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3 [12pt] $$ \,_^$$ R α N d a Where = radius of a vessel in the network, = the number of downstream endpoints from that vessel, =the radial scaling exponent.
|
[
{
"end": 125,
"label": "Tissue",
"start": 119,
"text": "vessel"
},
{
"end": 55,
"label": "Tissue",
"start": 49,
"text": "vessel"
},
{
"end": 70,
"label": "Tissue",
"start": 63,
"text": "network"
}
] |
Single_Cell
|
Plotting the log-log relation of these two variables allows a to be estimated by regression analysis.
|
[] |
Single_Cell
|
Source paper: PMC12408821
Segmentation of the compartments within the human kidney, including cortex, medulla, intermedullary pillars and hilum, was performed in Dragonfly (version: 2021.3) using a 2D convolutional neural network (CNN).
|
[
{
"end": 102,
"label": "Tissue",
"start": 96,
"text": "cortex"
},
{
"end": 84,
"label": "Tissue",
"start": 72,
"text": "human kidney"
},
{
"end": 111,
"label": "Tissue",
"start": 104,
"text": "medulla"
},
{
"end": 135,
"label": "Tissue",
"start": 113,
"text": "intermedullary pillars"
},
{
"end": 145,
"label": "Tissue",
"start": 140,
"text": "hilum"
},
{
"end": 60,
"label": "Tissue",
"start": 48,
"text": "compartments"
}
] |
Single_Cell
|
The final hyperparameters of the CNN are given in Supplementary Table 4 .
|
[] |
Single_Cell
|
Correction of the CNN output was manually performed in by an expert in Amira-Avizo v2021.1 to provide the final compartment delineations.
|
[] |
Single_Cell
|
These compartments were used to group and then analyse vascular network parameters.
|
[
{
"end": 18,
"label": "Tissue",
"start": 6,
"text": "compartments"
}
] |
Single_Cell
|
Source paper: PMC12408821
40 3D patches (512 × 512 × 512) of the highest resolution data, captured at 2.6–5.6 µm per voxel, were extracted from multiple human kidneys scanned by HiP-CT, and the glomeruli were manually segmented.
|
[
{
"end": 205,
"label": "Tissue",
"start": 196,
"text": "glomeruli"
},
{
"end": 168,
"label": "Tissue",
"start": 155,
"text": "human kidneys"
}
] |
Single_Cell
|
The widely utilised network nnU-net was trained using 35:5 cubes for a train:test split and a 70:30 training validation split.
|
[] |
Single_Cell
|
Training using 5-fold cross validation achieved a final DICE score of 0.928, 0.860, 0.906 for training, validation and test data, respectively.
|
[] |
Single_Cell
|
See Supplementary Note 3 for training results and nnU-net configuration.
|
[] |
Single_Cell
|
The plan files detailing all parameters for the training nnU-net are provided in Supplementary data .
|
[] |
Single_Cell
|
This trained network was used to perform inference of two VOIs of high-resolution data from the human kidney in this study, and count the number of glomeruli in each.
|
[
{
"end": 157,
"label": "Tissue",
"start": 148,
"text": "glomeruli"
},
{
"end": 108,
"label": "Tissue",
"start": 96,
"text": "human kidney"
},
{
"end": 62,
"label": "Tissue",
"start": 58,
"text": "VOIs"
}
] |
Single_Cell
|
Utilising the kidney anatomical compartment segmentation from above, the volume of cortical tissue within these high-resolution VOIs was calculated.
|
[
{
"end": 20,
"label": "Tissue",
"start": 14,
"text": "kidney"
},
{
"end": 98,
"label": "Tissue",
"start": 83,
"text": "cortical tissue"
},
{
"end": 132,
"label": "Tissue",
"start": 112,
"text": "high-resolution VOIs"
}
] |
Single_Cell
|
For each VOI, the number of glomeruli and the volume of cortex in each VOI were used to estimate the total number of glomeruli in the entire kidney.
