scholarly journals The Anti-Proliferative Lichen-Compound Protolichesterinic Acid Inhibits Oxidative Phosphorylation and Is Processed via the Mercapturic Pathway in Cancer Cells

Planta Medica ◽  
2021 ◽  
Author(s):  
Freyr Jóhannsson ◽  
Paulina Cherek ◽  
Maonian Xu ◽  
Óttar Rolfsson ◽  
Helga M. Ögmundsdóttir
Keyword(s):  
Oxidative Phosphorylation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Mitochondrial Function ◽  
Structural Changes ◽  
Morphological Changes ◽  
Redox Balance ◽  
Cancer Cell Lines ◽  
Atp Assay ◽  
Different Origin

AbstractThe lichen compound protolichesterinic acid (PA) has an anti-proliferative effect against several cancer cell lines of different origin. This effect cannot be explained by the known inhibitory activity of PA against 5- and 12-lipoxygenases. The aim was therefore to search for mechanisms for the anti-proliferative activity of PA. Two cancer cell lines of different origin, both sensitive to anti-proliferative effects of PA, were selected for this study, T-47D from breast cancer and AsPC-1 from pancreatic cancer. Morphological changes were assessed by transmission electron microscopy, HPLC coupled with TOF spectrometry was used for metabolomics, mitochondrial function was measured using the Agilent Seahorse XFp Real-time ATP assay and glucose/lactate levels by radiometry. Levels of glutathione, NADP/NADPH and reactive oxygen species [ROS] were measured by luminescence. Following exposure to PA both cell lines showed structural changes in mitochondria that were in line with a measured reduction in oxidative phosphorylation and increased glycolysis. These changes were more marked in T-47D, which had poorer mitochondrial function at baseline. PA was processed and expelled from the cells via the mercapturic pathway, which consumes glutathione. Nevertheless, glutathione levels were increased after 24 hours of exposure to PA, implying enhanced synthesis. Redox balance was not much affected and ROS levels were not increased. We conclude that PA is metabolically processed and expelled from cells, leading indirectly to increased glutathione levels with minimal effects on redox balance. The most marked effect was on mitochondrial structure and metabolic function implying that effects of PA may depend on mitochondrial fitness.

scholarly journals Fusaproliferin, a Fungal Phytotoxin Shows Rapid and Potent Cytotoxicity against Pancreatic Cancer Cell Lines

2018 ◽  
Author(s):  
Nazia Hoque ◽  
Choudhury Mahmood Hasan ◽  
Md. Sohel Rana ◽  
Amrit Varsha ◽  
Md. Hossain Sohrab ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Fusarium Solani ◽  
Pancreatic Cancer Cell ◽  
Morphological Changes ◽  
Cancer Cell Lines ◽  
Microscopy Imaging ◽  
Ongoing Research ◽  
Synthetic Agents

As a part of our ongoing research on endophytic fungi, we have isolated a sesterterpene mycotoxin, fusaproliferin (FUS), from Fusarium solani strain associated with the plant Aglaonema hookerianum Schott. FUS showed rapid and sub-micromolar IC50 against pancreatic cancer cell lines. Time dependent survival analysis and microscopy imaging showed rapid morphological changes in cancer cell lines 4 hours after incubation with FUS. This provides a new chemical scaffold that can be further developed to obtain more potent synthetic agents against pancreatic cancer.

scholarly journals APOPTOSIS INDUCTION EFFECT OF CURCUMIN AND ITS ANALOGS PENTAGAMAVUNON-0 AND PENTAGAMAVUNON-1 ON CANCER CELL LINES

2017 ◽  
Vol 10 (3) ◽  
pp. 373 ◽  
Author(s):  
Muhammad Da'i ◽  
Andi Suhendi ◽  
Edi Meiyanto ◽  
Umar Anggoro Jenie ◽  
Masashi Kawaichi
Keyword(s):  
Cell Growth ◽  
Western Blot ◽  
Cell Lines ◽  
Cancer Cell ◽  
Morphological Changes ◽  
Cancer Cell Line ◽  
T47d Cell ◽  
Cancer Cell Lines ◽  
Induction Effect ◽  
Apoptosis Induction

