CircSAMD4A accelerates cell proliferation of osteosarcoma by sponging miR-1244 and regulating MDM2 mRNA expression

2019 ◽  
Vol 516 (1) ◽  
pp. 102-111 ◽  
Author(s):  
Zhao Yanbin ◽  
Zhang Jing
Keyword(s):  
Cell Proliferation ◽  
Mrna Expression ◽  
Mdm2 Mrna

scholarly journals Follicle-Stimulating Hormone Inhibits Adenosine 5′-Monophosphate-Activated Protein Kinase Activation and Promotes Cell Proliferation of Primary Granulosa Cells in Culture through an Akt-Dependent Pathway

Endocrinology ◽  
2009 ◽  
Vol 150 (2) ◽  
pp. 929-935 ◽  
Author(s):  
Pradeep P. Kayampilly ◽  
K. M. J. Menon
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Protein Kinase ◽  
Mrna Expression ◽  
Granulosa Cell ◽  
Granulosa Cells ◽  
Ampk Activation ◽  
Cyclin D2 ◽  
Cell Cycle Inhibitor ◽  
Dependent Pathway

FSH, acting through multiple signaling pathways, regulates the proliferation and growth of granulosa cells, which are critical for ovulation. The present study investigated whether AMP-activated protein kinase (AMPK), which controls the energy balance of the cell, plays a role in FSH-mediated increase in granulosa cell proliferation. Cells isolated from immature rat ovaries were grown in serum-free, phenol red free DMEM-F12 and were treated with FSH (50 ng/ml) for 0, 5, and 15 min. Western blot analysis showed a significant reduction in AMPK activation as observed by a reduction of phosphorylation at thr 172 in response to FSH treatment at all time points tested. FSH also reduced AMPK phosphorylation in a dose-dependent manner with maximum inhibition at 100 ng/ml. The chemical activator of AMPK (5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside, 0.5 mm) increased the cell cycle inhibitor p27 kip expression significantly, whereas the AMPK inhibitor (compound C, 20 μm) and FSH reduced p27kip expression significantly compared with control. FSH treatment resulted in an increase in the phosphorylation of AMPK at ser 485/491 and a reduction in thr 172 phosphorylation. Inhibition of Akt phosphorylation using Akt inhibitor VIII reversed the inhibitory effect of FSH on thr 172 phosphorylation of AMPK, whereas ERK inhibitor U0126 had no effect. These results show that FSH, through an Akt-dependent pathway, phosphorylates AMPK at ser 481/495 and inhibits its activation by reducing thr 172 phosphorylation. AMPK activation by 5-amino-imidazole-4-carboxamide-1-β-d-ribofuranoside treatment resulted in a reduction of cell cycle regulatory protein cyclin D2 mRNA expression, whereas FSH increased the expression by 2-fold. These results suggest that FSH promotes granulosa cell proliferation by increasing cyclin D2 mRNA expression and by reducing p27 kip expression by inhibiting AMPK activation through an Akt-dependent pathway. FSH stimulates granulosa cell proliferation by reducing cell cycle inhibitor p27 kip through AMP kinase inhibition.

scholarly journals Identification of CTRP1 as a Prognostic Biomarker and Oncogene in Human Glioblastoma

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Liyan Chen ◽  
Gang Su
Keyword(s):  
Cell Proliferation ◽  
Mrna Expression ◽  
Genetic Alterations ◽  
Expression Levels ◽  
Cell Proliferation And Migration ◽  
Ccl2 Expression ◽  
Human Gbm ◽  
And Migration ◽  
Mrna Expression Levels ◽  
Proliferation And Migration