|
[
{
"end": 62,
"label": "Tissue",
"start": 56,
"text": "cortex"
},
{
"end": 37,
"label": "Tissue",
"start": 28,
"text": "glomeruli"
},
{
"end": 126,
"label": "Tissue",
"start": 117,
"text": "glomeruli"
},
{
"end": 147,
"label": "Tissue",
"start": 134,
"text": "entire kidney"
},
{
"end": 12,
"label": "Tissue",
"start": 9,
"text": "VOI"
},
{
"end": 74,
"label": "Tissue",
"start": 71,
"text": "VOI"
}
] |
Single_Cell
|
Estimates of total glomerular number extrapolated to the entire kidney, from each VOI, were: 1.28 × 10 and 1.12 × 10 for VOI 3.1 and VOI 2.1, respectively.
|
[
{
"end": 70,
"label": "Tissue",
"start": 57,
"text": "entire kidney"
},
{
"end": 85,
"label": "Tissue",
"start": 82,
"text": "VOI"
},
{
"end": 128,
"label": "Tissue",
"start": 121,
"text": "VOI 3.1"
},
{
"end": 140,
"label": "Tissue",
"start": 133,
"text": "VOI 2.1"
}
] |
Single_Cell
|
Source paper: PMC12408821
Statistical comparisons of vascular network morphology between human and rat kidney were performed in GraphPad Prism (version: 10.1.2).
|
[
{
"end": 96,
"label": "Tissue",
"start": 91,
"text": "human"
},
{
"end": 111,
"label": "Tissue",
"start": 101,
"text": "rat kidney"
}
] |
Single_Cell
|
For all statistical tests, a p -value of less than 0.05 was considered statistically significant.
|
[] |
Single_Cell
|
In both the rat and human datasets, the segmental/feeding renal arteries were identified to be at Strahler orders 8 and truncated Strahler order 9, respectively.
|
[
{
"end": 72,
"label": "Tissue",
"start": 40,
"text": "segmental/feeding renal arteries"
}
] |
Single_Cell
|
Radius against Strahler order were normalised to the 9th truncated Strahler order of the human data.
|
[] |
Single_Cell
|
Log of radius against truncated Strahler generation for the human kidney; and radius against Strahler Order of the rat kidney, were plotted facilitating a linear least squares regression analysis.
|
[
{
"end": 72,
"label": "Tissue",
"start": 60,
"text": "human kidney"
},
{
"end": 125,
"label": "Tissue",
"start": 115,
"text": "rat kidney"
}
] |
Single_Cell
|
A sum of squares F test was performed with the null hypothesis that a single set of global parameters for slope and intercept would fit vessel radius or vessel length for both the rat and human cases.
|
[] |
Single_Cell
|
For calculating the fit of the radial scaling exponent ( a ), we followed the approach of ref.
|
[] |
Single_Cell
|
applying a Standard major axis regression to account for measurement error in both variables.
|
[] |
Single_Cell
|
This was performed in Matlab 2023a using the gmregress.m function with an alpha significance set to 0.05.
|
[] |
Single_Cell
|
Source paper: PMC12408821
|
[] |
Single_Cell
|
The fact that the Mediterranean diet could represent a source of natural compounds with cancer-preventive and therapeutic activity has been the object of great interest, especially with regard to the mechanisms of action of polyphenols found in olive oil and olive leaves.
|
[] |
ChemBL_V1
|
Secoiridoid oleuropein (OLE) and its derivative hydroxytyrosol (3,4-dihydroxyphenylethanol, HT) have demonstrated anti-proliferative properties against a variety of tumors and hematological malignancies both in vivo and in vitro, with measurable effects on cellular redox status, metabolism, and transcriptional activity.
