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Accordingly, the phosphorylated form of JNK target, c-jun, was also increased in HT-29 cells as a response to treatment with HT.
|
[
{
"end": 86,
"label": "CellLine",
"start": 81,
"text": "HT-29"
}
] |
ChemBL_V1
|
Both JNK and c-jun phosphorylations seem to reach a peak after 30 min and 4 h of incubation.
|
[] |
ChemBL_V1
|
In addition, 400 μM HT induced activator protein 1 (AP-1) transcriptional activity (responsible for the expression of cell cycle regulator genes) , promoted a dynamic phosphorylation of ERK1/2 (with two peaks of phosphorylation—after 30 min and 2 h of incubation—both followed by a reduction in phospho-ERK1/2 levels), and abolished Akt phosphorylation.
|
[] |
ChemBL_V1
|
All HT-dependent effects producing apoptosis as a result seemed to be mediated by protein phosphatase 2A (PP2A) .
|
[] |
ChemBL_V1
|
Moreover, 400 μM HT reduced HIF-1α protein levels and augmented the protein levels of proliferation and inflammation modulator peroxisome proliferator-activated receptor γ (PPARγ) after 48 h incubation; 400 μM HT also elicited an increase in p53 levels starting after 16 h and lasting for 48 h .
|
[] |
ChemBL_V1
|
Similarly, 800 μM HT had analogous effects on HIF-1α and PPARγ protein expression starting after 24 h of incubation, but did not change p53 levels .
|
[] |
ChemBL_V1
|
Finally, treatment of HT-29 cells with 200 μM HT caused mobilization of endoplasmic reticulum Ca depots, but the contribution of this ionic species to HT-induced apoptosis/effects was not explained .
|
[
{
"end": 27,
"label": "CellLine",
"start": 22,
"text": "HT-29"
}
] |
ChemBL_V1
|
In SW620 cells, HT reduced cell viability at all tested concentrations (10–100 μM), with a mechanism related to a decrease in FASN transcription and activity after 72 h exposure.
|
[
{
"end": 8,
"label": "CellLine",
"start": 3,
"text": "SW620"
}
] |
ChemBL_V1
|
A detailed analysis of the cell cycle revealed that 10–50 μM HT produced S phase cell cycle arrest, with apoptosis induction when HT was used at a concentration of 100 μM .
|
[] |
ChemBL_V1
|
Treatment of HCT116 cell line with 100–300 μM HT and LoVo cell line with 100–400 HT μM for 72 h led to a dose-dependent decrease in cell viability, with IC50 calculated as 92.83 μM and 140.8 μM for HCT116 and LoVo cells, respectively.
|
[
{
"end": 19,
"label": "CellLine",
"start": 13,
"text": "HCT116"
},
{
"end": 57,
"label": "CellLine",
"start": 53,
"text": "LoVo"
},
{
"end": 204,
"label": "CellLine",
"start": 198,
"text": "HCT116"
},
{
"end": 213,
"label": "CellLine",
"start": 209,
"text": "LoVo"
}
] |
ChemBL_V1
|
Cell cycle analysis revealed that 72 h incubation of HCT116 and LoVo cells with 0.0154 mg/mL (≈100 μM) HT and 0.0231 mg/mL (≈150 μM) HT, respectively, caused G2/M cell cycle arrest and promoted apoptosis .
|
[
{
"end": 59,
"label": "CellLine",
"start": 53,
"text": "HCT116"
},
{
"end": 68,
"label": "CellLine",
"start": 64,
"text": "LoVo"
}
] |
ChemBL_V1
|
As regards the role of ROS in high-dose HT-mediated effects, a report documented a dose-dependent reduction in cell viability of SW480 (mean IC50 ± S.D. = 82 ± 10) and HCT116 (mean IC50 ± S.D. = 55 ± 7) cells treated with 50–100 μM for 72 h, in conditions favoring the accumulation of extracellular H2O2 .
