Cell proliferation rate and tumor volume in human osteosarcoma during exposure to methotrexate

Apmis ◽  
1991 ◽  
Vol 99 (7-12) ◽  
pp. 898-904 ◽  
Author(s):  
STAFFAN Smeds ◽  
THOMAS Walz ◽  
LENA Blomquist ◽  
SVEN-ERIC Larsson
2021 ◽  
Vol 22 (8) ◽  
pp. 3804
Author(s):  
Luisa Siculella ◽  
Laura Giannotti ◽  
Benedetta Di Chiara Stanca ◽  
Matteo Calcagnile ◽  
Alessio Rochira ◽  
...  

Reactive intermediate deaminase (Rid) proteins are enzymes conserved in all domains of life. UK114, a mammalian member of RidA subfamily, has been firstly identified as a component of liver perchloric acid-soluble proteins (L-PSP). Although still poorly defined, several functions have been attributed to the mammalian protein UK114/RIDA, including the reactive intermediate deamination activity. The expression of UK114/RIDA has been observed in some tumors, arousing interest in this protein as an evaluable tumor marker. However, other studies reported a negative correlation between UK114/RIDA expression, tumor differentiation degree and cell proliferation. This work addressed the question of UK114/RIDA expression in human non-tumor HEK293 cell lines and in some human tumor cell lines. Here we reported that human RIDA (hRIDA) was expressed in all the analyzed cell line and subjected to lysine (K-)succinylation. In HEK293, hRIDA K-succinylation was negatively correlated to the cell proliferation rate and was under the control of SIRT5. Moreover, K-succinylation clearly altered hRIDA quantification by immunoblotting, explaining, at least in part, some discrepancies about RIDA expression reported in previous studies. We found that hRIDA was able to deaminate reactive enamine-imine intermediates and that K-succinylation drastically reduced deaminase activity. As predicted by in silico analysis, the observed reduction of deaminase activity has been related to the drastic alterations of hRIDA structure inferred by K-succinylation. The role of hRIDA and the importance of its K-succinylation in cell metabolism, especially in cancer biology, have been discussed.


2008 ◽  
Vol 54 (6) ◽  
pp. 512-516 ◽  
Author(s):  
Petros M Pavlopoulos ◽  
Anastasia E Konstantinidou ◽  
Emmanuel Agapitos ◽  
Panagiotis Davaris

2002 ◽  
Vol 282 (3) ◽  
pp. E557-E563 ◽  
Author(s):  
Bernard Halloran ◽  
Per Udén ◽  
Quan-Yang Duh ◽  
Shoichi Kikuchi ◽  
Tracy Wieder ◽  
...  

To examine the pathophysiology of the age-related rise in the plasma concentration of parathyroid hormone (PTH), we studied the relationships among plasma immunoreactive PTH (iPTH), parathyroid gland volume, parathyroid cell proliferation rate, renal function, and blood Ca2+ in male Fischer 344 rats aged 6–28 mo. Plasma iPTH increased 2.5-fold between 6 and 28 mo and correlated with parathyroid gland volume ( r = 0.87). Gland volume began to increase as early as 6–12 mo of age and by 28 mo was threefold greater than at 6 mo. Gland expansion was a consequence of hyperplasia stimulated in part by an increase in cell proliferative activity late in life. Blood Ca2+ and plasma inorganic phosphorus did not change significantly with age. Glomerular filtration rate decreased with age but only after the age of 24 mo. Unlike what has been observed in the human, these data suggest that the age-related increase in plasma iPTH in the rat is linked to parathyroid gland hyperplasia and that early gland growth does not appear to be associated with hypocalcemia or renal insufficiency, but rather to developmentally related metabolic changes. Later in life (>24 mo), the increase in parathyroid cell proliferation rate, further hyperplastic expansion of the gland, and increase in iPTH secretion appear to be associated with renal insufficiency.


