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Tytuł:
Modulation of Doxorubicin Cytotoxicity by Isoliquiritin and Cynarin Combination on Different Cancer Cell Lines
Autorzy:
Al-AdamI, Salat G.
Al-Khateeb, EKBAL H.
NUMAN, NAWFAL A.
ABBAS, Mannal M.
Tawfiq, FATIMA A.
Shakya, Ashok K.
Powiązania:
https://bibliotekanauki.pl/articles/895633.pdf
Data publikacji:
2020-06-29
Wydawca:
Polskie Towarzystwo Farmaceutyczne
Tematy:
cytotoxicity
doxorubicin
cancer cells
Modulation
Cynarin
Isoliquiritin
Opis:
Natural polyphenolic compounds produced by plant exhibit many pharmacological effects including antioxidant, chemopreventive as well as anticancer properties. This study was conducted to investigate the effect of cynarin ( from Artichoke, Cynara scolymus) and isoliquiritin (from Licorice, Glycyrrhiza uralensis) on doxorubicin (positive control) cytotoxicity in different cell lines including normal (Fibroblasts MCR-5 and Myoblasts H9c2) and cancer (colorectal HCT-116 and hepatocellular HEP-G2) cell lines. The cytotoxic effect of doxorubicin, isoliquiritin and cynarin alone or in different combination was studied on cancer cell lines as well as normal cell lines. The results obtained indicated that both cynarin and isoliquiritin enhance the cytotoxicity of doxorubicin. Both cynarin and isoliquiritin also reduce the cardiotoxicity of doxorubicin on normal cardiac cell lines. The combination of the three compounds (cynarin, isoliquiritin and doxorubicin) result in decrease the cytotoxicity of doxorubicin, which may indicate the presence of interaction and/or antagonism effect between cynarin and isoliquiritin. Cynarin was found to enhance the growth of (HCT-116 and HEP-G2) this might suggest avoiding use of Artichoke in subjects’ susceptibility for these cancers. All results were evaluated using statistical path and showed significant findings. The mechanism of enhanced doxorubicin’s cytotoxicity by cynarin or isoliquiritin also require further investigation to explain the increasing and/or the decreasing effect of these polyphenolic compounds on cytotoxicity of doxorubicin. The current finding can help to start with safe minimum dose of two or three combination of compounds in the context of clinical trials and practice.
Źródło:
Acta Poloniae Pharmaceutica - Drug Research; 2020, 77, 3; 475-484
0001-6837
2353-5288
Pojawia się w:
Acta Poloniae Pharmaceutica - Drug Research
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Reactive oxygen species in BCR-ABL1-expressing cells - relevance to chronic myeloid leukemia
Autorzy:
Antoszewska-Smith, Joanna
Pawlowska, Elzbieta
Blasiak, Janusz
Powiązania:
https://bibliotekanauki.pl/articles/1038675.pdf
Data publikacji:
2017
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
chronic myeloid leukemia
reactive oxygen species
DNA damage
DNA repair
cancer stem cells
imatinib resistance
Opis:
Chronic myeloid leukemia (CML) results from the t(9;22) reciprocal chromosomal translocation producing the BCR-ABL1 gene, conferring growth and proliferation advantages in the CML cells. CML progresses from chronic, often syndrome-free, to blast phase, fatal if not treated. Although the involvement of BCR-ABL1 in some signaling pathways is considered as the cause of CML, the mechanisms resulting in its progression are not completely known. However, BCR-ABL1 stimulates the production of reactive oxygen species (ROS), which levels increase with CML progression and induce BCR-ABL1 self-mutagenesis. Introducing imatinib and other tyrosine kinase inhibitors (TKIs) to CML therapy radically improved its outcome, but TKIs-resistance became an emerging problem. TKI resistance can be associated with even higher ROS production than in TKI-sensitive cells. Therefore, ROS-induced self-mutagenesis of BCR-ABL1 can be crucial for CML progression and TKI resistance and in this way should be taken into account in therapeutic strategies. As a continuous production of ROS by BCR-ABL1 would lead to its self-destruction and death of CML cells, there must be mechanisms controlling this phenomenon. These can be dependent on DNA repair, which is modulated by BCR-ABL1 and can be different in CML stem and progenitor cells. Altogether, the mechanisms of the involvement of BCR-ABL1 in ROS signaling can be engaged in CML progression and TKI-resistance and warrant further study.
