Over-Expression of the Cell-Cycle Gene LaCDKB1;2 Promotes Cell Proliferation and the Formation of Normal Cotyledonary Embryos during Larix kaempferi Somatic Embryogenesis

Somatic embryogenesis is an effective tool for the production of forest tree seedlings with desirable characteristics; however, the low initiation frequency and productivity of high-quality mature somatic embryos are still limiting factors for Larix kaempferi (Japanese larch). Here, we analyzed the expression pattern of L. kaempferi cyclin-dependent kinase B 1;2 (LaCDKB1;2) during somatic embryogenesis in L. kaempferi and its relationship with the cell proliferation rate. We also analyzed the effect of LaCDKB1;2 over-expression on somatic embryo quality. The results revealed a positive correlation between LaCDKB1;2 expression and the cell proliferation rate during the proliferation stage. After LaCDKB1;2 over-expression, the proliferation rate of cultures increased, and the number of somatic embryos in transgenic cultures was 2.69 times that in non-transformed cultures. Notably, the number of normal cotyledonary embryos in transgenic cultures was 3 times that in non-transformed cultures, indicating that LaCDKB1;2 not only increases the proliferation of cultures and the number of somatic embryos but also improves the quality of somatic embryos. These results provide insight into the regulatory mechanisms of somatic embryogenesis as well as new Larix breeding material.

Download Full-text

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.

Download Full-text

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

Download Full-text

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

Download Full-text

LncRNA AB209371 up-regulated Survivin gene by down-regulating miR-203 in ovarian carcinoma

Journal of Ovarian Research ◽

10.1186/s13048-019-0559-4 ◽

2019 ◽

Vol 12 (1) ◽

Cited By ~ 1

Author(s):

Zi-Hui Zheng ◽

Dong-Mei Wu ◽

Shao-Hua Fan ◽

Xin Wen ◽

Xin-Rui Han ◽

...

Keyword(s):

Cell Proliferation ◽

Liver Cancer ◽

Ovarian Carcinoma ◽

Proliferation Rate ◽

Survivin Gene ◽

Over Expression

Abstract AB209371 gene has been characterized as an oncogenic lncRNA in liver cancer. However, its involvement in ovarian carcinoma (OC) is unknown. In the present study, we analyzed the roles of AB209371 in OC. We found that AB209371 gene and Survivin gene were up-regulated in OC and positively correlated with OC development. AB209371 over-expression led to up-regulated Survivin in OC cells, while Survivin over-expression failed to affect AB209371. In addition, AB209371 over-expression led to down-regulated miR-203. However, miR-203 over-expression failed to affect AB209371, but down-regulated the expression of Survivin. In addition, over-expressions of AB209371 and Survivin resulted in the increased proliferation rate of OC cells. Over-expression MiR-203 played the opposite role and attenuated the effects of AB209371 over-expression. Therefore, AB209371 may down-regulate miR-203 to up-regulate Survivin, thereby promoting OC cell proliferation. Our study provided novel insights into the pathogenesis of OC.

Download Full-text

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.

Download Full-text

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.

Download Full-text