Copper(II):phenanthroline complexes with l-asparagine and l-methionine: Synthesis, crystal structure and in-vitro cytotoxic effects on prostate, breast and melanoma cancer cells

Polyhedron ◽  
2020 ◽  
Vol 191 ◽  
pp. 114807
Author(s):  
Jessica Andreza Oliveira Rodrigues ◽  
João Gomes de Oliveira Neto ◽  
Aline Oliveira da Silva de Barros ◽  
Alejandro Pedro Ayala ◽  
Ralph Santos-Oliveira ◽  
...  
2018 ◽  
Author(s):  
F Guo ◽  
Z Yang ◽  
J Xu ◽  
J Sehouli ◽  
AE Albers ◽  
...  

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Carmela Martini ◽  
Mark DeNichilo ◽  
Danielle P. King ◽  
Michaelia P. Cockshell ◽  
Brenton Ebert ◽  
...  

Abstract Background The formation of blood vessels within solid tumors directly contributes to cancer growth and metastasis. Until recently, tumor vasculature was thought to occur exclusively via endothelial cell (EC) lined structures (i.e. angiogenesis), but a second source of tumor vasculature arises from the cancer cells themselves, a process known as vasculogenic mimicry (VM). While it is generally understood that the function of VM vessels is the same as that of EC-lined vessels (i.e. to supply oxygen and nutrients to the proliferating cancer cells), the molecular mechanisms underpinning VM are yet to be fully elucidated. Methods Human VM-competent melanoma cell lines were examined for their VM potential using the in vitro angiogenesis assays (Matrigel), together with inhibition studies using small interfering RNA and blocking monoclonal antibodies. Invasion assays and adhesion assays were used to examine cancer cell function. Results Herein we demonstrate that CD36, a cell surface glycoprotein known to promote angiogenesis by ECs, also supports VM formation by human melanoma cancer cells. In silico analysis of CD36 expression within the melanoma cohort of The Cancer Genome Atlas suggests that melanoma patients with high expression of CD36 have a poorer clinical outcome. Using in vitro ‘angiogenesis’ assays and CD36-knockdown approaches, we reveal that CD36 supports VM formation by human melanoma cells as well as adhesion to, and invasion through, a cancer derived extracellular matrix substrate. Interestingly, thrombospondin-1 (TSP-1), a ligand for CD36 on ECs that inhibits angiogenesis, has no effect on VM formation. Further investigation revealed a role for laminin, but not collagen or fibronectin, as ligands for CD36 expressing melanoma cells. Conclusions Taken together, this study suggests that CD36 is a novel regulator of VM by melanoma cancer cells that is facilitated, at least in part, via integrin-α3 and laminin. Unlike angiogenesis, VM is not perturbed by the presence of TSP-1, thus providing new information on differences between these two processes of tumor vascularization which may be exploited to combat cancer progression.


2018 ◽  
Vol 34 (5) ◽  
pp. 659-667 ◽  
Author(s):  
Abel Joël Yaya Gbaweng ◽  
Hadidjatou Daïrou ◽  
Stephane Zingué ◽  
Talla Emmanuel ◽  
Alembert Tiabou Tchinda ◽  
...  

2020 ◽  
Vol 10 (2) ◽  
pp. 2117-2125

Cold atmosphere plasma has been shown as a promising technology for certain cancer treatments. In this paper, we report indirect plasma treatment using CAP discharged in cell culture medium and study the effect of identical plasma stimulated culture medium on melanoma cancer cells and fibroblast cells cultured in vitro. The results of MTT assay, migration assay, ROS detection, and alizarin red assay show that plasma-treated medium can have a strong negative effect on melanoma cancer cells compared with the control group. However, the plasma-treated medium has a less cytotoxic effect on fibroblast cells than that on melanoma cancer cells at the same treatment. This result is attributed to the production of reactive oxygen species in the plasma-treated medium to induce apoptosis and inhibit melanoma cell proliferation and further cell metastasis. According to the results, this study shows the potential of CAP plasma treatment for anti-cancer therapy.