Źródło:
Acta Biochimica Polonica; 2017, 64, 1; 1-10
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Trastuzumab Efficacy Quantified by Fluorine-19 Magnetic Resonance Imaging
Autorzy:
Bartusik-Aebisher, Dorota
Aebisher, David
Czmil, Mrs Anna
Mazur, Damian
Powiązania:
https://bibliotekanauki.pl/articles/895489.pdf
Data publikacji:
2020-06-29
Wydawca:
Polskie Towarzystwo Farmaceutyczne
Tematy:
trastuzumab
magnetic resonance imaging
breast cancer cells
three-dimensional cell culture
Trastuzumab conjugates
Opis:
The purpose of this study was to conjugate Trastuzumab with fluorine-bearing PAMAM dendrimer to compare activities in three-dimensional (3D) cultured breast cancer cells with parent Trastuzumab. An in vitro study was performed to determine cellular responses to fluorinated Trastuzumab conjugates by Magnetic Resonance Imaging (MRI). Breast cancer cells were cultured in 3D geometry. Proton (1H) MRI and Fluorine-19 (19F) MRI were used for visualization of cellular locations within a Hollow Fiber Bioreactor (HFBR) device and to monitor the cellular response to treatment. The results of this study confirm that cell growth is significantly decreased following treatment with Trastuzumab conjugates. The use of fluorinated Trastuzumab conjugates decreases breast cancer cell growth in 3D cultures and allows for tracking of drug delivery to cancer cells via 19F.
Źródło:
Acta Poloniae Pharmaceutica - Drug Research; 2020, 77, 3; 495-503
0001-6837
2353-5288
Pojawia się w:
Acta Poloniae Pharmaceutica - Drug Research
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Detection of circulating tumour cells in the breast cancer using CytoTrack system
Autorzy:
Bogacz, A.
Wolek, M.
Górska, A.
Leporowska, E.
Procyk, D.
Kolenda, P.
Litwiniuk, M.
Uzar, I.
Gryszczyńska, A.
Łowicki, Z.
Czerny, B.
Powiązania:
https://bibliotekanauki.pl/articles/2048955.pdf
Data publikacji:
2019
Wydawca:
Instytut Włókien Naturalnych i Roślin Zielarskich
Tematy:
circulating tumour cells
breast cancer
CytoTrack CT11
liquid biopsy
wolnokrążące komórki nowotworowe
rak piersi
CytroTrack CT11
płynna biopsja
Opis:
Introduction: Plants are a rich source of healing substances. Cancer is a leading cause of death worldwide while breast cancer is the most common cancer among women. Circulating tumour cells (CTCs) are potential founder cells for metastasis. Therefore, their assessment may be used for monitoring of treatment as well as detecting cancer metastatis. Hence, it is suggested that the number of CTCs may be a valuable tumour biomarker during therapy. Objective: The purpose of this study was to detect CTCs in breast cancer and to validate the method of assessment of CTC count using CytoTrack CT11 technology. Methods: MCF-7 cells were sorted by a FACSARIA flow cytometer from blood samples derived from patients who have not been diagnosed with cancer. Identification and quantitative assessment of MCF-7 cells in blood samples were determined by flow sorting. Then, blood samples containing MCF-7 cells or without MCF-7 were scanned with the use of an automated fluorescence scanning microscope. Results: In in vitro model analysing the glass CytoDisc™ with stained MCF-7 cells, we noted the correlation between the amount of observed tumour cells and expected number of tumour cells. Moreover, coefficient of variation in case of the recovery rate of the assumed number of MCF-7 cells was 30%, 17%, 18% and 15%, respectively. Conclusion: Our study suggest that CTCs could be predictive factor in patients with metastatic cancer especially in breast cancer.