|
[
{
"end": 134,
"label": "CellLine",
"start": 129,
"text": "SW480"
},
{
"end": 174,
"label": "CellLine",
"start": 168,
"text": "HCT116"
}
] |
ChemBL_V1
|
Pancreatic cancer, or pancreatic ductal adenocarcinoma, arises from the malignant transformation of pancreatic ductal cells, and represents the third leading cause of cancer-related death worldwide, with extremely low 5-year and overall survival rates .
|
[] |
ChemBL_V1
|
Up to now, the study of OLE and HT effects in pancreatic cancer in vivo has been limited.
|
[] |
ChemBL_V1
|
In an in vivo orthotopic model of pancreatic cancer, obtained by injecting mouse pancreatic cancer cells Panc02 in C57BL/6 mice, proved that 200 mg/kg HT for 10 days suppressed tumor growth and proliferation.
|
[
{
"end": 111,
"label": "CellLine",
"start": 105,
"text": "Panc02"
},
{
"end": 122,
"label": "CellLine",
"start": 115,
"text": "C57BL/6"
}
] |
ChemBL_V1
|
These results seem to depend on the modulation of the tumor microenvironment, since HT was able to reduce the accumulation of myeloid-derived suppressor cells in lymphoid organs, bone marrow, and tumor tissues .
|
[] |
ChemBL_V1
|
Results in vitro underline the diverse sensitivity that cell lines exhibit against OLE- and HT-mediated effects on cell growth.
|
[] |
ChemBL_V1
|
Neither OLE nor HT exhibited a cytotoxic effect on pancreatic ductal adenocarcinoma cell lines BxPC-3 and CFPAC-1 for doses up to 300 μM, but both were able to decrease cell viability of pancreatic ductal adenocarcinoma cell line MIA PaCa-2 (IC50 = 150.1 μM for OLE and 75.1 for HT) after 72 h incubation.
|
[
{
"end": 101,
"label": "CellLine",
"start": 95,
"text": "BxPC-3"
},
{
"end": 113,
"label": "CellLine",
"start": 106,
"text": "CFPAC-1"
},
{
"end": 240,
"label": "CellLine",
"start": 230,
"text": "MIA PaCa-2"
}
] |
ChemBL_V1
|
Both 200 μM OLE and 100 μM HT produced G2 phase cell cycle arrest after 24 h treatment.
|
[] |
ChemBL_V1
|
The 48 h incubation with the same concentrations of OLE and HT led to caspase-3-mediated apoptosis.
|
[] |
ChemBL_V1
|
The observed effects may be dependent on OLE- and HT-mediated upregulation of AP-1 components c-jun and fos .
|
[] |
ChemBL_V1
|
Similarly, treatment of pancreatic ductal adenocarcinoma cell line PANC-1 with 10 μM, 32 μM, 100 μM, and 320 μM HT for 24, 48, and 72 h reduced cell viability in a dose- and time-dependent fashion; doses as low as 19 μM were able to induce apoptosis (as detected after 24 h), with caspase-9 and Bax upregulation, and MMP-2 and MMP-9 downregulation at mRNA levels after 72 h incubation .
|
[
{
"end": 73,
"label": "CellLine",
"start": 67,
"text": "PANC-1"
}
] |
ChemBL_V1
|
Treatment of mouse pancreatic cancer cell line Panc02 with 50 μM, 150 μM, and 200 μM HT for 48 h elicited a dose-dependent inhibition of cell proliferation and induction of apoptosis.
|
[
{
"end": 53,
"label": "CellLine",
"start": 47,
"text": "Panc02"
}
] |
ChemBL_V1
|
Further experimental evidence revealed that 100 μM HT inhibited the expression of phospho-STAT3 and Cyclin D1 after 24 h .
|
[] |
ChemBL_V1
|
Cervical cancer is the fourth most common cancer among women worldwide, and the protagonist of an internationally shared effort towards prevention.
|
[] |
ChemBL_V1
|
Cervical cancer cases may be classified into two major histological subtypes: squamous cell carcinoma and adenocarcinoma .
