Enhanced OXPHOS, glutaminolysis and β-oxidation constitute the metastatic phenotype of melanoma cells

2016 ◽  
Vol 473 (6) ◽  
pp. 703-715 ◽  
Author(s):  
Mariana F. Rodrigues ◽  
Emilie Obre ◽  
Fabiana H.M. de Melo ◽  
Gilson C. Santos ◽  
Antonio Galina ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Primary Tumour ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Metastatic Phenotype ◽  
Metastatic Cells ◽  
Extra Energy

Detachment from the primary tumour, migration and invasion of target tissues by metastatic cells require extra energy. Among melanoma cells displaying different stages of aggressiveness, only the metastatic ones exhibited increased mitochondrial function, reflected mainly by glutamine catabolism, by β-oxidation.

scholarly journals Mitochondrial function is controlled by melatonin and its metabolites in vitro in human melanoma cells

2021 ◽  
Vol 70 (3) ◽  
Author(s):  
Bernadetta Bilska ◽  
Fiona Schedel ◽  
Anna Piotrowska ◽  
Joanna Stefan ◽  
Michal Zmijewski ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Human Melanoma Cells

scholarly journals Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression

2021 ◽  
Author(s):  
Lijun Wu ◽  
Ke Li ◽  
Wei Lin ◽  
Jianjiang Liu ◽  
Qiang Qi ◽  
...  
Keyword(s):  
Colony Formation ◽  
Noncoding Rna ◽  
Melanoma Cells ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Tumor Xenograft ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Competing Endogenous Rna ◽  
Melanoma Tumor

AbstractStudies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291’s role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma.

Luteolin inhibits the proliferation, adhesion, migration and invasion of choroidal melanoma cells in vitro

2021 ◽  
pp. 108643
Author(s):  
Meng-Lin Shi ◽  
Yu-Fen Chen ◽  
Wei-Qi Wu ◽  
Yao Lai ◽  
Qi Jin ◽  
...  
Keyword(s):  
Choroidal Melanoma ◽  
Melanoma Cells ◽  
Migration And Invasion

Induction of the metastatic phenotype of human melanoma cells by wild type P53 and P21

1997 ◽  
Vol 7 (Supplement 1) ◽  
pp. S97
Author(s):  
S Rauth ◽  
A Green ◽  
J Kichina ◽  
A Silkaitis
Keyword(s):  
Melanoma Cells ◽  
Human Melanoma ◽  
Wild Type ◽  
Metastatic Phenotype ◽  
Human Melanoma Cells ◽  
Wild Type P53

scholarly journals In-depth Characterization of the Secretome of Colorectal Cancer Metastatic Cells Identifies Key Proteins in Cell Adhesion, Migration, and Invasion

2013 ◽  
Vol 12 (6) ◽  
pp. 1602-1620 ◽  
Author(s):  
Rodrigo Barderas ◽  
Marta Mendes ◽  
Sofia Torres ◽  
Rubén A. Bartolomé ◽  
María López-Lucendo ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Adhesion ◽  
Migration And Invasion ◽  
Metastatic Cells

Mechanism of miR‐137 regulating migration and invasion of melanoma cells by targeting PIK3R3 gene

2018 ◽  
Vol 120 (5) ◽  
pp. 8393-8400 ◽  
Author(s):  
Jia Qi ◽  
Wei‐wei Wang ◽  
Wei Chen ◽  
Wen‐ying Lu ◽  
An‐quan Shang
Keyword(s):  
Melanoma Cells ◽  
Migration And Invasion

scholarly journals Elevated METTL9 is associated with peritoneal dissemination in human scirrhous gastric cancers

2021 ◽  
Author(s):  
Toshifumi Hara ◽  
Yuuki Tominaga ◽  
Koji Ueda ◽  
Keichiro Mihara ◽  
Kazuyoshi Yanagihara ◽  
...  
Keyword(s):  
Cancer Metastasis ◽  
Peritoneal Dissemination ◽  
Migration And Invasion ◽  
Gastric Cancers ◽  
Metastatic Cells ◽  
Metastatic Activity ◽  
Gastric Cancer Patients ◽  
Cellular Components ◽  
Complex I Activity ◽  
The Relationship

Methylation, the most common chemical modification of cellular components such as DNA, RNA, and proteins, impacts biological processes including transcription, RNA processing, and protein dynamics. Although abnormal expression of methyltransferase can lead to various diseases including cancers, little is known about the relationship between methyltransferase and cancers. Here we aimed to understand the role of methyltransferase in cancer metastasis. We found that elevated methyltransferase-like 9 (METTL9) is closely associated with the acquisition of metastatic activity in human scirrhous gastric cancers. The stable knockdown of METTL9 via an shRNA vector technique in our original metastatic cells from scirrhous gastric cancer patients significantly inhibited migration and invasion. In metastatic cells, METTL9 protein is predominantly localized in mitochondria, and the METTL9 knockdown significantly reduced mitochondrial Complex I activity. METTL9 can be a promising molecular target to inhibit peritoneal dissemination of scirrhous gastric cancers. This report is the first to describe the relationship between METTL9 and cancer metastasis.