|
[] |
ChemBL_V1
|
With this review, we aim to summarize the most up-to-date information on the potential use of OLE and HT for cancer treatment, making important considerations about OLE and HT bioavailability, OLE- and HT-mediated effects on drug metabolism, and OLE and HT dual activity as both pro- and antioxidants, likely hampering their use in clinical routine.
|
[] |
ChemBL_V1
|
Also, we focus on the details available on the effects of nutritionally relevant concentrations of OLE and HT on cell viability, redox homeostasis, and inflammation in order to evaluate if both compounds could be considered cancer-preventive agents or new potential chemotherapy drugs whenever their only source is represented by diet.
|
[] |
ChemBL_V1
|
Cancer insurgence and progression are complex processes, depending on the combination of unmodifiable genetic and modifiable environmental/lifestyle-related factors.
|
[] |
ChemBL_V1
|
With this premise, it sounds perfectly understandable that scientific evidence has corroborated the role of a healthy diet and dietary intervention as potentially beneficial approaches contributing to cancer prevention .
|
[] |
ChemBL_V1
|
Epidemiological and experimental evidence has confirmed that the so-called Mediterranean diet is a source of molecules that may mitigate cancer risk factors like chronic inflammation and redox imbalance, thus participating in the prevention of carcinogenesis in terms of loss of cell cycle regulation and proper immune modulation, as well as in the inhibition of angiogenesis and metastasis.
|
[] |
ChemBL_V1
|
Moreover, some of these natural compounds may have a cytotoxic effect, making them interesting alternatives to or candidates for integration into conventional therapeutic approaches .
|
[] |
ChemBL_V1
|
Among Mediterranean diet phenols, secoiridoid oleuropein (OLE) is the most abundant phenolic compound in Olea europaea L. tree leaves (OLE content up to 14–19% in olive leaves), followed by its degradation derivative hydroxytyrosol (3,4-dihydroxyphenylethanol, HT, 2.28 mg/g of olive leaf extract) (Figure 1) .
|
[] |
ChemBL_V1
|
OLE and HT are also found in the fruit of Olea europaea L. and in olive oil; thus, they are easily ingested as part of a routine diet, but they can also be obtained from other sources, e.g., olive mill wastewater .
|
[] |
ChemBL_V1
|
Both compounds have attracted attention for their accessibility, safe profile, powerful antioxidant and scavenging activity against reactive oxygen species (ROS), and controversial anti-inflammatory action.
|
[] |
ChemBL_V1
|
For more than two decades, OLE and HT (together or alone) have been the focus of intense research efforts in the context of infectious diseases and prevention/management of chronic non-communicable diseases, including cancer, with encouraging results from in vitro and in vivo models .
|
[] |
ChemBL_V1
|
On this basis, it would be difficult to understand the reasons behind the lack of systematic testing of OLE and HT as supplements to prevent the insurgence of cancer or support the management of hematological malignancies and solid tumors.
|
[] |
ChemBL_V1
|
This becomes clearer considering that, despite promising proof in the field, experimental evidence about OLE and HT bioavailability in humans and animals clearly demonstrates that OLE and HT act as cancer-preventive agents and cytotoxic drugs mainly at concentrations far from plasma levels reachable through nutrition, an aspect often interpreted as marginal that we discuss in detail in this review.
|
[] |
ChemBL_V1
|
Also, as explained in the following paragraphs, the complexity and diversity of molecular mechanisms resulting in net OLE and HT action has led to questions regarding the possibility that these compounds might even facilitate the expansion of neoplastic clones at nutritionally relevant concentrations.
|
[] |
ChemBL_V1
|
In this review, we discuss the available data on the use of OLE and HT as anti-cancer drugs and the feasibility of their application in the context of clinical routine now or in the near future.
|
[] |
ChemBL_V1
|
OLE and HT activity against solid tumor insurgence and development has been challenged in a large number of experimental models, both in vivo and in vitro.
