scholarly journals Tumor cell intrinsic TLR4 signaling promotes melanoma progression and metastatic dissemination

2021 ◽  
Author(s):  
Meri Rogava ◽  
Andreas Dominik Braun ◽  
Tetje Cornelia Sluis ◽  
Naveen Shridhar ◽  
Thomas Tüting ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Tlr4 Signaling ◽  
Metastatic Dissemination ◽  
Melanoma Progression

scholarly journals Lipid metabolic Reprogramming: Role in Melanoma Progression and Therapeutic Perspectives

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3147
Author(s):  
Laurence Pellerin ◽  
Lorry Carrié ◽  
Carine Dufau ◽  
Laurence Nieto ◽  
Bruno Ségui ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Tumor Cell ◽  
Fatty Acid Synthase ◽  
Lipid Synthesis ◽  
Metabolic Reprogramming ◽  
Acid Uptake ◽  
Oncogenic Signaling ◽  
Tumor Cell Migration ◽  
Melanoma Progression

Metabolic reprogramming contributes to the pathogenesis and heterogeneity of melanoma. It is driven both by oncogenic events and the constraints imposed by a nutrient- and oxygen-scarce microenvironment. Among the most prominent metabolic reprogramming features is an increased rate of lipid synthesis. Lipids serve as a source of energy and form the structural foundation of all membranes, but have also emerged as mediators that not only impact classical oncogenic signaling pathways, but also contribute to melanoma progression. Various alterations in fatty acid metabolism have been reported and can contribute to melanoma cell aggressiveness. Elevated expression of the key lipogenic fatty acid synthase is associated with tumor cell invasion and poor prognosis. Fatty acid uptake from the surrounding microenvironment, fatty acid β-oxidation and storage also appear to play an essential role in tumor cell migration. The aim of this review is (i) to focus on the major alterations affecting lipid storage organelles and lipid metabolism. A particular attention has been paid to glycerophospholipids, sphingolipids, sterols and eicosanoids, (ii) to discuss how these metabolic dysregulations contribute to the phenotype plasticity of melanoma cells and/or melanoma aggressiveness, and (iii) to highlight therapeutic approaches targeting lipid metabolism that could be applicable for melanoma treatment.

TAMI-06. TUMOR CELL-DERIVED CYTOKINE EXPRESSION CHANGES ASSOCIATED WITH BRAIN METASTASIS IN A SYNGENEIC MOUSE MODEL OF BREAST CANCER

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi199-vi199
Author(s):  
Ramin Morshed ◽  
Alexander Haddad ◽  
Saket Jain ◽  
Sabraj Gill ◽  
Jordan Spatz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Mouse Model ◽  
Tumor Cell ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Cytokine Expression ◽  
Metastatic Dissemination ◽  
Syngeneic Mouse ◽  
Syngeneic Mouse Model

Abstract Breast cancer is the most common malignancy in women in the United States, and brain metastases occur in almost a third of patients with metastatic dissemination. Immunoediting is a critical component of metastatic tumor cell elimination, and tumor clones that develop immune-escape mechanisms are associated with progression and metastatic dissemination. We hypothesized that breast cancer brain metastatic cells harbor immunomodulatory cytokine expression changes that promote an immunosuppressive environment to avoid immune cell-mediated elimination. To study this, a syngeneic mouse model of metastatic breast cancer was used. A brain metastatic line derived from the 4T1 breast cancer parental cell line was created by serially selecting brain metastatic populations of cells after intracardiac injection (4T1 BrM). A gene-expression analysis using an 800-gene cancer immunology-specific microarray panel was performed comparing the 4T1 parental and 4T1 BrM lines. 4T1 BrM cells demonstrate gene expression changes promoting immunosuppression including significant upregulation of IL18 and Lgals9 (Galectin-9) and downregulation of CD40, IL2rg, CCL2, and EOMES. When compared to 4T1 parental lines, the 4T1 BrM line demonstrated decreased expression of CCL2 and increased expression of GM-CSF on a cytokine array, corresponding to results obtained from gene expression analysis. These results suggest tumor-intrinsic cytokine expression changes that may mediate an immunosuppressive environment.

scholarly journals NAADP-Dependent Ca2+ Signaling Controls Melanoma Progression, Metastatic Dissemination and Neoangiogenesis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Annarita Favia ◽  
Irene Pafumi ◽  
Marianna Desideri ◽  
Fabrizio Padula ◽  
Camilla Montesano ◽  
...  
Keyword(s):  
Metastatic Dissemination ◽  
Melanoma Progression

scholarly journals New Insights into the Role of Sphingolipid Metabolism in Melanoma