scholarly journals RUNX2 is overexpressed in melanoma cells and mediates their migration and invasion

2014 ◽  
Vol 348 (1-2) ◽  
pp. 61-70 ◽  
Author(s):  
Rajeev K. Boregowda ◽  
Oyenike O. Olabisi ◽  
Walid Abushahba ◽  
Byeong-Seon Jeong ◽  
Keneshia K. Haenssen ◽  
...  
Keyword(s):  
Melanoma Cells ◽  
Migration And Invasion

scholarly journals Bornyl cis-4-Hydroxycinnamate Suppresses Cell Metastasis of Melanoma through FAK/PI3K/Akt/mTOR and MAPK Signaling Pathways and Inhibition of the Epithelial-to-Mesenchymal Transition

2018 ◽  
Vol 19 (8) ◽  
pp. 2152 ◽  
Author(s):  
Tzu-Yen Yang ◽  
Mei-Li Wu ◽  
Chi-I Chang ◽  
Chih-I Liu ◽  
Te-Chih Cheng ◽  
...  
Keyword(s):  
Cell Migration ◽  
Signaling Pathways ◽  
Melanoma Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion ◽  
Cell Metastasis ◽  
A375 Melanoma

Bornyl cis-4-hydroxycinnamate, a bioactive compound isolated from Piper betle stems, has the potential for use as an anti-cancer agent. This study investigated the effects of bornyl cis-4-hydroxycinnamate on cell migration and invasion in melanoma cells. Cell migration and invasion were compared in A2058 and A375 melanoma cell lines treated with/without bornyl cis-4-hydroxycinnamate (1–6 µM). To examine whether bornyl cis-4-hydroxycinnamate has a potential anti-metastatic effect on melanoma cells, cell migration and invasion assays were performed using a Boyden chamber assay and a transwell chamber in A2058 and A375 cells. Gelatin zymography was employed to determine the enzyme activities of MMP-2 and MMP-9. Cell lysates were collected for Western blotting analysis of matrix metalloproteinase (MMP)-2, MMP-9 and tissue inhibitors of metalloproteinase-1/2 (TIMP-1/2), as well as key molecules in the mitogen-activated protein kinase (MAPK), focal adhesion kinase (FAK)/ phosphatidylinositide-3 kinases (PI3K)/Akt/ mammalian target of rapamycin (mTOR), growth factor receptor-bound protein 2 (GRB2) signaling pathways. Our results demonstrated that bornyl cis-4-hydroxycinnamate is a potentially useful agent that inhibits melanoma cell migration and invasion, and altered melanoma cell metastasis by reducing MMP-2 and MMP-9 expression through inhibition of the FAK/PI3K/Akt/mTOR, MAPK, and GRB2 signaling pathways. Moreover, bornyl cis-4-hydroxycinnamate inhibited the process of the epithelial-to-mesenchymal transition in A2058 and A375 melanoma cells. These findings suggested that bornyl cis-4-hydroxycinnamate has potential as a chemotherapeutic agent, and warrants further investigation for its use in the management of human melanoma.

scholarly journals An Autocrine Wnt5a Loop Promotes NF-κB Pathway Activation and Cytokine/Chemokine Secretion in Melanoma

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 1060 ◽  
Author(s):  
Gastón Barbero ◽  
María Victoria Castro ◽  
María Belén Villanueva ◽  
María Josefina Quezada ◽  
Natalia Brenda Fernández ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Epithelial Mesenchymal Transition ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Melanoma Cells ◽  
Dominant Negative ◽  
Migration And Invasion ◽  
Soluble Receptor ◽  
Mesenchymal Transition ◽  
Cytokines And Chemokines

Wnt5a signaling has been implicated in the progression of cancer by regulating multiple cellular processes, largely migration and invasion, epithelial-mesenchymal transition (EMT), and metastasis. Since Wnt5a signaling has also been involved in inflammatory processes in infectious and inflammatory diseases, we addressed the role of Wnt5a in regulating NF-κB, a pivotal mediator of inflammatory responses, in the context of cancer. The treatment of melanoma cells with Wnt5a induced phosphorylation of the NF-κB subunit p65 as well as IKK phosphorylation and IκB degradation. By using cDNA overexpression, RNA interference, and dominant negative mutants we determined that ROR1, Dvl2, and Akt (from the Wnt5a pathway) and TRAF2 and RIP (from the NF-κB pathway) are required for the Wnt5a/NF-κB crosstalk. Wnt5a also induced p65 nuclear translocation and increased NF-κB activity as evidenced by reporter assays and a NF-κB-specific upregulation of RelB, Bcl-2, and Cyclin D1. Further, stimulation of melanoma cells with Wnt5a increased the secretion of cytokines and chemokines, including IL-6, IL-8, IL-11, and IL-6 soluble receptor, MCP-1, and TNF soluble receptor I. The inhibition of endogenous Wnt5a demonstrated that an autocrine Wnt5a loop is a major regulator of the NF-κB pathway in melanoma. Taken together, these results indicate that Wnt5a activates the NF-κB pathway and has an immunomodulatory effect on melanoma through the secretion of cytokines and chemokines.

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