|
[] |
ChemBL_V1
|
No single shared molecular mechanism and/or triggered cellular response seems implicated in OLE and HT cytotoxicity, resulting in an articulated frame that imposes a separate dissertation for every type of studied solid tumor.
|
[] |
ChemBL_V1
|
To facilitate critical interpretation, in each subsection, OLE and HT assayed doses are indicated, with the half-maximal inhibitory concentration (IC50) and the half-maximal effective concentration (EC50) reported as exact values, mean ± standard deviation (S.D.), or mean ± standard error of the mean (S.E.M.) whenever provided by the authors.
|
[] |
ChemBL_V1
|
A list of experimental models used to study OLE and HT cytotoxicity in cancer cells is reported in Table 1.
|
[] |
ChemBL_V1
|
Malignant melanoma is a malignancy arising from the transformation of melanocytes, with increasing incidence worldwide.
|
[] |
ChemBL_V1
|
On the basis of the tissue where the primary lesion appears, four major subtypes can be distinguished: cutaneous melanoma (non-glabrous skin), acral melanoma (glabrous skin), mucosal melanoma (melanocytes in the mucosal tissues), and uveal melanoma (uveal tract of the eye).
|
[] |
ChemBL_V1
|
Among these major subtypes, it is possible to distinguish some particular variants: amelanotic/hypomelanotic melanoma, a subtype of cutaneous melanoma with low or absent melanin; desmoplastic melanoma, a spindle cell tumor exhibiting signs of dense scar-like fibrosis; spitzoid melanoma, sharing histopathological characteristics with Spitz nevi; acral lentiginous melanoma, with a lentiginous growth pattern .
|
[] |
ChemBL_V1
|
OLE seems to be effective in the prevention of skin carcinogenesis in vivo.
|
[] |
ChemBL_V1
|
Orally administered 10 mg/kg and 25 mg/kg OLE reduced skin carcinogenesis (expressed in terms of number of tumors per mouse) in UVB-irradiated albino hairless HOS: HR-1 mice .
|
[
{
"end": 162,
"label": "CellLine",
"start": 159,
"text": "HOS"
},
{
"end": 168,
"label": "CellLine",
"start": 164,
"text": "HR-1"
}
] |
ChemBL_V1
|
For 25 mg/kg OLE, this effect was associated with a persistent reduction in (I) the total volume of tumors per mouse, (II) the expression levels of invasion enzymes matrix metalloproteinase 2 (MMP2), pro-MMP9, and MMP9, (III) tissue angiogenesis marker vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2) levels, and (IV) the percentage of skin Ki-67+ cells and platelet endothelial cell adhesion molecule-1 (PECAM-1 or CD31)+ areas .
|
[] |
ChemBL_V1
|
OLE also seems effective in the prevention of melanoma growth and metastasis.
|
[] |
ChemBL_V1
|
In an in vivo B16F10 (mouse melanoma cell line) allograft model of high-fat diet (HFD)-induced melanoma progression in C57BL/6N mice, HFD containing 0.02% and 0.04% OLE reduced HFD-driven tumor growth and lymph node metastasis, with a mechanism involving (I) inhibition of cell proliferation, as indicated by the reduction in the percentage of cells positive for proliferation markers Ki67, Cyclin D1, and cyclin-dependent kinase 4 (CDK4) cells, (II) suppression of angiogenesis (reduction in CD31, VE-cadherin expression, VEGF-A, VEGF-C, VEGF-D, VEGF receptor 2 -VEGFR2- and VEGFR3), and (III) inhibition of lymphangiogenesis, as proved by staining for lymphatic vessel endothelial hyaluronan receptor (LYVE-1).
|
[
{
"end": 20,
"label": "CellLine",
"start": 14,
"text": "B16F10"
},
{
"end": 127,
"label": "CellLine",
"start": 119,
"text": "C57BL/6N"
}
] |
ChemBL_V1
|
According to further in vitro experimental assays, OLE anti-angiogenetic and lymphangiogenetic action relies on the inhibition of lipid and M2-macrophage accumulation .