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1967 ◽  
Author(s):  
Lorry Carrié ◽  
Mathieu Virazels ◽  
Carine Dufau ◽  
Anne Montfort ◽  
Thierry Levade ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Skin Cancer ◽  
Immune Responses ◽  
Cutaneous Melanoma ◽  
Sphingolipid Metabolism ◽  
Metastatic Dissemination ◽  
Resistance To Treatment ◽  
Melanoma Progression ◽  
The Impact

Cutaneous melanoma is a deadly skin cancer whose aggressiveness is directly linked to its metastatic potency. Despite remarkable breakthroughs in term of treatments with the emergence of targeted therapy and immunotherapy, the prognosis for metastatic patients remains uncertain mainly because of resistances. Better understanding the mechanisms responsible for melanoma progression is therefore essential to uncover new therapeutic targets. Interestingly, the sphingolipid metabolism is dysregulated in melanoma and is associated with melanoma progression and resistance to treatment. This review summarises the impact of the sphingolipid metabolism on melanoma from the initiation to metastatic dissemination with emphasis on melanoma plasticity, immune responses and resistance to treatments.

scholarly journals The Fate of Fusions

Cells ◽  
2018 ◽  
Vol 8 (1) ◽  
pp. 13 ◽  
Author(s):  
Gary Clawson
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Fusion ◽  
Cancer Progression ◽  
Genetic Instability ◽  
Cell Heterogeneity ◽  
Metastatic Dissemination ◽  
Tumor Cell Heterogeneity ◽  
Long Time

The concept of leukocyte-tumor cell fusion as a significant driver of cancer progression has been around a long time, and has garnered growing support over the last several years. The underlying idea seems quite simple and attractive: Fusion of tumor cells (with their inherent genetic instability) with leukocytes, particularly macrophages, could produce hybrids with high invasive capabilities, greatly facilitating their metastatic dissemination, while potentially accelerating tumor cell heterogeneity. While there are a number of attractive features with this story on the surface, the various studies seem to leave us with a conundrum, namely, what is the fate of such fusions?

scholarly journals Activation of STAT3 is a key event in TLR4 signaling-mediated melanoma progression

2020 ◽  
Vol 11 (4) ◽  
Author(s):  
Xiu-Qiong Fu ◽  
Bin Liu ◽  
Ya-Ping Wang ◽  
Jun-Kui Li ◽  
Pei-Li Zhu ◽  
...  
Keyword(s):  
Tlr4 Signaling ◽  
Melanoma Progression

Metastatic Growth of a Murine Tumor: Evidence of Dissemination to the Lungs in the Absence of Subcutaneous Growth

1986 ◽  
Vol 72 (4) ◽  
pp. 345-350 ◽  
Author(s):  
Saverio Alberti ◽  
Stefania Filippeschi ◽  
Federico Spreafico ◽  
Elsa Alberti ◽  
Francesco Colotta
Keyword(s):  
Tumor Growth ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Primary Tumor ◽  
Lung Metastases ◽  
Colon Adenocarcinoma ◽  
Cell Injection ◽  
Metastatic Dissemination ◽  
Metastatic Growth ◽  
Cell Inoculation

Growth of MCA-38/B colon adenocarcinoma was detectable 30-33 days after subcutaneous (s.c.) tumor cell inoculation in mice. Seventy percent of the mice receiving 107 tumor cells, 50 % of those receiving 104, and 15% of the mice given 105 cells developed s.c. tumors (mean of 4 experiments, total of 80 mice per group). Metastases in the presence of a primary tumor were observed in 11% of 107 and in 10% of 106 tumor-cell injected animals. Lung metastases were detected in the absence of tumor growth at the site of s.c. cell injection in 19% of 107, in 8% of 106 and in 5% of 105 and 104 tumor-cell inoculated mice. In parallel experiments an intravenous (i.v.) inoculum of tumor cells produced lung colonies in 40% of 106 and in 14% of 105 tumor-cell injected animals. Smaller inocula did not give rise to lung colonies, thus making it unlikely that accidental i.v. inoculations of tumor cells during the s.c. injections caused the observed metastatic dissemination to the lungs.

Sign in / Sign up

Export Citation Format

Share Document