Źródło:
Herba Polonica; 2019, 65, 4; 31-36
0018-0599
Pojawia się w:
Herba Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Growth suppression of human breast carcinoma stem cells by lipid peroxidation product 4-hydroxy-2-nonenal and hydroxyl radical-modified collagen
Autorzy:
Cipak, Ana
Mrakovcic, Lidija
Ciz, Milan
Lojek, Antonin
Mihaylova, Boryana
Goshev, Ivan
Jaganjac, Morana
Cindric, Marina
Sitic, Sanda
Margaritoni, Marko
Waeg, Georg
Balic, Marija
Zarkovic, Neven
Powiązania:
https://bibliotekanauki.pl/articles/1040399.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
collagen
4-hydroxynonenal
breast cancer stem cells
extracellular matrix
oxidative homeostasis
SUM159
Opis:
Breast cancer is a leading cause of mortality and morbidity in women, mostly due to high metastatic capacity of mammary carcinoma cells. It has been revealed recently that metastases of breast cancer comprise a fraction of specific stem-like cells, denoted as cancer stem cells (CSCs). Breast CSCs, expressing specific surface markers CD44+CD24-/lowESA+ usually disseminate in the bone marrow, being able to spread further and cause late metastases. The fundamental factor influencing the growth of CSCs is the microenvironment, especially the interaction of CSCs with extracellular matrix (ECM). The structure and function of ECM proteins, such as the dominating ECM protein collagen, is influenced not only by cancer cells but also by various cancer treatments. Since surgery, radio and chemotherapy are associated with oxidative stress we analyzed the growth of breast cancer CD44+CD24-/lowESA+ cell line SUM159 cultured on collagen matrix in vitro, using either native collagen or the one modified by hydroxyl radical. While native collagen supported the growth of CSCs, oxidatively modified one was not supportive. The SUM159 cell cultures were further exposed to a supraphysiological (35 µM) dose of the major bioactive lipid peroxidation product 4-hydroxynonenal (HNE), a well known as 'second messenger of free radicals', which has a strong affinity to bind to proteins and acts as a cytotoxic or as growth regulating signaling molecule. Native collagen, but not oxidised, abolished cytotoxicity of HNE, while oxidized collagen did not reduce cytotoxicity of HNE at all. These preliminary findings indicate that beside direct cytotoxic effects of anticancer therapies consequential oxidative stress and lipid peroxidation modify the microenvironment of CSCs influencing oxidative homeostasis that could additionally act against cancer.
Źródło:
Acta Biochimica Polonica; 2010, 57, 2; 165-171
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Simvastatin modulates β-catenin/MDR1 expression on spheres derived from CF41.Mg canine mammary carcinoma cells
Autorzy:
Cruz, P.
Reyes, F.
Torres, C.G.
Powiązania:
https://bibliotekanauki.pl/articles/2087784.pdf
Data publikacji:
2018
Wydawca:
Polska Akademia Nauk. Czytelnia Czasopism PAN
Tematy:
β-catenin
MDR1
simvastatin
canine mammary carcinoma cells
cancer stem cells
Źródło:
Polish Journal of Veterinary Sciences; 2018, 21, 1; 95-99
1505-1773
Pojawia się w:
Polish Journal of Veterinary Sciences
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The expression of CD44, CD90 and CD133 in response to cisplatin in hepatocellular cancer cells
Autorzy:
Donmez Cakıl, Yaprak
Gunes Ozunal, Zeynep
Gokceoglu Kayalı, Damla
Gulhan Aktas, Ranan
Powiązania:
https://bibliotekanauki.pl/articles/2040155.pdf
Data publikacji:
2021-03-30
Wydawca:
Uniwersytet Rzeszowski. Wydawnictwo Uniwersytetu Rzeszowskiego
Tematy:
cancer
cisplatin
hepatocellular
stem cells
Opis:
Introduction. Cancer is a leading cause of mortality. Hepatocellular cancer is one of the malignancies associated with poor outcome and resistance to pharmacotherapy. Cancer stem cells (CSCs) contribute to resistance to therapy and hence lead to the treatment failure of tumors. Aim. This study aims to explore the expression of CSCs in response to cisplatin treatment in HepG2 hepatocellular cancer cell line. Material and methods. Cell proliferation test, CCK-8, was used to evaluate the cell proliferation following cisplatin treatment for 72 hours. The expressions of CSC markers CD44, CD90, and CD133 were assessed by flow cytometric analysis. Results. The results showed a dose-dependent decrease in cell proliferation and increased expression of CSC markers CD44 and CD90 in response to cisplatin. Conclusion. Understanding the roles of CSC markers may point to new targets and therapeutic strategies to predict and overcome cisplatin resistance.