|
[] |
ChemBL_V1
|
In vitro results for OLE are conflicting.
|
[] |
ChemBL_V1
|
Incubation of human amelanotic melanoma cell line C32 with 100 μM, 400 μM, and 1000 μM OLE for 72 h promoted cell viability .
|
[
{
"end": 53,
"label": "CellLine",
"start": 50,
"text": "C32"
}
] |
ChemBL_V1
|
On the contrary, incubation of human melanoma cell lines A375, WM266-4, and M21 with 250 μM, 500 μM, and 800 μM OLE for 72 h produced a dose-dependent decrease in cell viability.
|
[
{
"end": 61,
"label": "CellLine",
"start": 57,
"text": "A375"
},
{
"end": 70,
"label": "CellLine",
"start": 63,
"text": "WM266-4"
},
{
"end": 79,
"label": "CellLine",
"start": 76,
"text": "M21"
}
] |
ChemBL_V1
|
As deepened in A375 cells, an increase in OLE effectiveness with time may be detected.
|
[
{
"end": 19,
"label": "CellLine",
"start": 15,
"text": "A375"
}
] |
ChemBL_V1
|
OLE induced inhibition of cell viability after 24 h at a concentration of 800 μM, whereas after 48 and 72 h, a decrease in the percentage of viable cells became significant with a concentration as low as 250 μM .
|
[] |
ChemBL_V1
|
After 48 h treatment, 500 μM OLE increased the rate of apoptosis in A375 cells.
|
[
{
"end": 72,
"label": "CellLine",
"start": 68,
"text": "A375"
}
] |
ChemBL_V1
|
In addition, 24 h incubation with 250 μM OLE was sufficient to reduce invasiveness of A375 cells, while 48 h incubation with the same OLE concentration reduced the phosphorylation of pro-survival kinase Akt .
|
[
{
"end": 90,
"label": "CellLine",
"start": 86,
"text": "A375"
}
] |
ChemBL_V1
|
As regards in vitro evidence for HT, the effects on cell growth seem to be cell line-dependent.
|
[] |
ChemBL_V1
|
Treatment of C32 cells with 100 μM HT for 72 h increased cell viability, which was instead reduced by incubation with 400 μM and 1000 μM HT .
|
[
{
"end": 16,
"label": "CellLine",
"start": 13,
"text": "C32"
}
] |
ChemBL_V1
|
Incubation of human melanoma cell line A375 with 100 μM and 200 μM HT significantly diminished cell viability after 48 h. On the contrary, 48 h treatment of melanoma cell line MNT1 with 100 μM and 200 μM HT had no significant effect on cell viability.
|
[
{
"end": 43,
"label": "CellLine",
"start": 39,
"text": "A375"
},
{
"end": 180,
"label": "CellLine",
"start": 176,
"text": "MNT1"
}
] |
ChemBL_V1
|
The authors attributed this dissimilarity between the mentioned cell lines to differences in the active metabolic pathways.
|
[] |
ChemBL_V1
|
Expression analysis revealed a significant transcriptional upregulation of lactate dehydrogenase B (LDHB) and LDHC (accounting for lactate conversion into pyruvate) and glutamine synthetase (GLUL) in MNT1 cells in comparison with the A375 cell line, while sodium-coupled neutral amino acid transporter 1 (SNAT1) and SNAT2 (involved in glutamine transport within the cell), monocarboxylate transporter 4 (MCT4, accounting for lactate export), glycolytic enzyme glucose-6-phosphate dehydrogenase (G6PD), and excitatory amino acid transporter 3 (EEAT3) were downregulated in MNT1 cells vs. A375 .
