoma cells. They also reduced the melanin formation in α-melanocyte-stimulating hormone (MSH)-stimulated melanoma cells. Furthermore, BV and melittin induced the apoptosis of melanoma cells by enhancing the activities of caspase-3 and -9. In addition, we demonstrated that the antimelanoma effect of BV and melittin is associated with the downregulation of PI3K/AKT/mTOR and MAPK signaling pathways. We also found that the combination of melittin with the chemotherapeutic agent temozolomide (TMZ) significantly increases the inhibition of growth as well as invasion in melanoma cells compared to melittin or TMZ alone. Taken together, these results suggest that melittin could be potentially applied for the prevention and treatment of malignant melanoma.

scholarly journals MicroRNA-9 inhibits the proliferation and migration of malignant melanoma cells via targeting sirituin 1

2017 ◽  
Vol 14 (2) ◽  
pp. 931-938 ◽  
Author(s):  
Pingyuan Bu ◽  
Chengqun Luo ◽  
Quanyong He ◽  
Ping Yang ◽  
Xi Li ◽  
...  
Keyword(s):  
Malignant Melanoma ◽  
Melanoma Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Inhibition Effect of Chloroquine and Integrin-Linked Kinase Knockdown on Translation in Melanoma Cells

2021 ◽  
Vol 22 (7) ◽  
pp. 3682
Author(s):  
Dorota Gil ◽  
Piotr Laidler ◽  
Marta Zarzycka ◽  
Joanna Dulińska-Litewka
Keyword(s):  
Signaling Pathways ◽  
Melanoma Cell ◽  
Melanoma Cells ◽  
Antitumor Effects ◽  
Regulatory Pathways ◽  
Scratch Wound ◽  
Integrin Linked Kinase ◽  
And Migration ◽  
Cell Signaling Pathways

The twofold role of autophagy in cancer is often the therapeutic target. Numerous regulatory pathways are shared between autophagy and other molecular processes needed in tumorigenesis, such as translation or survival signaling. Thus, we have assumed that ILK knockdown should promote autophagy, and used together with chloroquine, an autophagy inhibitor, it could generate a better anticancer effect by dysregulation of common signaling pathways. Expression at the protein level was analyzed using Western Blot; siRNA transfection was done for ILK. Analysis of cell signaling pathways was monitored with phospho-specific antibodies. Melanoma cell proliferation was assessed with the crystal violet test, and migration was evaluated by scratch wound healing assays. Autophagy was monitored by the accumulation of its marker, LC3-II. Our data show that ILK knockdown by siRNA suppresses melanoma cell growth by inducing autophagy through AMPK activation, and simultaneously initiates apoptosis. We demonstrated that combinatorial treatment of melanoma cells with CQ and siILK has a stronger antitumor effect than monotherapy with either of these. It generates the synergistic antitumor effects by the decrease of translation of both global and oncogenic proteins synthesis. In our work, we point to the crosstalk between translation and autophagy regulation.

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