|
[] |
ChemBL_V1
|
In human cervical adenocarcinoma HeLa cells, 50–100 μM OLE promoted the accumulation of S phase cells with only a modest increase in the percentage of sub-G1 cells, whereas 200 μM OLE was able to induce G2/M cell cycle arrest and apoptosis through the augmented expression of pro-apoptotic Bax protein, the reduction in anti-apoptotic Bcl-2, the release of mitochondrial cytochrome c in the cytosol, and caspase-9 mediated activation of caspase-3.
|
[
{
"end": 37,
"label": "CellLine",
"start": 33,
"text": "HeLa"
}
] |
ChemBL_V1
|
These effects were connected to (I) an increase in the phosphorylated form of apoptosis regulator JNK, which in turn ruled an increase in the phosphorylated forms of cell cycle controller activator protein 1 (AP-1) components c-Jun and ATF-2, and (II) an increase in the levels of tumor suppressors p53 and p21 .
|
[] |
ChemBL_V1
|
Another report documented the cytotoxic effect of 100–1200 μg/mL (≈185–2220 μM) OLE in HeLa cells after 24 and 48 h treatments in a dose- and time-dependent manner, with 24 h IC50 = 600 μg/mL and 48 h IC50 = 300 μg/mL. A 50 μg/mL, 100 μg/mL, 200 μg/mL, 400 μg/mL, and 600 μg/mL OLE-dependent increase in the apoptotic cell rate was detected after 48 h incubation .
|
[
{
"end": 91,
"label": "CellLine",
"start": 87,
"text": "HeLa"
}
] |
ChemBL_V1
|
Treatment with 300 μg/mL OLE downregulated invasion-promoting miR-181b-3p, miR-221-3p, radiosensitivity-promoting miR-16-5p, and anti-apoptotic Bcl-2 and Mcl1, while upregulating invasion-inhibiting miR-29a-3p, miR-34a-5p, miR-125-5p and apoptosis-promoter Fas, p53, TNF receptor superfamily member 10b (TNFRSF10B9, also known as TRAIL), and Bid .
|
[] |
ChemBL_V1
|
Ovarian cancer is a highly aggressive neoplasm whose complex management (due to molecular and cellular heterogeneity) together with its commonly delayed diagnosis have made it the fifth cause of death in women.
|
[] |
ChemBL_V1
|
The great majority of ovarian cancers are classified as epithelial belonging to the serous subtype .
|
[] |
ChemBL_V1
|
Treatment of high-grade ovarian serous adenocarcinoma cell line HEY with 200 μM and 400 μM OLE led to a reduction in cell viability, with accumulation of cells in G2/M phase and induction of apoptosis.
|
[
{
"end": 67,
"label": "CellLine",
"start": 64,
"text": "HEY"
}
] |
ChemBL_V1
|
A detailed analysis revealed that 400 μM OLE acted as a pro-oxidant agent, increasing oxygen radical generator labile iron pool (LIP) and ROS levels .
|
[] |
ChemBL_V1
|
Similarly, treatment of ovarian serous adenocarcinoma OVCAR-3 cell line with 200 μg/mL olive leaf extract containing 87% OLE for 24 h induced S/G2M phase cell cycle arrest and apoptosis.
|
[
{
"end": 61,
"label": "CellLine",
"start": 54,
"text": "OVCAR-3"
}
] |
ChemBL_V1
|
These effects were dependent on OLE-mediated ROS accumulation and reduction in CAT and SOD2 protein levels .
|
[] |
ChemBL_V1
|
Prostate cancer is the fifth leading cause of cancer-related deaths among men, whose therapeutic options are mainly defined on the basis of a combination of life expectancy, disease stage/risk classification/presence of metastasis, and cancer sensitivity towards androgens .
|
[] |
ChemBL_V1
|
Treatment of benign prostatic hyperplasia (BPH) epithelial cell line BPH-1 and prostate cancer cell lines LNCaP and DU145 with 100 μM and 500 μM OLE for 72 h determined a reduction in cell viability, probably as a consequence of the reduction in Akt phosphorylation levels, with cells showing signs of necrosis for the highest of the two tested OLE doses.