|
[
{
"end": 204,
"label": "CellLine",
"start": 200,
"text": "MNT1"
},
{
"end": 238,
"label": "CellLine",
"start": 234,
"text": "A375"
},
{
"end": 576,
"label": "CellLine",
"start": 572,
"text": "MNT1"
},
{
"end": 591,
"label": "CellLine",
"start": 587,
"text": "A375"
}
] |
ChemBL_V1
|
In a further report, treatment of human melanoma cell lines A375, HT-144, and M74 with 50–250 μM HT produced a dose- and time-dependent decrease in cell viability after 24, 48, and 72 h .
|
[
{
"end": 64,
"label": "CellLine",
"start": 60,
"text": "A375"
},
{
"end": 72,
"label": "CellLine",
"start": 66,
"text": "HT-144"
},
{
"end": 81,
"label": "CellLine",
"start": 78,
"text": "M74"
}
] |
ChemBL_V1
|
A detailed analysis on A375 cells (treated with 250 μM, 375 μM, and 500 μM HT) and HT-144 cells (incubated with 250 μM, 350 μM, and 450 μM HT) performed for 24 and 48 h revealed an increase in the rate of apoptosis in both cell lines, with a dose- and time-dependent increase in tumor suppressor p53 and reduction in growth-promoting kinase Akt protein levels .
|
[
{
"end": 27,
"label": "CellLine",
"start": 23,
"text": "A375"
},
{
"end": 89,
"label": "CellLine",
"start": 83,
"text": "HT-144"
}
] |
ChemBL_V1
|
The activation of apoptosis pathway was further confirmed by an increase in apoptosis markers pro-activated and cleaved (activated) forms of caspase-3, a dose- and time-dependent increase in cleavage (activation) of poly ADP-ribose polymerase 1 (PARP-1), and a dose-dependent increase in the phosphorylation of histone H2AX (γH2AX) .
|
[] |
ChemBL_V1
|
HT-mediated induction of apoptosis was related to ROS accumulation in both cell lines at the indicated HT concentrations, which was detected after 24 and 48 h .
|
[] |
ChemBL_V1
|
Thyroid cancer is a category of neoplastic lesions with a highly variable degree of aggressiveness, arising from parafollicular C cells (resulting in medullary thyroid cancers) and follicular thyroid cells (producing follicular thyroid cancer, papillary thyroid cancer, poorly differentiated thyroid cancer, Hürthle cell cancers, and anaplastic thyroid cancer) .
|
[] |
ChemBL_V1
|
In vitro, treatment of human papillary thyroid carcinoma cell line TPC-1 and poorly differentiated thyroid gland carcinoma cell line BCPAP with 50–100 μM OLE for 48 h produced a significant reduction in cell viability attributable to S phase and G2/M phase cell cycle block, respectively.
|
[
{
"end": 72,
"label": "CellLine",
"start": 67,
"text": "TPC-1"
},
{
"end": 138,
"label": "CellLine",
"start": 133,
"text": "BCPAP"
}
] |
ChemBL_V1
|
In both cell lines, 50–100 μM OLE exerted an antioxidant activity against hydrogen peroxide (H2O2)-induced perturbation of ROS homeostasis.
|
[] |
ChemBL_V1
|
Also, 100 μM OLE caused a short-lasting (30 to 60 min) reduction in phosphorylated forms pro-survival kinases ERK (phospho-ERK) and Akt (phospho-Akt) in TPC-1 and BCPAP cells .
|
[
{
"end": 158,
"label": "CellLine",
"start": 153,
"text": "TPC-1"
},
{
"end": 168,
"label": "CellLine",
"start": 163,
"text": "BCPAP"
}
] |
ChemBL_V1
|
Incubation of papillary thyroid cancer cell lines TPC-1 and FB-2 with 324–973 μM HT decreased cell viability after 24 and 48 h in a dose-dependent manner.
