Effect of nano-selenium loaded with lycium barbarum polysaccharide on the proliferation of lens epithelial cells after UVB damage in vitro

AIM: To investigate the effect of nano-selenium loaded with different concentrations of lycium barbarum polysaccharide (LBP-SeNPs) on the proliferation of human lens epithelial cells (HLECs) from UV irradiation. METHODS: LBP-SeNPs were prepared and their particle size was detected. HLECs (SRA01/04) were irradiated with UVB for different time (0, 10, 20, 30, 40, 50, 60min) to construct a damaged model, the survival rate of cells was determined by methylthiazol tetrazolium (MTT) assay. The 4',6-Diamidine-2'-phenylindole dihydrochloride (DAPI) staining was used to observe the status of cell nucleus and drug entering cytoplasm through cell membrane in SRA01/04 cells after adding LBP-SENPS loaded with coumarin fluorescence agent 24h under fluorescence microscope. SRA01/04 normal and UVB-damaged cells were treated with different amounts of LBP-SeNPs at different concentrations, cells proliferation were observed. RESULTS: The particle size of LBP-SeNPs was stable in the range of 150-200 nm. The survival rate changes with time after UVB irradiation were statistically significant. The 10min of UVB exposure as the time was chosen to construct the cell damage model. With DAPI staining, LBP-SeNPs were observed to enter the cytoplasm through the cell membrane under fluorescence inverted microscope. Cytotoxicity of SRA01/04 at different concentrations of LBP-SeNPs were measured. Cell survival rate was statistically different compared with the control group. The higher the loading concentration of LBP in nano-Se drugs was, the higher the cell proliferation rate was (P<0.05). The lower the concentration of LBP-SeNPs, the higher the cell proliferation rate, showing a negative growth trend (P<0.05). The group with the highest average cell proliferation rate was 0.5 µmol/L 2.0 mg/mL LBP-SeNPs (128.80%). When the 2.0 mg/mL LBP-SeNPs group was selected for cell photography, the cell density was higher at 0.5 μmol/L. With the increase of concentration, SRA01/04 cells appeared more cytoplasm dehydration, cell shrinkage and apoptotic bodies, and cell density decreased. CONCLUSION: LBP-SeNPs has moderate particle size and good stability. LBP-SeNPs can protect HLECs (SRA01/04) from UVB-induced damage, and the cell proliferation rate is further increased with increasing the amount of loaded LBP and decreasing nano-selenium concentration.

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Evidence for a Negative Correlation between Human Reactive Enamine-Imine Intermediate Deaminase A (RIDA) Activity and Cell Proliferation Rate: Role of Lysine Succinylation of RIDA

International Journal of Molecular Sciences ◽

10.3390/ijms22083804 ◽

2021 ◽

Vol 22 (8) ◽

pp. 3804

Author(s):

Luisa Siculella ◽

Laura Giannotti ◽

Benedetta Di Chiara Stanca ◽

Matteo Calcagnile ◽

Alessio Rochira ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Negative Correlation ◽

Cancer Biology ◽

Human Tumor ◽

In Silico Analysis ◽

Proliferation Rate ◽

Reactive Intermediate ◽

Cell Proliferation Rate

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.

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Cell proliferation rate and nuclear morphometry in Roberts syndrome

Clinical Genetics ◽

10.1111/j.1399-0004.1998.tb03772.x ◽

2008 ◽

Vol 54 (6) ◽

pp. 512-516 ◽

Cited By ~ 6

Author(s):

Petros M Pavlopoulos ◽

Anastasia E Konstantinidou ◽

Emmanuel Agapitos ◽

Panagiotis Davaris

Keyword(s):

Cell Proliferation ◽

Proliferation Rate ◽

Roberts Syndrome ◽

Nuclear Morphometry ◽

Cell Proliferation Rate

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Analysis of cell proliferation rate in Oral Leukoplakia and Oral Squamous Cell Carcinoma

Journal of Clinical and Experimental Dentistry ◽

10.4317/jced.2.e173 ◽

2010 ◽

pp. e173-177 ◽

Cited By ~ 2

Author(s):

S. Mehkri ◽

AR. Iyengar ◽

KS. Nagesh ◽

MB. Bharati

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Oral Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Proliferation Rate ◽

Oral Leukoplakia ◽

Cell Proliferation Rate

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Parathyroid gland volume increases with postmaturational aging in the rat

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00261.2001 ◽

2002 ◽

Vol 282 (3) ◽

pp. E557-E563 ◽

Cited By ~ 7

Author(s):

Bernard Halloran ◽

Per Udén ◽

Quan-Yang Duh ◽

Shoichi Kikuchi ◽

Tracy Wieder ◽

...

Keyword(s):

Cell Proliferation ◽

Renal Insufficiency ◽

Parathyroid Gland ◽

Inorganic Phosphorus ◽

Proliferation Rate ◽

Parathyroid Cell ◽

Fischer 344 ◽

Gland Volume ◽

Cell Proliferation Rate ◽

Age Related

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.

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The Novel Long Noncoding RNA TUSC7 Inhibits Proliferation by Sponging MiR-211 in Colorectal Cancer

Cellular Physiology and Biochemistry ◽

10.1159/000457938 ◽

2017 ◽

Vol 41 (2) ◽

pp. 635-644 ◽

Cited By ~ 57

Author(s):

Jian Xu ◽

Rui Zhang ◽

Jian Zhao

Keyword(s):

Colorectal Cancer ◽

Cell Proliferation ◽

Tumor Suppressor ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Proliferation Rate ◽

Expression Level ◽

The Novel ◽

Cell Proliferation Rate ◽

Potential Tumor Suppressor

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.

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