Źródło:
European Journal of Clinical and Experimental Medicine; 2021, 1; 18-22
2544-2406
2544-1361
Pojawia się w:
European Journal of Clinical and Experimental Medicine
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
c-myc Oncogene gene dosage, serum CEA and CA-15.3 antigen levels, and cellular DNA values in relation to ex vivo chemosensitivity of primary human breast cancer.
Autorzy:
Falkiewicz, Bogdan
Schlotter, Claus
Bosse, Ulrich
Bielawski, Krzysztof
Vogt, Ulf
Powiązania:
https://bibliotekanauki.pl/articles/1044409.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
cultured tumor cells
antitumor drug screening assays
oncogenes
antineoplastic agents
drug resistance
breast cancer
Opis:
A pilot study on relationships of selected molecular factors (c-myc oncogene average gene copy numbers (AGCN); serum CEA and CA 15.3 antigen levels; tumor cells' DNA values), to the ex vivo chemosensitivity of primary female human breast cancer in a modified adenosine triphosphate cell viability chemosensitivity assay (ATP-CVA), was performed. Four drug combinations were tested. A group of 75 cases of female primary breast cancer was assessed. Numerous correlations were found among molecular factors tested but none, with the exception of tumor grading, of these reflected ex vivo chemosensitivity of tumors tested. The results suggest that the parameters tested may not be important factors related to adjuvant chemoresponsiveness of primary human breast cancer to tested drug combinations.
Źródło:
Acta Biochimica Polonica; 2000, 47, 1; 149-156
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Strategie odżywcze komórek nowotworowych – przegląd wybranych typów nowotworów z uwzględnieniem zmian w poziomie i wzorze ekspresji transporterów glukozy
Nutritional strategies of tumor cells – review of selected cancer types involving changes of expression level and pattern of glucose
Autorzy:
Gajek, K.
Wiatrak, B.
Ślęzak, A.
Ussowicz, M.
Powiązania:
https://bibliotekanauki.pl/articles/261959.pdf
Data publikacji:
2017
Wydawca:
Politechnika Wrocławska. Wydział Podstawowych Problemów Techniki. Katedra Inżynierii Biomedycznej
Tematy:
GLUT1
SGLT1
hipoksja
komórki nowotworowe
transport glukozy
hypoxia
cancer cells
glucose transport
Opis:
Zaburzona równowaga pomiędzy proliferacją a dojrzewaniem i różnicowaniem komórek nowotworowych powoduje szybki wzrost guza, prowadząc do zwiększenia zapotrzebowania na składniki odżywcze, m.in. glukozę i tlen. Pierwszą odpowiedzią komórek nowotworowych na niewystarczającą ilość składników odżywczych jest zmiana metabolizmu na beztlenowy (efekt Warburga). Glukoza niezbędna do przeprowadzenia tego procesu dostarczana jest za pomocą transporterów – najczęściej białek GLUT1 i SGLT1. Zmiana poziomu i wzoru ekspresji transporterów glukozy w komórkach nowotworowych w porównaniu z komórkami odpowiednich tkanek prawidłowych świadczy o adaptacji, do której doszło w obrębie guza. Dotychczasowe badania pozwoliły ustalić, w których rodzajach nowotworów dochodzi do zmian w ekspresji białek GLUT1 i SGLT1 oraz pokazały, że zmiany te mogą mieć bezpośredni związek z zaawansowaniem choroby i rokowaniem dla pacjentów. Niniejsza praca ma charakter przeglądowy i stanowi zestawienie zmian w poziomie ekspresji transporterów glukozy w niektórych typach nowotworów. Określenie poziomu ekspresji tych białek w komórkach nowotworowych może mieć kluczowe znaczenie dla spersonalizowanej terapii przeciwnowotworowej.