Introduction. Glioblastoma (GBM) is the most frequent and malignant type of primary brain tumors in adults. The valuable prognostic biomarkers and therapeutic targets for GBM remain to be elucidated. The association of adipokines with cancer has been well documented. The C1q/TNF-related protein 1 (CTRP1), a novel adipokine, belongs to the CTRP family.Methods. In the present study, the expression and potential roles of CTRP1 in GBM were explored based on in silico evaluation, including GEPIA, the Pathology Atlas of the Human Protein Atlas, cBioPortal, TIMER, and SurvExpress. The CCK8, transwell, and wound healing assays were used to detect cell proliferation and migration.Results. It was found that mRNA expression levels ofCTRP1were significantly upregulated in GBM tissues compared with those in nontumor tissues according to the analysis on public dataset and immunohistochemical results of GBM tissues (P<0.05). CTRP1 was mainly localized in the cytoplasm and cell membrane of GBM cells. The genetic alterations of CTRP1 occurred at a low rate in GBM (2 of 591 sequenced cases/patients, 0.33%). The mRNA expression levels ofCTRP1were positively associated with the tumor-infiltrating macrophages and CCL2 in GBM (P<0.05, respectively). The higher mRNA expression levels ofCTRP1were significantly correlated with higher risk and shorter overall survival time in GBM (P<0.05). CTRP1 knockdown significantly inhibited the proliferation and migration in human GBM cells, suggesting the inhibition of CTRP1 on human GMB progression. Moreover, CTRP1 knockdown inhibited CCL2 expression, and CCL2 overexpression reversed the inhibition of cell proliferation and migration induced by CTRP1 knockdown, suggesting that CTRP1 promoted tumor progression by regulating CCL2 expression.Conclusions. These findings suggest that CTRP1 potentially indicates poor prognosis in GBM and promotes the progression of human GBM.

scholarly journals Rapamycin inhibits human renal epithelial cell proliferation: Effect on cyclin D3 mRNA expression and stability

2005 ◽  
Vol 67 (6) ◽  
pp. 2422-2433 ◽  
Author(s):  
Nicolas Pallet ◽  
Eric Thervet ◽  
Delphine Le Corre ◽  
Bertrand Knebelmann ◽  
Patrick Nusbaum ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Mrna Expression ◽  
Cyclin D3 ◽  
Epithelial Cell Proliferation ◽  
Renal Epithelial Cell

Down expression of activin A receptor type 2A in relation to metastatic potential and prognosis of patients with colon cancer.

2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 712-712
Author(s):  
Changhua Zhuo ◽  
Dan Hu ◽  
Xiandong Lin ◽  
Ying Chen ◽  
Xiongwei Zheng ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Mrna Expression ◽  
Tissue Microarray ◽  
Validation Cohort ◽  
Activin A ◽  
Receptor Type ◽  
Primary Tumors

712 Background: The ACVR2A (activin A receptor type 2A) is a membrane receptor in TGF-β signal pathway, which is involved in the regulation of cell proliferation, migration and apoptosis. The expression profiles and biological functions of ACVR2A in colon cancer is largely unknown so far. Methods: ACVR2A expression was investigated using GSE39582 database and two validation cohorts. The in vitro study of the cell proliferation and migration of human colon cell lines was also performed. Results: In GSE39582 database (n = 497), lower mRNA expression of ACVR2A was identified as an inferior prognostic factor by linear regression analysis. In one validation cohort of 15 stage IV patients, the mRNA expression of ACVR2A was significantly reduced in metastatic lesions and primary tumors compared with adjacent normal controls (P = 0.001). In another validation cohort of tissue microarray (TMA) cohort consisting 193 cases, reduced ACVR2A expression was correlated with advanced N stage (P = 0.001) and positive lymphovascular invasion (P = 0.005). Strong correlations between lower ACVR2A mRNA or protein expression and worse survival were also observed in GSE39582 database and TMA validation cohort (all P< 0.05). Moreover, our in vitro studies showed a remarkable increase of cell migration in cell ACVR2A knockdown cells. Conclusions: Taken together, our findings indicate that loss of ACVR2A has an important role in cancer progression and distant metastasis, and may serve as a prognostic marker in patients with colon cancer. Keywords: Activin a receptor type 2A (ACVR2A), Colon Cancer, tissue microarray, Metastasis, Cell proliferation, Cell migration

Endothelin-1 stimulates c-fos mRNA expression and acts as a modulator on cell proliferation of rat FRTL5 thyroid cells