|
[
{
"end": 74,
"label": "CellLine",
"start": 69,
"text": "BPH-1"
},
{
"end": 111,
"label": "CellLine",
"start": 106,
"text": "LNCaP"
},
{
"end": 121,
"label": "CellLine",
"start": 116,
"text": "DU145"
}
] |
ChemBL_V1
|
Treatment with 100 μM and 500 μM OLE for 72 h also produced different effects on ROS homeostasis in the three cell lines.
|
[] |
ChemBL_V1
|
In BPH-1, a reduction in ROS was measured, while no effect was recorded for LNCaP cells, and a pro-oxidant activity with a marked ROS increase was exerted by OLE on DU145 cells.
|
[
{
"end": 8,
"label": "CellLine",
"start": 3,
"text": "BPH-1"
},
{
"end": 81,
"label": "CellLine",
"start": 76,
"text": "LNCaP"
},
{
"end": 170,
"label": "CellLine",
"start": 165,
"text": "DU145"
}
] |
ChemBL_V1
|
Measurement of non-protein thiol groups as a marker of oxidative stress defense revealed that OLE caused a dose-dependent increase in thiol groups in both BPH-1 and LNCaP cells, but only 100 μM OLE augmented thiol groups in DU145 cells; on the contrary, 500 μM OLE diminished thiol groups in this cell line.
|
[
{
"end": 160,
"label": "CellLine",
"start": 155,
"text": "BPH-1"
},
{
"end": 170,
"label": "CellLine",
"start": 165,
"text": "LNCaP"
},
{
"end": 229,
"label": "CellLine",
"start": 224,
"text": "DU145"
}
] |
ChemBL_V1
|
As regards oxidative damage protecting enzyme heme oxygenase-1 (HO-1), both 100 μM and 500 μM OLE increased HO-1 protein levels in BHP-1 and LNCaP cells, while in DU145 cells, OLE treatment decreased HO-1 enzyme expression.
|
[
{
"end": 136,
"label": "CellLine",
"start": 131,
"text": "BHP-1"
},
{
"end": 146,
"label": "CellLine",
"start": 141,
"text": "LNCaP"
},
{
"end": 168,
"label": "CellLine",
"start": 163,
"text": "DU145"
}
] |
ChemBL_V1
|
The levels of γ-glutamylcysteine synthetase (γ-GCS) (involved in reduced glutathione synthesis) were not affected by OLE treatment in the three studied cell lines .
|
[] |
ChemBL_V1
|
ROS homeostasis also seems to play a fundamental role in HT cytotoxic action on prostate cancer cells.
|
[] |
ChemBL_V1
|
Treatment of prostate cancer cell line PC3 with 80 μM HT caused mitochondrial dysfunction and triggered O2-dependent apoptosis .
|
[
{
"end": 42,
"label": "CellLine",
"start": 39,
"text": "PC3"
}
] |
ChemBL_V1
|
Similarly, 50–150 μM HT reduced cell viability of PC3 and LNCaP cells after 72 h treatment in a dose-dependent fashion (mean IC50 ± S.D. = 103 ± 7 μM and 146 ± 12 μM for PC3 and LNCaP cells, respectively), with a mechanism that seemed dependent on the ability of culture conditions to favor H2O2 accumulation (quantified in the medium after 24 h incubation with 100 μM HT as mean ± S.D. = 12.0 ± 2.9 and 8.8 ± 3.4 for PC3 and LNCaP cells, respectively) .
|
[
{
"end": 53,
"label": "CellLine",
"start": 50,
"text": "PC3"
},
{
"end": 63,
"label": "CellLine",
"start": 58,
"text": "LNCaP"
},
{
"end": 173,
"label": "CellLine",
"start": 170,
"text": "PC3"
},
{
"end": 183,
"label": "CellLine",
"start": 178,
"text": "LNCaP"
},
{
"end": 421,
"label": "CellLine",
"start": 418,
"text": "PC3"
},
{
"end": 431,
"label": "CellLine",
"start": 426,
"text": "LNCaP"
}
] |
ChemBL_V1
|
HT action might overcome androgen sensitivity.