Due to imbalance between proliferation, differentiation and maturation, cancer cells grow rapidly and require elevated levels of oxygen and glucose. The main strategy of cancer cells is to prevent starvation is the anaerobic adaptation of cellular metabolism known as the Warburg’s effect. Increased glucose uptake is maintained by alterating the level and the pattern of glucose transporters expression, mainly GLUT1 and SGLT1. In many cancer types, these proteins are present despite their absence in healthy tissue. Previous researches revealed cancer types in which GLUT1 and SGLT1 expression are altered. There is a strong direct correlation between their expression pattern, cancer stage and prognosis for the patient. This review provides an overview of changes in the level of glucose transporters expression in some cancer types. Determination of glucose transporters expression levels in cancer cells could be crucial for personalized cancer treatment.
Źródło:
Acta Bio-Optica et Informatica Medica. Inżynieria Biomedyczna; 2017, 23, 2; 133-146
1234-5563
Pojawia się w:
Acta Bio-Optica et Informatica Medica. Inżynieria Biomedyczna
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Correlation of clinico-pathologic data with inflammatory cells infiltration in colorectal cancer
Autorzy:
Grudzińska, M.
Jakubowska, K.
Kańczuga-Koda, L.
Kisielewski, W.
Famulski, W.
Smereczański, N.M.
Lomperta, K.
Płoński, M.A.
Rogoz-Jezierska, N.
Koda, M.
Powiązania:
https://bibliotekanauki.pl/articles/1918914.pdf
Data publikacji:
2020-06-10
Wydawca:
Uniwersytet Medyczny w Białymstoku
Tematy:
Colorectal cancer
inflammatory cells
fibrosis
Opis:
Introduction: Colorectal cancer (CRC) is the third most common cancer worldwide. At every phase of cancer development, the inflammatory process has an important impact. Accurate assessment inflammatory cells in the tumour environment in conjunction with clinico-pathologic features can be a relevant prognostic or predictive parameter. Purpose: To analyse inflammatory cell infiltration in CRC tumour mass and correlate with chosen clinico-pathologic parameters. Materials and methods: The study group consisted of 160 patients (64 women, 96 men) diagnosed with colorectal cancer who underwent surgery. Tissue material obtained from routine histopathological diagnosis was stained with H&E and used to assess the type of inflammatory cells in the invasive front and centre of the tumour. Results were subjected to statistical analysis with the age and gender of patients, tumour localization, tumour growth and size, TNM stage, adenocarcinoma type, fibrosis, necrosis, metastasis and tumour invasion (by the Spearman’s correlation coefficient test). Results: The presence of neutrophils in the invasive front of tumour mass was associated with fibrosis and inflammatory cell infiltration in the invasive front of tumour. Macrophages in the invasive front of tumour were found to correlate with tumour growth (expanding and infiltrate). Macrophages and eosinophils were associated with inflammatory cell infiltration in the invasive front and in the centre of tumour. Conclusions: The type of inflammatory cells in the invasive front or centre of the tumour may be useful to prognoses clinical features of colorectal cancer
Źródło:
Progress in Health Sciences; 2020, 10(1); 69-76
2083-1617
Pojawia się w:
Progress in Health Sciences
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Use of cell therapy as a means of targeting chemotherapy to inoperable pancreatic cancer
Autorzy:
Günzburg, Walter
Salmons, Brian
Powiązania:
https://bibliotekanauki.pl/articles/1041363.pdf
Data publikacji:
2005
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
cytochrome P450
chemotherapy
genetically modified cells
cell therapy
encapsulated cells
pancreatic cancer
Opis:
Although approved for the treatment of pancreatic cancer, the chemotherapeutic agent ifosfamide is not an effective therapy for this type of tumour. Ifosfamide must be activated by cytochrome P450 (P450) enzymes in the liver, initially to a short lived intermediate and then to toxic metabolites that are subsequently distributed by the circulatory system. Particularly for pancreatic cancer, this liver-mediated conversion results in relatively high systemic toxicities and poor therapeutic concentrations at the liver-distant site of the tumour. Activation of ifosfamide at the site of the tumour may allow lower doses to be used, while increasing the therapeutic index due to the resultant active concentrations generated locally. A cell-based therapy has been conceived where encapsulated, 293-derived cells genetically modified to overexpress a cytochrome P450 enzyme, are implanted near solid tumours. The cells are encapsulated in polymers of cellulose sulphate in order to provide a means of immunoprotection in vivo as well as to physically constrain them to the vicinity of the tumour. A major advantage of this strategy is that it allows one standard cell line to be applied to all patients and this approach can be extended to the treatment of other tumour types. After proof of principle studies in animal models, a phase I/II clinical trial was initiated in patients with stage III/IV nonresectable pancreatic cancer. Encapsulated cells were angiographically placed into the tumour vasculature of 14 patients and followed by systemic low dose ifosfamide treatment. Angiographic delivery of encapsulated cells proved feasible in all but one patient, and was well tolerated with no capsule or ifosfamide treatment-related adverse events. Four of the treated patients showed tumour regressions after capsule delivery and ifosfamide treatment in computer-tomography scans. The other 10 patients showed no further tumour growth (i.e. stable disease) during 20 weeks observation period. The median life expectancy of the patient collective was extended two fold as compared to age and status matched historical controls, with a 3-fold improvement in one year survival being attained. Evidence for a clinical benefit of the treatment was also obtained on the basis of standard parameters for quality of life. This approach has been evaluated by the European Medicines Evaluation Agency (EMEA) and orphan drug status has been granted. A pivotal clinical trial is now being planned with the help of the EMEA. Taken together, the data from this clinical trial suggest that encapsulated cytochrome P450-expressing cells combined with chemotherapy may be useful for the local treatment of a number of solid tumours and support the performance of further clinical studies of this new treatment.