2017 ◽  
Vol 45 (8) ◽  
pp. 1769-1777 ◽  
Author(s):  
Mohammad Hossein Abdolmohammadi ◽  
Faranak Fallahian ◽  
Zahra Fakhroueian ◽  
Mozhgan Kamalian ◽  
Peyman Keyhanvar ◽  
...  

2020 ◽  
Author(s):  
Atikul Islam ◽  
Pei-Fang Hsieh ◽  
Jou-Chun Chou ◽  
Jiunn-Wang Liao ◽  
Ming-Kun Hsieh ◽  
...  

Abstract Background: Although considered a rare form of skin cancer, malignant melanoma has steadily increased internationally and is a main cause of cancer-associated death worldwide. The treatment options for malignant melanoma are very limited. Accumulating data suggest that the natural compound, capsaicin, exhibits preferential anticancer properties to act as a nutraceutical agent. Here, we explored the underlying molecular events involved in the inhibitory effects of capsaicin on the growth of melanoma cells.Methods: The cellular thermal shift assay (CETSA) and isothermal dose response fingerprint (ITDRFCETSA) were utilized to validate the binding of capsaicin with the tumor-associated NADH oxidase, tNOX (ENOX2) in melanoma cells. We also assessed the cellular impact of capsaicin-targeting of tNOX on A375 cells by flow cytometry and protein analysis. The essential role of tNOX in tumor- and melanoma-growth limiting abilities of capsaicin was evaluated in C57BL/6 mice.Results: Our data show that capsaicin directly targets cellular tNOX to inhibit its enzymatic activity and enhance protein degradation capacity. The inhibition of tNOX by capsaicin is accompanied by the attenuation of SIRT1, a NAD+-dependent deacetylase that enhances ULK1 acetylation to induce ROS-dependent autophagy in melanoma cells. Capsaicin treatment of mice implanted with melanoma cancer cells suppressed tumor growth by down-regulating tNOX and SIRT1, which was also seen in an in vivo xenograft study with tNOX-depleted melanoma cells. Conclusions: Together, our findings suggest that tNOX expression is important for the growth of melanoma cancer cells both in vitro and in vivo, and that inhibition of the tNOX-SIRT1 axis contributes to inducting cytotoxic ROS-dependent autophagy in melanoma cells.


Pharmaceutics ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 45 ◽  
Author(s):  
Hany Marei ◽  
Patrizia Casalbore ◽  
Asmaa Althani ◽  
Valentina Coccè ◽  
Carlo Cenciarelli ◽  
...  

Exploitation of the potential ability of human olfactory bulb (hOB) cells to carry, release, and deliver an effective, targeted anticancer therapy within the central nervous system (CNS) milieu remains elusive. Previous studies have demonstrated the marked ability of several types of stem cells (such as mesenchymal stem cells (MSCs) to carry and release different anti-cancer agents such as paclitaxel (PTX). Herein we investigate the ability of human olfactory bulb neural stem cells (Hu-OBNSCs) to carry and release paclitaxel, producing effective cytotoxic effects against cancer cells. We isolated Hu-OBNSCs from the hOB, uploaded them with PTX, and studied their potential cytotoxic effects against cancer cells in vitro. Interestingly, the Hu-OBNSCs displayed a five-fold increase in their resistance to the cytotoxicity of PTX, and the PTX-uploaded Hu-OBNSCs were able to inhibit proliferation and invasion, and to trigger marked cytotoxic effects on glioblastoma multiforme (GBM) cancer cells, and Human Caucasian fetal pancreatic adenocarcinoma 1 (CFPAC-1) in vitro. Despite their ability to resist the cytotoxic activity of PTX, the mechanism by which Hu-OBNSCs acquire resistance to PTX is not yet explained. Collectively our data indicate the ability of the Hu-OBNSCs to resist PTX, and to trigger effective cytotoxic effects against GBM cancer cells and CFPAC-1. This indicates their potential to be used as a carrier/vehicle for targeted anti-cancer therapy within the CNS.


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