|
[
{
"end": 55,
"label": "CellLine",
"start": 50,
"text": "TPC-1"
},
{
"end": 64,
"label": "CellLine",
"start": 60,
"text": "FB-2"
}
] |
ChemBL_V1
|
A stronger action was exerted on follicular thyroid cancer cell line WRO, whose cell viability was reduced even at lower doses of HT after 24 h (162 μM) and 48 h (65 μM) treatment .
|
[
{
"end": 72,
"label": "CellLine",
"start": 69,
"text": "WRO"
}
] |
ChemBL_V1
|
After 24 h incubation, 324 μM HT elicited an increase in the percentage of apoptotic and necrotic cells in all the three mentioned cell lines (with a concomitant downregulation of pro-proliferative cyclin D1 and upregulation of tumor suppressor p21 at both mRNA and protein levels), increased protein level of tumor suppressor p53, and activated the intrinsic pathway of apoptosis, as corroborated by the increase in cleaved PARP and cleaved caspase-3 levels, Bcl-2-associated agonist of cell death (Bad) and caspase-9 protein levels, and the release of mitochondrial cytochrome c .
|
[] |
ChemBL_V1
|
Currently, lung cancer represents the most commonly diagnosed cancer and the main cause of cancer-related deaths worldwide, including small cell carcinoma and more common non-small cell carcinoma .
|
[] |
ChemBL_V1
|
In adenocarcinomic human alveolar epithelial cells A549 (a model for non-small cell lung cancer), 50 μM and 150 μM OLE-induced apoptosis after 24 h incubation was mediated by the decrement in Bcl-2 and Bcl-XL anti-apoptotic proteins flanked by the increase in (I) mitochondrial-located pro-apoptotic protein Bax, (II) cytochrome c release from the mitochondria, (III) activation of apoptosome component apoptotic protease activating factor-1 (Apaf-1), (IV) activation of caspase-3, and (V) mitochondrial methylglyoxal detoxicating enzyme Glo2 (mGlo2), which physically interacted with Bax .
|
[
{
"end": 55,
"label": "CellLine",
"start": 51,
"text": "A549"
}
] |
ChemBL_V1
|
Consistent with these data, incubation of non-small cell lung cancer cell line H1299 with 50–200 μM OLE for 24 h elicited a dose-dependent G2/M phase cell cycle block and apoptosis, with effects on Bcl-2, Bax, cytochrome c, and caspase-3 that were similar to those documented for A549 cells .
|
[
{
"end": 84,
"label": "CellLine",
"start": 79,
"text": "H1299"
},
{
"end": 284,
"label": "CellLine",
"start": 280,
"text": "A549"
}
] |
ChemBL_V1
|
However, the underlying molecular mechanism ruling OLE activity differed between the two cell lines.
|
[] |
ChemBL_V1
|
The effects elicited by 150 μM OLE on mGlo2 levels in A549 cells were strictly dependent on OLE-induced increase in superoxide dismutase 2 (SOD2) detoxicating action against superoxide (O2), and on the inhibition of the Akt signalling pathway.
|
[
{
"end": 58,
"label": "CellLine",
"start": 54,
"text": "A549"
}
] |
ChemBL_V1
|
This was not surprising, since in A549 cells, O2 supports Akt activations, promoting cell survival .
|
[
{
"end": 38,
"label": "CellLine",
"start": 34,
"text": "A549"
}
] |
ChemBL_V1
|
In H1299 cells, the observed apoptosis was instead determined by OLE-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), accompanied by an increased rate of phosphorylation of activating transcription factor-2 (ATF-2), involved in cell cycle regulation, as documented in both tumorigenesis and cell death, and the upregulation of genes ruling cell metabolism and apoptosis .
|
[
{
"end": 8,
"label": "CellLine",
"start": 3,
"text": "H1299"
}
] |
ChemBL_V1
|
In A549 cell line, HT showed an increase in effectiveness of its anti-proliferative activity with respect to time, with the IC50 values changing from 230.60 μM to 149.36 μM in 72 h .