Źródło:
Acta Biochimica Polonica; 2005, 52, 3; 601-607
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Salinomycyna – przełom w leczeniu raka jajnika?
Salinomycin – a breakthrough in the treatment of ovarian cancer?
Autorzy:
Huczyński, Adam
Markowska, Janina
Ramlau, Rodryg
Sajdak, Stefan
Szubert, Sebastian
Stencel, Katarzyna
Powiązania:
https://bibliotekanauki.pl/articles/1030100.pdf
Data publikacji:
2016
Wydawca:
Medical Communications
Tematy:
cancer stem cells
ovarian cancer
salinomycin
komórki macierzyste raka
rak jajnika
salinomycyna
Opis:
It is believed that cancer stem cells are the primary cause of cancer chemotherapy resistance, metastasis and relapse. The cancer stem cells form a small population of cells present in the tumor (accounting for less than 2% of the tumor mass) and have properties which enable them to survive chemo- and radiotherapy. These cells have the ability to self-renew, do not undergo apoptosis, display overexpression of the ALDH1A1 enzyme and ABC genes which encode transport proteins, and furthermore make use of various signaling pathways (Wnt, Notch, Hedgehog). Cancer stem cells may be identified and isolated from the tumor based on the characteristic biomarkers (CD44+, CD133+, CD117+, BMi1, Oct-4, nestin). It has been demonstrated that salinomycin, an antibiotic obtained from Streptomyces albus, eliminates cancer stem cells, which are resistant to treatment with cytostatics. Salinomycin causes apoptosis of these cells through a number of mechanisms, including the disruption of the Na+/K+ ion balance in biological membranes, inhibition of the Wnt pathway and resistance to transporters, increase in the activity of caspases, activation of the MAPKp38 pathway and inhibition of the nuclear transcription factor NF-κB. Salinomycin has an effect on many types of cancer. It may turn out to be a breakthrough in the therapy of chemotherapy-resistant cancers.
Uważa się, że główną przyczyną chemiooporności, przerzutów i nawrotów raka jajnika są komórki macierzyste raka. Jest to obecna w guzie mała populacja komórek (stanowiąca mniej niż 2% jego masy), których właściwości pozwalają im przetrwać chemio- i radioterapię. Komórki te mają zdolność do samoodnowy, nie podlegają apoptozie, wykazują nadekspresję genów ABC kodujących białka transportowe, enzymu ALDH1A1 i korzystają z różnych szlaków sygnałowania (Wnt, Notch, Hedgehog). Komórki macierzyste raka można zidentyfikować oraz izolować z guza na podstawie charakterystycznych biomarkerów (CD44+, CD133+, CD117+, BMi1, Oct-4, nestyna). Wykazano, że salinomycyna, antybiotyk uzyskany ze Streptomyces albus, eliminuje komórki macierzyste raka, które są oporne na leczenie cytostatykami. Salinomycyna powoduje apoptozę tych komórek poprzez wiele mechanizmów, w tym poprzez zakłócenie jonowego bilansu Na+/K+ w błonach biologicznych, hamowanie szlaku Wnt i oporności na działanie transporterów, wzrost aktywności kaspaz, aktywację szlaku MAPKp38 oraz hamowanie jądrowego czynnika transkrypcyjnego NF-κB. Salinomycyna jest aktywna w wielu rodzajach nowotworów. Może okazać się przełomem w terapii nowotworów chemioopornych.
