The role of polymorphonuclear leukocytes (PMN) on the growth and metastatic potential of 13762nf mammary adenocarcinoma cells

1988 ◽  
Vol 42 (5) ◽  
pp. 748-759 ◽  
Author(s):  
Paul A. Aeed ◽  
Motowo Nakajima ◽  
Danny R. Welch
Author(s):  
Alejandro Urtreger ◽  
Santiago Werbajh ◽  
Frank Verrecchia ◽  
Alain Mauviel ◽  
Lydia Puricelli ◽  
...  

2018 ◽  
Vol 17 (4) ◽  
pp. 180-186
Author(s):  
E. V. Shakhristova ◽  
E. A. Stepovaya ◽  
O. L. Nosareva ◽  
L. S. Litvinova ◽  
D. A. Skuratovskaya ◽  
...  

Redox proteins (thioredoxin, glutaredoxin) are key macromolecules capable of modulating intracellular processes. This determines research choices in the field of redox-dependent cell proliferation management. The study of the molecular mechanisms of the onset, development and progression of malignant neoplasms underlies the search for tumor-associated markers and potential targets for personalized antitumor therapy.Purpose.To establish the role of the “thioredoxin – thioredoxin-reductase” system in the impaired proliferation of mammary adenocarcinoma cells under the action of the cyclin-dependent protein kinase roskovitin blocker.Materials and methods.The study was carried out using the culture of mammary adenocarcinoma cells of the MCF-7 line incubated in the presence and absence of roskovitin at a final concentration of 20 μM for 18 h. The intracellular content of thioredoxin and protein regulators of proliferation (cyclin E and cyclin-dependent protein kinase 2) were determined by Western blotting technique, the expression level of thioredoxin mRNA was determined by real-time polymerase chain reaction and the activity of thioredoxin-reductase was measured by a spectrophotometric method.Results.It was established that the decrease in proliferative activity of MCF-7 tumor cells incubated in the presence of roskovitin was accompanied by a decrease in the content of cyclin E and cyclin-dependent kinase on the background of a decrease in the expression level of thioredoxin mRNA and an increase in the activity of thioredoxin-reductase.Conclusion.The involvement of the components of the thioredoxin system (thioredoxin, thioredoxinreductase) in disrupting the proliferation of MCF-7 tumor cells was detected under the action of the cyclindependent protein kinases of roskovitin.


The role of vitamin D is implicated in carcinogenesis through numerous biological processes like induction of apoptosis, modulation of immune system inhibition of inflammation and cell proliferation and promotion of cell differentiation. Its use as additional adjuvant drug with cancer treatment may be novel combination for improved outcome of different cancers. Numerous preclinical, epidemiological and clinical studies support the role of vitamin D as an anticancer agent. Anticancer properties of vitamin D have been studied widely (both in vivo and in vitro) among various cancers and found to have promising results. There are considerable data that indicate synergistic potential of calcitriol and antitumor agents. Possible mechanisms for modulatory anticancer activity of vitamin D include its antiproliferative, prodifferentiating, and anti-angiogenic and apoptic properties. Calcitriol reduces invasiveness and metastatic potential of many cancer cells by inhibiting angiogenesis and regulating expression of the key molecules involved in invasion and metastasis. Anticancer activity of vitamin D is synergistic or additive with the antineoplastic actions of several drugs including cytotoxic chemotherapy agents like paclitaxel, docetaxel, platinum base compounds and mitoxantrone. Benefits of addition of vitamin D should be weighed against the risk of its toxicity.


2021 ◽  
Vol 22 (13) ◽  
pp. 6726
Author(s):  
Agata M. Gaweł ◽  
Maciej Ratajczak ◽  
Ewa Gajda ◽  
Małgorzata Grzanka ◽  
Agnieszka Paziewska ◽  
...  

Background: Thyroid carcinoma (TC) is the most common endocrine system malignancy, and papillary thyroid carcinoma (PTC) accounts for >80% of all TC cases. Nevertheless, PTC pathogenesis is still not fully understood. The aim of the study was to elucidate the role of the FRMD5 protein in the regulation of biological pathways associated with the development of PTC. We imply that the presence of certain genetic aberrations (e.g., BRAF V600E mutation) is associated with the activity of FRMD5. Methods: The studies were conducted on TPC1 and BCPAP (BRAF V600E) model PTC-derived cells. Transfection with siRNA was used to deplete the expression of FRMD5. The mRNA expression and protein yield were evaluated using RT-qPCR and Western blot techniques. Proliferation, migration, invasiveness, adhesion, spheroid formation, and survival tests were performed. RNA sequencing and phospho-kinase proteome profiling were used to assess signaling pathways associated with the FRMD5 expressional status. Results: The obtained data indicate that the expression of FRMD5 is significantly enhanced in BRAF V600E tumor specimens and cells. It was observed that a drop in intracellular yield of FRMD5 results in significant alternations in the migration, invasiveness, adhesion, and spheroid formation potential of PTC-derived cells. Importantly, significant divergences in the effect of FRMD5 depletion in both BRAF-wt and BRAF-mutated PTC cells were observed. It was also found that knockdown of FRMD5 significantly alters the expression of multidrug resistant genes. Conclusions: This is the first report highlighting the importance of the FRMD5 protein in the biology of PTCs. The results suggest that the FRMD5 protein can play an important role in controlling the metastatic potential and multidrug resistance of thyroid tumor cells.


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