|
[
{
"end": 7,
"label": "CellLine",
"start": 3,
"text": "A549"
}
] |
ChemBL_V1
|
This piece of data was confirmed in another report.
|
[] |
ChemBL_V1
|
In fact, for A549 cells, mean IC50 ± S.E.M. = 147.0 ± 16.5 μM was reported after 48 h incubation .
|
[
{
"end": 17,
"label": "CellLine",
"start": 13,
"text": "A549"
}
] |
ChemBL_V1
|
Malignant pleural mesothelioma arises from mesothelial cells and is characterized by a pronounced aggressiveness and poor prognosis.
|
[] |
ChemBL_V1
|
On the basis of histological features, mesothelioma is classified as epithelioid, sarcomatoid, or biphasic, with epithelioid type offering the best median survival .
|
[] |
ChemBL_V1
|
Pleural epithelioid mesothelioma REN cell line was utilized to demonstrate that OLE exhibited a cytotoxic activity (IC50 = 25 μg/mL, ≈46 μM), and that both OLE and HT (10–100 μM) mobilized extracellular Ca in a dose-dependent manner .
|
[
{
"end": 36,
"label": "CellLine",
"start": 33,
"text": "REN"
}
] |
ChemBL_V1
|
Breast cancer is the most frequent malignant tumor in women worldwide, with a constantly rising incidence .
|
[] |
ChemBL_V1
|
Treatment of breast cancer is based on the molecular subtype, a classification that in the first instance takes into account the immunohistochemically assayed expression of hormone receptors estrogen receptor (ER) and progesterone receptor (PR), and gene amplification or overexpression of human epidermal growth factor receptor 2 (HER2).
|
[] |
ChemBL_V1
|
Triple negative breast cancer identifies a category of tumors lacking the three mentioned receptors .
|
[] |
ChemBL_V1
|
In an in vivo model of tumor xenograft (triple negative MDA-MB-231 cell line) in BALB/c OlaHsd-foxn1 mice, animals receiving 50 mg/kg OLE for 4 weeks showed a decrease in tumor size, together with a reduction in actors involved in cell growth/proliferation: transcription factor NF-κB and cyclin D1 .
|
[
{
"end": 66,
"label": "CellLine",
"start": 56,
"text": "MDA-MB-231"
},
{
"end": 87,
"label": "CellLine",
"start": 81,
"text": "BALB/c"
}
] |
ChemBL_V1
|
Instead, levels of tumor suppressor p21 increased after OLE injection.
|
[] |
ChemBL_V1
|
The effects elicited by OLE were accompanied by the induction of apoptosis, as demonstrated by caspase-3 activation, increase in Bax levels, and reduction in Bcl-2 protein expression .
|
[] |
ChemBL_V1
|
In vitro, OLE action appears to be independent of HER2 gene amplification/overexpression and hormone receptor status.
|
[] |
ChemBL_V1
|
Using MCF-7 cell line, which is devoid of HER-2 overexpression , 200 μg/mL (≈370 μM) OLE for 48 h showed a specific cytotoxic effect on MCF-7 cell line, leaving the non-cancerous cell line MCF-10A unharmed.
|
[
{
"end": 11,
"label": "CellLine",
"start": 6,
"text": "MCF-7"
},
{
"end": 141,
"label": "CellLine",
"start": 136,
"text": "MCF-7"
},
{
"end": 196,
"label": "CellLine",
"start": 189,
"text": "MCF-10A"
}
] |
ChemBL_V1
|
The observed effect on cell viability was accompanied by the upregulation of the expression of Prdx1-Prdx6, encoding for antioxidant and chaperone proteins peredoxins .
|
[] |
ChemBL_V1
|
The induction of apoptosis triggered by the same concentration of OLE in MCF-7 cells was confirmed in another study after 12 h incubation .
|
[
{
"end": 78,
"label": "CellLine",
"start": 73,
"text": "MCF-7"
}
] |
ChemBL_V1
|
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