Źródło:
Current Gynecologic Oncology; 2016, 14, 3; 156-161
2451-0750
Pojawia się w:
Current Gynecologic Oncology
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Surface-modified SPION systems for cancer therapy
Autorzy:
Karewicz, Anna
Karnas, Karolina
Dulińska-Litewka, Joanna
Kapusta, Czesław
Lekka, Małgorzata
Powiązania:
https://bibliotekanauki.pl/articles/1844916.pdf
Data publikacji:
2020
Wydawca:
Akademia Górniczo-Hutnicza im. Stanisława Staszica w Krakowie. Polskie Towarzystwo Biominerałów
Tematy:
SPION systems
cancer therapy
tumor cells
system SPION
terapia
komórki rakowe
Źródło:
Engineering of Biomaterials; 2020, 23, 158 spec. iss.; 13
1429-7248
Pojawia się w:
Engineering of Biomaterials
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Multidirectional effects of triterpene saponins on cancer cells - mini-review of in vitro studies
Autorzy:
Koczurkiewicz, Paulina
Czyż, Jarosław
Podolak, Irma
Wójcik, Katarzyna
Galanty, Agnieszka
Janeczko, Zbigniew
Michalik, Marta
Powiązania:
https://bibliotekanauki.pl/articles/1038965.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
triterpene saponins
cancer cells
invasiveness
apoptosis
proliferation
Opis:
Triterpene saponins (saponosides) are found in a variety of higher plants and display a wide range of pharmacological activities, including expectorant, anti-inflamatory, vasoprotective, gastroprotective and antimicrobial properties. Recently, a potential anticancer activity of saponins has been suggested by their cytotoxic, cytostatic, pro-apoptotic and anti-invasive effects. At high concentrations (more than 100 µM) saponins exert cytotoxic and haemolytic effects via permeabilization of the cell membranes. Noteworthy, the inhibition of cancer cell proliferation, the induction of apoptosis and attenuation of cell invasiveness is observed in the presence of low saponin concentrations. Saponins might affect the expression of genes associated with malignancy. These alterations are directly related to the invasive phenotype of cancer cells and depend on "cellular context". It illustrates the relationships between the action of saponins, and the momentary genomic/proteomic status of cancer cells. Here, we discuss the hallmarks of anti-cancer activity of saponins with the particular emphasis on anti-invasive effect of diverse groups of saponins that have been investigated in relation to tumor therapy.
Źródło:
Acta Biochimica Polonica; 2015, 62, 3; 383-393
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Numerical experiments with model equations of cancer invasion of tissue
Autorzy:
Kolev, M.
Zubik-Kowal, B.
Powiązania:
https://bibliotekanauki.pl/articles/206179.pdf
Data publikacji:
2011
Wydawca:
Polska Akademia Nauk. Instytut Badań Systemowych PAN
Tematy:
in vivo tumorigenicity
cancer cells
proliferation
chemotaxis
haptotaxis
extracellular matrix
tumour invasion
mathematical model
animal models
approximations
Opis:
In this paper we investigate a mathematical model of cancer invasion of tissue, which incorporates haptotaxis, chemotaxis, proliferation and degradation rates for cancer cells and the extracellular matrix, kinetics of urokinase receptor, and urokinase plasminogen activator cycle. We solve the model using spectrally accurate approximations and compare its numerical solutions with laboratory data. The spectral accuracy allows to use low-dimensional matrices and vectors, which speeds up the computations of the numerical solutions and thus to estimate the parameter values for the model equations. Our numerical results demonstrate correlations between numerical data computed from the mathematical model and in vivo tumour growth rates from prostate cell lines.
Źródło:
Control and Cybernetics; 2011, 40, 3; 779-791
0324-8569
Pojawia się w:
Control and Cybernetics
Dostawca treści:
Biblioteka Nauki
Artykuł

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