|
[] |
ChemBL_V1
|
Incubation of androgen-sensitive LNCaP and castration-resistant C4-2 cell lines with 50–400 μM HT for 48 and 72 h reduced cell viability in a dose-dependent manner, with the IC50 values for LNCaP = 190 μM and 86.9 μM after 48 and 72 h, respectively, and the IC50 values measured for C4–2 = 176 μM and 76.5 μM after 48 and 72 h, respectively.
|
[
{
"end": 38,
"label": "CellLine",
"start": 33,
"text": "LNCaP"
},
{
"end": 68,
"label": "CellLine",
"start": 64,
"text": "C4-2"
},
{
"end": 195,
"label": "CellLine",
"start": 190,
"text": "LNCaP"
},
{
"end": 287,
"label": "CellLine",
"start": 283,
"text": "C4–2"
}
] |
ChemBL_V1
|
Cell cycle analysis after 48 h incubation with 100–300 μM demonstrated a dose-dependent cellular accumulation in the G1 phase and apoptosis induction, with (I) caspase-3/7 and PARP activation, (II) reduction in Bcl-2, Bcl-XL, cell cycle progression drivers cyclins D1 and E, and CDK2 and CDK4 protein levels, (III) increased Bax protein levels, (IV) reduced NF-κB p65 nuclear localization, (V) reduction in activation levels of cell growth regulators Akt and STAT3, and (VI) decreased androgen receptor protein levels and activity .
|
[] |
ChemBL_V1
|
The 48 h incubation of human prostate cancer cell lines LNCaP, 22Rv1, and PC-3 with 30–300 μM HT decreased cell viability in a dose-dependent fashion.
|
[
{
"end": 61,
"label": "CellLine",
"start": 56,
"text": "LNCaP"
},
{
"end": 68,
"label": "CellLine",
"start": 63,
"text": "22Rv1"
},
{
"end": 78,
"label": "CellLine",
"start": 74,
"text": "PC-3"
}
] |
ChemBL_V1
|
As indicated by the authors, mean IC50 ± S.E.M. = 41.17 ± 2.79 μM for LNCaP cells, 9.32 ± 0.50 for 22Rv1 cell line, and 28.88 ± 2.25 for PC-3 cells.
|
[
{
"end": 75,
"label": "CellLine",
"start": 70,
"text": "LNCaP"
},
{
"end": 104,
"label": "CellLine",
"start": 99,
"text": "22Rv1"
},
{
"end": 141,
"label": "CellLine",
"start": 137,
"text": "PC-3"
}
] |
ChemBL_V1
|
Treatment of PC-3 cells with 30 μM and 100 μM HT for 24 h reduced the migration rate in a dose-dependent manner.
|
[
{
"end": 17,
"label": "CellLine",
"start": 13,
"text": "PC-3"
}
] |
ChemBL_V1
|
Treatment of 22Rv1 cells with 10 μM HT reduced prostatosphere number and size after 10 days, and phosphorylation of ERK1/2, cAMP response element-binding (CREB) protein, and JNK after 24 h .
|
[
{
"end": 18,
"label": "CellLine",
"start": 13,
"text": "22Rv1"
}
] |
ChemBL_V1
|
Osteosarcoma is a primary malignant bone tumor historically known for its extremely low survival rates even in the case of surgical resection/amputation, which have been improved by the introduction of neoadjuvant and adjuvant chemotherapy .
|
[] |
ChemBL_V1
|
Data about OLE cytotoxic effect in vitro are conflicting, and partially dependent on the used cell line and the duration of the treatment.
|
[] |
ChemBL_V1
|
In human 143B osteosarcoma cells, OLE showed a dose-dependent inhibition of proliferation when used at concentrations of 62.5 μM, 125 μM, and 250 μM for 24 h, and 1 μM–250 μM for 48 h. Also, 100 μM OLE induced autophagy after 48 h and exhibited an anti-migratory effect after 60 h incubation .
|
[
{
"end": 13,
"label": "CellLine",
"start": 9,
"text": "143B"
}
] |
ChemBL_V1
|
In human MG-63 cells, 3–50 μg/mL (≈5–92.5 μM) OLE for 24 h reduced cell viability in a dose-dependent manner with IC50 = 22 μg/mL ± 3.6 .