ABSTRACTObjectives: This experiment aims to investigate the apoptosis effect of curcumin and its analogs pentagamavunon-0 (PGV-0) and PGV-1 on normaland other cancer cell lines.Methods: Growth inhibition effect was investigated using the MTT method. Double staining used acridine orange, 2-(4-aminodiphenyl)-6-indolcarbamidine dihydrochloride and ethidium bromide was performed to determine morphological changes of cells. Detection of PARP, caspase-3,PUMA and BAX using a western blot method was conducted to elucidate the apoptosis effect of the compounds.Results: PGV-1 (2.5 μM) and PGV-0 (5.0 μM) could inhibit T47D-cell growth on 72 h observation, but not for curcumin. DNA staining showed PGV-1has the strongest apoptosis induction effect on T47D-cells compared to PGV-0 and curcumin as well. Western blot analysis resulted in cleavage PARP(83 kD) on HeLa, T47D, and MCF-7 cells treated with PGV-1 (2.5 μM), PGV-0 (5.0 μM). Curcumin (10.0 μM) just induced apoptosis on T47D-cell andMCF-7 cell, but not HeLa cell. Cleavage PARP resulted by apoptosis process in the cell. PGV-1 (2.5 μM) had a stronger apoptosis effect compared toPGV-0 (5.0 μM) and curcumin (10.0 μM) based on cleaved PARP result qualitatively. On the normal cell (NH3T3), cells that were treated with thecompounds resulted in a negative cleavage PARP. This result indicated that the compounds were part of a selectively induced cancer cell line apoptosisprocess.Conclusion: Curcumin, PGV-0 and PGV-1 could inhibit cell growth by induce apoptosis on cancer cells but not on normal cells, which PGV-1 hasstrongest apoptosis induction effect on cancer cell lines.Keywords: Curcumin and analogs, Apoptosis, Cancer cell lines.

scholarly journals Quantitative Analysis of Actin Cytoskeleton's Morphological Changes during EMT in Lung Cancer and Pre-Cancer Cell Lines

2021 ◽  
Vol 120 (3) ◽  
pp. 346a
Author(s):  
Arkaprabha Basu ◽  
Manash K. Paul ◽  
Mitchel Alioscha-Perez ◽  
Anna Grosberg ◽  
Hichem Sahli ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Quantitative Analysis ◽  
Cell Lines ◽  
Cancer Cell ◽  
Morphological Changes ◽  
Cancer Cell Lines

Induction of Apoptosis in Human Oral Cancer Cell Lines, OC2 and TSCCa, by Chingwaysan

2005 ◽  
Vol 33 (01) ◽  
pp. 21-27 ◽  
Author(s):  
Pao-Hsin Liao ◽  
Shiow-Ling Chen ◽  
Hung-Che Shih ◽  
Ming-Yung Chou
Keyword(s):  
Oral Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Morphological Changes ◽  
Cell Activity ◽  
Cancer Cell Lines ◽  
Dependent Manner ◽  
Dna Ladder ◽  
Bax Protein ◽  
Oral Cancer Cell

Chingwaysan, a Chinese herbal formula, contains Cimicfugae Rhizoma, Rehmanniae Radixet Rhizoma, Moutan Radicis Cortex, Coptidis Rhizoma and Angelicae Sinensis Radix. This medicine is well-known for its curing power for ulcerated gums, toothaches, cheek boils and bleeding gingiva. However, no reports can be found on its application in the treatment of oral cancers. We are therefore interested in whether Chingwaysan is capable of causing abnormal apoptosis processes, and whether this condition can be rectified through Chingwaysan herb treatment. We used aqueous extract to treat OC2 and TSCCa cells (both are human oral cancer cell lines) with different Chingwaysan concentrations (0, 10, 25, 50, 75 and 100 μl/ml). The MTT (3, (4, 5-dimethyl-thiazol) 2, 5-diphenyl-tetraxolium bromide) reduction assay was employed to quantify the differences in cell activity and viability. DNA ladder formation on agarose electrophoresis was also performed. The bax expression level was monitored using immunoblotting techniques. The patterns of the changes in expression were scanned and analyzed by NIH image 1.56 software. Taken together, drastic morphological changes, reduced cell viability and the presence of inter-nucleosomal DNA fragmentation all indicated that Chingwaysan is capable of inducing apoptosis in OC2 and TSCCa cell lines. Furthermore, the accumulation of wild type bax protein significantly increased in a dose-dependent manner upon treatment with Chingwaysan. In conclusion, Chingwaysan can induce apoptosis via a bax-dependent pathway in cells from these two particular oral cancer cell lines.

