scholarly journals Curcumin acts as anti-tumorigenic and hormone-suppressive agent in murine and human pituitary tumour cells in vitro and in vivo

2009 ◽  
Vol 16 (4) ◽  
pp. 1339-1350 ◽  
Author(s):  
C Schaaf ◽  
B Shan ◽  
M Buchfelder ◽  
M Losa ◽  
J Kreutzer ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Lines ◽  
Tumour Cell ◽  
Curcuma Longa ◽  
Pituitary Tumour ◽  
Pituitary Cells ◽  
Facs Analysis ◽  
Human Pituitary ◽  
Tumour Cell Lines

Curcumin (diferuloylmethane) is the active ingredient of the spice plant Curcuma longa and has been shown to act anti-tumorigenic in different types of tumours. Therefore, we have studied its effect in pituitary tumour cell lines and adenomas. Proliferation of lactosomatotroph GH3 and somatotroph MtT/S rat pituitary cells as well as of corticotroph AtT20 mouse pituitary cells was inhibited by curcumin in monolayer cell culture and in colony formation assay in soft agar. Fluorescence-activated cell sorting (FACS) analysis demonstrated curcumin-induced cell cycle arrest at G2/M. Analysis of cell cycle proteins by immunoblotting showed reduction in cyclin D1, cyclin-dependent kinase 4 and no change in p27kip. FACS analysis with Annexin V-FITC/7-aminoactinomycin D staining demonstrated curcumin-induced early apoptosis after 3, 6, 12 and 24 h treatment and nearly no necrosis. Induction of DNA fragmentation, reduction of Bcl-2 and enhancement of cleaved caspase-3 further confirmed induction of apoptosis by curcumin. Growth of GH3 tumours in athymic nude mice was suppressed by curcumin in vivo. In endocrine pituitary tumour cell lines, GH, ACTH and prolactin production were inhibited by curcumin. Studies in 25 human pituitary adenoma cell cultures have confirmed the anti-tumorigenic and hormone-suppressive effects of curcumin. Altogether, the results described in this report suggest this natural compound as a good candidate for therapeutic use on pituitary tumours.

scholarly journals Doxorubicin treatment modulates chemoresistance and affects the cell cycle in two canine mammary tumour cell lines

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Michela Levi ◽  
Roberta Salaroli ◽  
Federico Parenti ◽  
Raffaella De Maria ◽  
Augusta Zannoni ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Tumour Cell ◽  
S Phase ◽  
Mammary Tumour ◽  
Cancer Resistance ◽  
Neoplastic Cells ◽  
Canine Mammary Tumour ◽  
Tumour Cell Lines

Abstract Background Doxorubicin (DOX) is widely used in both human and veterinary oncology although the onset of multidrug resistance (MDR) in neoplastic cells often leads to chemotherapy failure. Better understanding of the cellular mechanisms that circumvent chemotherapy efficacy is paramount. The aim of this study was to investigate the response of two canine mammary tumour cell lines, CIPp from a primary tumour and CIPm, from its lymph node metastasis, to exposure to EC50(20h) DOX at 12, 24 and 48 h of treatment. We assessed the uptake and subcellular distribution of DOX, the expression and function of P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), two important MDR mediators. To better understand this phenomenon the effects of DOX on the cell cycle and Ki67 cell proliferation index and the expression of p53 and telomerase reverse transcriptase (TERT) were also evaluated by immunocytochemistry (ICC). Results Both cell lines were able to uptake DOX within the nucleus at 3 h treatment while at 48 h DOX was absent from the intracellular compartment (assessed by fluorescence microscope) in all the surviving cells. CIPm, originated from the metastatic tumour, were more efficient in extruding P-gp substrates. By ICC and qRT-PCR an overall increase in both P-gp and BCRP were observed at 48 h of EC50(20h) DOX treatment in both cell lines and were associated with a striking increase in the percentage of p53 and TERT expressing cells by ICC. The cell proliferation fraction was decreased at 48 h in both cell lines and cell cycle analysis showed a DOX-induced arrest in the S phase for CIPp, while CIPm had an increase in cellular death without arrest. Both cells lines were therefore composed by a fraction of cells sensible to DOX that underwent apoptosis/necrosis. Conclusions DOX administration results in interlinked modifications in the cellular population including a substantial effect on the cell cycle, in particular arrest in the S phase for CIPp and the selection of a subpopulation of neoplastic cells bearing MDR phenotype characterized by P-gp and BCRP expression, TERT activation, p53 accumulation and decrease in the proliferating fraction. Important information is given for understanding the dynamic and mechanisms of the onset of drug resistance in a neoplastic cell population.