|
[
{
"end": 14,
"label": "CellLine",
"start": 9,
"text": "MG-63"
}
] |
ChemBL_V1
|
Another report documented no effect on MG-63 cell viability at OLE concentrations of 50 μM and 100 μM, while a dose-dependent cytotoxic effect was documented for 200 μM and 400 μM OLE after 24, 48, and 72 h incubation, with IC50 = 346 μM for 48 h incubation .
|
[
{
"end": 44,
"label": "CellLine",
"start": 39,
"text": "MG-63"
}
] |
ChemBL_V1
|
Treatment of MG-63 cells with 20 μg/mL (≈37 μM) OLE for 48 h boosted the transcription of autophagy-related genes unc-51, like autophagy activating kinase 1 (ULK1), activating molecule in BECN1-regulated autophagy protein 1 (AMBRA1), and Bcl-2 interacting protein 3 like (BniP3L), as well as protein levels of ubiquitin binding protein p62, suggesting that OLE activity relies on autophagy induction .
|
[
{
"end": 18,
"label": "CellLine",
"start": 13,
"text": "MG-63"
}
] |
ChemBL_V1
|
In Saos2 osteosarcoma cell line, 50 μM OLE caused no changes in cell viability after 24, 48, and 72 h incubation.
|
[
{
"end": 8,
"label": "CellLine",
"start": 3,
"text": "Saos2"
},
{
"end": 31,
"label": "CellLine",
"start": 9,
"text": "osteosarcoma cell line"
}
] |
ChemBL_V1
|
Treatment with 100 μM OLE affected cell viability only after 48 h incubation, causing no detectable effects after 24 and 72 h incubation.
|
[] |
ChemBL_V1
|
Instead, 200 μM OLE started being effective as a cytotoxic agent after 48 h incubation, with effects confirmed after 72 h incubation.
|
[] |
ChemBL_V1
|
On the contrary, 400 μM showed a consistent cytotoxic action at all the assayed time points (24, 48, and 72 h) .
|
[] |
ChemBL_V1
|
Neuroblastomas are clinically heterogeneous embryonal neuroendocrine tumors, driving important research efforts towards the improvement of survival rates for patients with high-risk disease .
|
[] |
ChemBL_V1
|
Both OLE and HT exhibit a cytotoxic action against human neuroblastoma cell line SH-SY5Y.
|
[
{
"end": 80,
"label": "CellLine",
"start": 57,
"text": "neuroblastoma cell line"
},
{
"end": 88,
"label": "CellLine",
"start": 81,
"text": "SH-SY5Y"
}
] |
ChemBL_V1
|
After 48 h treatment, IC50 for OLE was 350 μM. OLE induced cell cycle arrest and apoptosis through upregulation of CDK inhibitors p53, p21, p15, and p16, together with downregulation of cyclins D1, D2, and D3, and CDK4 and CDK6 .
|
[] |
ChemBL_V1
|
HT was also effective in the reduction in cell viability of SH-SY5Y cells after 72 h incubation, with mean EC50 ± S.D. = 114.02 ± 1.69 μM, inducing apoptosis .
|
[
{
"end": 67,
"label": "CellLine",
"start": 60,
"text": "SH-SY5Y"
}
] |
ChemBL_V1
|
Glioma, a neoplastic lesion arising from glial cells, is the most frequent tumor of the central nervous system, and glioblastoma multiforme accounts for the large majority of all gliomas.
|
[] |
ChemBL_V1
|
Glioblastomas are extremely aggressive and difficult-to-treat cancers, with very modest survival expectancy .
|
[] |
ChemBL_V1
|
Treatment of human glioblastoma cell lines A-172 and U-251 with 200 μM and 400 μM OLE for 24 h reduced cell viability in a dose-dependent fashion, triggering apoptosis and suppressing cell migration and invasion abilities with a mechanism involving the increase in Bax, MMP2, MMP9, and phospho-Akt levels, the reduction in Bcl-2 protein levels, and caspase-9 and caspase-3 activation .