Actinomycin D and nutlin-3a synergistically promote phosphorylation of p53 on serine 46 in cancer cell lines of different origin

2015 ◽  
Vol 27 (9) ◽  
pp. 1677-1687 ◽  
Author(s):  
Artur Zajkowicz ◽  
Agnieszka Gdowicz-Kłosok ◽  
Małgorzata Krześniak ◽  
Dorota Ścieglińska ◽  
Marek Rusin
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Actinomycin D ◽  
Cancer Cell Lines ◽  
Different Origin

Bovine lactoferrin and lactoferrin peptides affect endometrial and cervical cancer cell lines

2020 ◽  
Author(s):  
Diana A. Ramírez-Sánchez ◽  
Izamar G. Arredondo-Beltran ◽  
Adrian Canizalez-Roman ◽  
Hector Flores-Villaseñor ◽  
Kamran Nazmi ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Morphological Changes ◽  
Uterine Cancer ◽  
Female Genital Tract ◽  
Cancer Cell Lines ◽  
Bovine Lactoferrin ◽  
Additive Interaction ◽  
Induced Apoptosis

Cervical, uterine and ovarian cancers are the most common malignancies of the female genital tract worldwide. In spite of advances in prevention, early diagnosis, effective screening, and treatment programs, mortality remains high. Consequently, it is important to search for new treatments. The activity of bovine Lactoferrin (bLF) and LF-peptides against several types of cancer has been studied, however, there are only a few studies reporting the effect of bLF and LF-peptides against cervical and endometrial cancers. In this study, we explored the effect of bLF, LFchimera and its constituent peptides LFcin17-30 and LFampin265-284 on the viability of cervical (HeLa, SiHa) and endometrial (KLE, HEC-1A) cancer cell lines. Cell proliferation was quantified with an MTT assay; cell morphological changes and damage were determined by Giemsa and phalloidin-TRITC and DAPI staining; and apoptotic and necrotic cells were identified by Alexa Fluor® 488 Annexin V and PI staining. Additionally, the effect of combinations of bLF and LF-peptides with cisplatin was assessed. BLF and LF-peptides inhibited the proliferation of uterine cancer cells and caused cellular morphological changes and damage to cell monolayers. BLF induced apoptosis; LFcin17-30 and LFampin265-284 induced apoptosis and necrosis, and LFchimera induced necrosis. Additionally, bLF and LFchimera showed an additive interaction with cisplatin against uterine cancer cells.

scholarly journals Autophagy Mediates Leptin-Induced Migration and ERK Activation in Breast Cancer Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Alin García-Miranda ◽  
Karen Aylín Solano-Alcalá ◽  
José Benito Montes-Alvarado ◽  
Arely Rosas-Cruz ◽  
Julio Reyes-Leyva ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Morphological Changes ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Breast Cancer Patients ◽  
Erk Activation ◽  
Erk Phosphorylation

Autophagy is an intracellular recycling process active in eukaryotic cells that involves the formation of an autophagosome which delivers cytoplasmic components to the lysosome for degradation. This process occurs at low rates under basal conditions, but it can be induced by diverse types of stress such as starvation, hypoxia, metabolic disorders or in response to hormones, including leptin. Leptin is considered a pro-tumorigenic protein whose circulating levels have been related to bad prognosis in obese breast cancer patients. It has been recently demonstrated that leptin can induce autophagy in cancer cell lines from different tissues, suggesting that autophagy could modulate the pro-tumorigenic effects associated with leptin. In this study, the role of autophagy in leptin-induced proliferation, migration, apoptosis and ERK phosphorylation in breast cancer cell lines was evaluated. Although leptin differentially induced autophagy in the breast cancer cell lines tested, autophagy inhibition reduced leptin-induced cell proliferation in MCF7 cells and decreased cell migration, ERK activation, and impaired morphological changes in both cell lines. Our data demonstrates an important role for basal autophagy or leptin-induced autophagy in leptin-induced migration and ERK phosphorylation in breast cancer cell lines, suggesting a potential use for the inhibition of autophagy in breast cancer associated with obesity.

scholarly journals Fusaproliferin, a Fungal Mycotoxin, Shows Cytotoxicity against Pancreatic Cancer Cell Lines

Molecules ◽  
2018 ◽  
Vol 23 (12) ◽  
pp. 3288 ◽  
Author(s):  
Nazia Hoque ◽  
Choudhury Hasan ◽  
Md. Rana ◽  
Amrit Varsha ◽  
Md. Sohrab ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Fusarium Solani ◽  
Pancreatic Cancer Cell ◽  
Morphological Changes ◽  
Cancer Cell Lines ◽  
Microscopy Imaging ◽  
Ongoing Research ◽  
Synthetic Agents

As a part of our ongoing research on endophytic fungi, we have isolated a sesterterpene mycotoxin, fusaproliferin (FUS), from a Fusarium solani strain, which is associated with the plant Aglaonema hookerianum Schott. FUS showed rapid and sub-micromolar IC50 against pancreatic cancer cell lines. Time-dependent survival analysis and microscopy imaging showed rapid morphological changes in cancer cell lines 4 h after incubation with FUS. This provides a new chemical scaffold that can be further developed to obtain more potent synthetic agents against pancreatic cancer.

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