scholarly journals Masitinib Combined with Standard Gemcitabine Chemotherapy: In Vitro and In Vivo Studies in Human Pancreatic Tumour Cell Lines and Ectopic Mouse Model

PLoS ONE ◽  
2010 ◽  
Vol 5 (3) ◽  
pp. e9430 ◽  
Author(s):  
Martine Humbert ◽  
Nathalie Castéran ◽  
Sébastien Letard ◽  
Katia Hanssens ◽  
Juan Iovanna ◽  
...  
Keyword(s):  
Mouse Model ◽  
Cell Lines ◽  
Tumour Cell ◽  
In Vivo Studies ◽  
Pancreatic Tumour ◽  
Tumour Cell Lines

scholarly journals Conjugation of Daunorubicin to Monoclonal Antihuman Sarcoma Antibody by a Novel Method

1992 ◽  
Vol 3 (suppl b) ◽  
pp. 101-105
Author(s):  
Michel Pagé ◽  
Denis Thibeault ◽  
Hélène Tremblay ◽  
Christiane Noël ◽  
Marie-Josée Perron
Keyword(s):  
Cell Lines ◽  
Pharmacological Activity ◽  
Tumour Cell ◽  
Immunological Specificity ◽  
Coupling Procedure ◽  
Novel Method ◽  
Tumour Cell Lines

Most of the reported methods for coupling anthracycline drugs to antibody result in either a loss of pharmacological activity or yield antibodies which have lost much of their immunological specificity. The use of glutaraldehyde for coupling saves both the pharmacological and immunological activities but it causes some polymerization of the antibody or of the macromolecular carrier which is undesirable for in vivo use. A new coupling procedure is reported which uses an activated derivative of daunorubicin added to monoclonal antihuman sarcoma antibody. This coupling procedure has not resulted in significant polymerization of the antibody or Joss of pharmacological activity determined by testing normal and tumour cell Lines in vitro.

scholarly journals Cell-specific expression and function of adenylyl cyclases in rat pituitary tumour cell lines

1994 ◽  
Vol 222 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Ruth H. PAULSSEN ◽  
Per W. JOHANSEN ◽  
Jan O. GORDELADZE ◽  
Oystein NYMOEN ◽  
Eyvind J. PAULSSEN ◽  
...  
Keyword(s):  
Cell Lines ◽  
Tumour Cell ◽  
Pituitary Tumour ◽  
Adenylyl Cyclases ◽  
Specific Expression ◽  
Rat Pituitary ◽  
Tumour Cell Lines ◽  
And Function

scholarly journals Effect of aspirin on tumour cell colony formation and evolution

2017 ◽  
Vol 14 (134) ◽  
pp. 20170374 ◽  
Author(s):  
Dominik Wodarz ◽  
Ajay Goel ◽  
C. Richard Boland ◽  
Natalia L. Komarova
Keyword(s):  
Cell Lines ◽  
Cell Population ◽  
Tumour Cell ◽  
Evolutionary Potential ◽  
A Cell ◽  
Tumour Cell Lines ◽  
Underlying Mechanisms ◽  
Cell Colony

Aspirin is known to reduce the risk of colorectal cancer (CRC) incidence, but the underlying mechanisms are not fully understood. In a previous study, we quantified the in vitro growth kinetics of different CRC tumour cell lines treated with varying doses of aspirin, measuring the rate of cell division and cell death. Here, we use these measured parameters to calculate the chances of successful clonal expansion and to determine the evolutionary potential of the tumour cell lines in the presence and absence of aspirin. The calculations indicate that aspirin increases the probability that a single tumour cell fails to clonally expand. Further, calculations suggest that aspirin increases the evolutionary potential of an expanding tumour cell colony. An aspirin-treated tumour cell population is predicted to result in the accumulation of more mutations (and is thus more virulent and more difficult to treat) than a cell population of the same size that grew without aspirin. This indicates a potential trade-off between delaying the onset of cancer and increasing its evolutionary potential through chemoprevention. Further work needs to investigate to what extent these findings apply to in vivo settings, and to what degree they contribute to the epidemiologically documented aspirin-mediated protection.

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