2017 ◽  
Vol 41 (2) ◽  
pp. 635-644 ◽  
Author(s):  
Jian Xu ◽  
Rui Zhang ◽  
Jian Zhao

Background/Aims: The novel long noncoding RNA (lncRNA) tumor suppressor candidate 7 (TUSC7) has been reported as a potential tumor suppressor, while the functional role of TUSC7 is still unknown in colorectal cancer (CRC). Here, we characterized TUSC7 expression profile in CRC patients and investigated its biological function and potential molecular mechanism. Methods: RNA isolation, qRT-PCR, cell counter kit-8 assay, cell cycle assay, EdU assay, and western blot were performed. Statistical analyses were performed using SPSS 18.0 software and p value < 0.05 was considered as statistically significant. Results: In a cohort of CRC patients, we found TUSC7 was significantly downregulated in CRC tissues compared with adjacent non-tumor tissues (P < 0.01). Patients with high expression of TUSC7 had better survival than those with low expression of TUSC7 (HR = 0.342, 95% CI: 0.120-0.972, P = 0.044). Cell count kit 8 and EdU assays showed that ectopic expression of TUSC7 in HCT116 and SW480 cells significantly inhibited cell proliferation rate. After silence of TUSC7 with small interfering RNA, cell proliferation rate increased. Flow cytometry analyses revealed cycles were arrested at G1 phase after TUSC7 overexpression. We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p. Conclusion: To summary, we demonstrated that TUSC7 is a potential tumor suppressor in CRC, and TUSC7 could inhibit CRC cell proliferation by completely sponging miR-211-3p.


2001 ◽  
Vol 913 (2) ◽  
pp. 190-194 ◽  
Author(s):  
Almudena Velasco ◽  
Elena Cid ◽  
Juana Ciudad ◽  
Alberto Orfao ◽  
Jose Aijon ◽  
...  

2005 ◽  
Vol 80 (3) ◽  
pp. 203-207 ◽  
Author(s):  
Sandra Cristina de Souza ◽  
Egberto Munin ◽  
Leandro Procópio Alves ◽  
Miguel Angel Castillo Salgado ◽  
Marcos Tadeu Tavares Pacheco

1970 ◽  
Vol 16 (2) ◽  
Author(s):  
Basuki B Purnomo

Objective: Alpha tocopherol, other than its anti-oxidant activity, also has a non anti-oxidant activity that correlates with inhibition of PKC-alpha isozyme activity. Several studies had confirmed its role in inhibition of vascular smooth muscle proliferation. Inhibition of stromal cell proliferation is an alternative method of prevention in BPH development. The aim of this in vitro study is to confirm that alpha-tocopherol, by its ability to inhibit PKC-alpha activity, has the capability to inhibit human prostatic stromal cell proliferation rate. Materials & Method: Primary cultures of human prostatic stromal muscle cells were obtained from 4 patients with bladder outlet obstruction caused by benign prostatic enlargement. The effects of various concentrations of alpha-tocopherol (20, 30, 40, 50, and 60 microM) were examined by cell proliferation and PKC-alpha isozyme activity assay. Cell proliferation study was performed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay method. Caspase-3 activity assay was also performed to examine apoptotic mechanism. Results: MTT method, which is used to count viable cells, showed that exposures to various doses of alpha-tocopherol resulted in decreased proliferation rate. The decrement of proliferation rate is linear with the increment of alpha-tocopherol dose. Immunocytochemistry staining with anti caspase-3 antibody showed that no cells developed apoptosis. Alpha-tocopherol also inhibits PKC-alpha activity. Isozyme activity is reduced along with the increment of the dose (dose-dependent). There is a correlation between PKC-alpha activity with cell proliferation rate after exposure to alpha-tocopherol (R2=0,9279; p=0,000). Conclusion: Alpha-tocopherol at different concentrations reduces prostatic stromal cell proliferation rate, without effect on apoptosis. This antiproliferative property correlates with decreased activity of PKC-alpha isozyme.


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