|
[
{
"end": 48,
"label": "CellLine",
"start": 43,
"text": "A-172"
},
{
"end": 58,
"label": "CellLine",
"start": 53,
"text": "U-251"
}
] |
ChemBL_V1
|
In glioblastoma cell line T98G, 277.5 μM and 555 μM OLE for 24 h diminished cell viability in a dose-dependent manner.
|
[
{
"end": 30,
"label": "CellLine",
"start": 26,
"text": "T98G"
}
] |
ChemBL_V1
|
Treatment with 555 μM OLE strongly increased the expression of miRNAs inhibiting tumor growth: miR-181b, miR-137, and Let-7d.
|
[] |
ChemBL_V1
|
On the contrary, 277.5 μM OLE increased Let-7d levels only.
|
[] |
ChemBL_V1
|
Expression of miR-153 was not changed by OLE treatments .
|
[] |
ChemBL_V1
|
In this section, the most important results about less investigated malignancies are summarized.
|
[] |
ChemBL_V1
|
Head and neck squamous cell carcinoma is the sixth most common cancer and arises from mucosal epithelium in the oral cavity, pharynx, and larynx .
|
[] |
ChemBL_V1
|
Treatment of human cell lines Tu686 and CAL-27 with 50–200 μg/mL OLE (≈92.5–370 μM) significantly reduced cell viability, while no effect was elicited by concentrations ≤ 25 μg/mL (≈46 μM).
|
[
{
"end": 35,
"label": "CellLine",
"start": 30,
"text": "Tu686"
},
{
"end": 46,
"label": "CellLine",
"start": 40,
"text": "CAL-27"
}
] |
ChemBL_V1
|
Consistently, 25 μg/mL did not change the apoptotic rate in the mentioned cell lines, but inhibited epithelial-to-mesenchymal transition (EMT) induced by transforming growth factor-β1 TGF-β1 .
|
[] |
ChemBL_V1
|
The effects of OLE on EMT-related proteins were also verified in a in vivo model of 686LN-M2 cell line xenograft in BALB/c nude mice .
|
[
{
"end": 92,
"label": "CellLine",
"start": 84,
"text": "686LN-M2"
},
{
"end": 122,
"label": "CellLine",
"start": 116,
"text": "BALB/c"
}
] |
ChemBL_V1
|
Among gastric cancers, gastric adenocarcinoma is the most common subtype .
|
[] |
ChemBL_V1
|
Treatment of human gastric adenocarcinoma cell line CRL-1739 with 50–500 μM OLE for 24 h reduced cell viability in a dose-dependent fashion, with results becoming significant for values between 200 μM and 500 μM. The authors calculated that IC50 = 42 μM. As demonstrated by incubating the mentioned cell line with 200–500 μM OLE, 24 h exposure elicited the accumulation of ROS and apoptosis .
|
[
{
"end": 60,
"label": "CellLine",
"start": 52,
"text": "CRL-1739"
}
] |
ChemBL_V1
|
Seminoma is the result of germ cell malignant transformation.
|
[] |
ChemBL_V1
|
It is generally associated with an excellent prognosis, and may involve testicles or extra-gonadal sites .
|
[] |
ChemBL_V1
|
The 48 h incubation of human seminoma cell lines SEM-1 and TCAM-2 with 15–200 μM OLE reduced cell viability in a dose-dependent manner, with IC50 = 140 μM and 50 μM for SEM-1 and TCAM-2, respectively.
|
[
{
"end": 54,
"label": "CellLine",
"start": 49,
"text": "SEM-1"
},
{
"end": 65,
"label": "CellLine",
"start": 59,
"text": "TCAM-2"
},
{
"end": 174,
"label": "CellLine",
"start": 169,
"text": "SEM-1"
},
{
"end": 185,
"label": "CellLine",
"start": 179,
"text": "TCAM-2"
}
] |
ChemBL_V1
|
Treatment of the mentioned cell lines with OLE concentrations corresponding to their respective IC50 values produced apoptosis, the reduction in protein levels of cyclin D1 and nuclear localization of NF-κB, the increase in Bax and p21, and impaired cell migratory capacities through downregulation of TGF-β1 .
|
[] |
ChemBL_V1
|
Hematological malignancies arise from the loss of hematopoietic homeostasis, and may be configured as a large category including both myeloid and lymphatic neoplasms (leukemia, lymphoma, and multiple myeloma) whose incidence is pretty variable at the regional level .
|
[] |
ChemBL_V1
|
Only limited experimental evidence supporting OLE and HT preventive and anti-cancer properties is available in such a context (Table 1).
|
[] |
ChemBL_V1
|
Acute promyelocytic leukemia is a form of acute leukemia characterized by a chromosomal rearrangement involving PML::RARA fusion , making this malignancy sensitive to differentiating agents inducing PML-RARA fusion protein degradation by targeting the RARA or the PML part (all-trans-retinoic acid and arsenic-trioxide, respectively) .
|
[] |
ChemBL_V1
|
In vitro, treatment of promyelocytic leukemia cell line HL-60 with 50–100 μM HT reduced cell viability and triggered apoptosis, as indicated by the cleavage of PARP, the activation of caspase-3, and cytochrome c release .
|
[
{
"end": 61,
"label": "CellLine",
"start": 56,
"text": "HL-60"
}
] |
ChemBL_V1
|
According to another report, 100 μM HT reduced DNA synthesis in HL-60 cells, with promotion of cell differentiation, cell accumulation in G0/G1 phase, and apoptosis of S phase cells .
|
[
{
"end": 69,
"label": "CellLine",
"start": 64,
"text": "HL-60"
}
] |
ChemBL_V1
|
The detected cytotoxic effect of HT was caused by HT-mediated H2O2 accumulation in cell culture medium, overcoming HL-60 ability to clear ROS .
|
[
{
"end": 120,
"label": "CellLine",
"start": 115,
"text": "HL-60"
}
] |
ChemBL_V1
|
The accumulation of H2O2 and the extent of apoptosis were inversely correlated with cell density .
|
[] |
ChemBL_V1
|
As hypothesized by the authors, in their experimental setting, the first step of HT-mediated H2O2 accumulation is the auto-oxidation of HT by O2, with production of the corresponding o-quinone and superoxide O2; the process is accelerated by SOD .
|
[] |
ChemBL_V1
|
These findings were confirmed in a study using an HT-rich natural extract of the olive pulp as a source of HT .
|
[] |
ChemBL_V1
|
Effects of HT on cell cycle and induction of apoptosis in replicating cells seemed to be related to an increase in cyclin D3 flanked by a decrease in CDK6 when HT concentration was 100 μM, whereas it was linked to an increase in p21 and p27 mRNA and protein levels when HT was used at a concentration of 75 μM. As suggested by the authors, these observations may be explained in the light of cyclin D3-dependent CDK6-mediated phosphorylation of pRB, which in turn causes the release of E2F transcription factor and G1/S transition as well as DNA synthesis.
|
[] |
ChemBL_V1
|
Intriguingly, both p21 and p27 are able to inhibit CDK6-mediated pRB phosphorylation and accelerate HL-60 differentiation .
|
[
{
"end": 105,
"label": "CellLine",
"start": 100,
"text": "HL-60"
}
] |
ChemBL_V1
|
Chronic myelogenous leukemia (also known as chronic myeloid leukemia) is a myeloproliferative neoplastic disease characterized by the chromosomal translocation t(9;22)(q34;q11.2), resulting in the presence of the Philadelphia chromosome.
|
[] |
ChemBL_V1
|
The mentioned translocation produces the BCR- ABL1 fusion oncogene, encoding for a constitutively active tyrosine kinase, making leukemia cells sensitive to tyrosine kinase inhibition, with very good 5-year survival rates (90%) .
|
[] |
ChemBL_V1
|
Incubation of chronic myelogenous leukemia cell line K562 for 4 days with 200 μg/mL (≈370 μM) and 400 μg/mL (≈740 μM) OLE reduced cell density and viability.
|
[
{
"end": 57,
"label": "CellLine",
"start": 53,
"text": "K562"
}
] |
ChemBL_V1
|
After 48 h treatment with 200 μg/mL OLE, a significant activation of caspase-1 was measured.
|
[] |
ChemBL_V1
|
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