1992 ◽  
Vol 184 (1) ◽  
pp. 231-238 ◽  
Author(s):  
Megumi Miyakawa ◽  
Toshio Tsushima ◽  
Osamu Isozaki ◽  
Hiroshi Demura ◽  
Kazuo Shizume ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mrna Expression ◽  
Thyroid Cells ◽  
Endothelin 1

scholarly journals Latency-Associated Peptide of Transforming Growth Factor β Enhances Mycobacteriocidal Immunity in the Lung duringMycobacterium bovis BCG Infection in C57BL/6 Mice

2000 ◽  
Vol 68 (11) ◽  
pp. 6505-6508 ◽  
Author(s):  
K. A. Wilkinson ◽  
T. D. Martin ◽  
S. M. Reba ◽  
H. Aung ◽  
R. W. Redline ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Growth Factor ◽  
Mrna Expression ◽  
Mycobacterium Bovis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Gamma Interferon ◽  
T Cell Proliferation

ABSTRACT Latency-associated peptide of transforming growth factor β (TGF-β) (LAP) was used to determine whether in vivo modulation of TGF-β bioactivity enhanced pulmonary immunity to Mycobacterium bovis BCG infection in C57BL/6 mice. LAP decreased BCG growth in the lung and enhanced antigen-specific T-cell proliferation and gamma interferon mRNA expression. Thus, susceptibility of the lung to primary BCG infection may be partially mediated by the immunosuppressive effects of TGF-β.

scholarly journals Unique Roles of p160 Coactivators for Regulation of Breast Cancer Cell Proliferation and Estrogen Receptor-α Transcriptional Activity

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1588-1596 ◽  
Author(s):  
Sudipan Karmakar ◽  
Estrella A. Foster ◽  
Carolyn L. Smith
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Breast Cancer Cells ◽  
Transcriptional Activity ◽  
Interfering Rna ◽  
Mcf 7

Each of the three members of the p160 steroid receptor coactivator (SRC) family of coactivators (SRC-1, SRC-2 and SRC-3) stimulates estrogen receptor (ER)-α function in trans-activation assays. Consequently, we sought to elucidate their contributions to the ER-regulated processes of cell proliferation, apoptosis, and the expression of ERα target genes in MCF-7 breast cancer cells. The small interfering RNA depletion of SRC-2 or SRC-3 but not SRC-1 inhibited growth of MCF-7 cells, and this was reflected in decreased cell cycle progression and increased apoptosis in SRC-2- or SRC-3-depleted cells as well as a reduction in ERα transcriptional activity measured on a synthetic reporter gene. However, only SRC-3 depletion blocked estradiol stimulated cell proliferation. Depletion of SRC-1 did not affect these events, and together this reveals functional differences between each of the three SRC family coactivators. Regulation of the endogenous ERα target gene, c-myc was not affected by depletion of any of the p160 coactivators although depletion of each of them decreased pS2 mRNA expression in estradiol-treated MCF-7 cells. Moreover, progesterone receptor and cyclin D1 gene expression were decreased in SRC-3 small interfering RNA-treated cells. Expression of mRNA and protein levels for the antiapoptotic gene, Bcl-2 was dependent on SRC-3 expression, whereas Bcl-2 protein but not mRNA expression also was sensitive to SRC-1 depletion. Together these data indicate that the closely related p160 coactivators are not functionally redundant in breast cancer cells because they play gene-specific roles in regulating mRNA and protein expression, and they therefore are likely to make unique contributions to breast tumorigenesis.

The potential anti-proliferative effect of β-sitosterol on human mast cell line-1 cells

2015 ◽  
Vol 93 (11) ◽  
pp. 979-983 ◽  
Author(s):  
Na-Ra Han ◽  
Hyung-Min Kim ◽  
Hyun-Ja Jeong
Keyword(s):  
Cell Proliferation ◽  
Mast Cell ◽  
Mrna Expression ◽  
Cell Line ◽  
Allergic Diseases ◽  
Human Mast Cell ◽  
Ki 67 ◽  
Proliferative Effect ◽  
P53 Activation ◽  
Mast Cell Line

Thymic stromal lymphopoietin (TSLP) was reported to induce mast cell proliferation and aggravate allergic reactions through activation of mouse double minute 2 (MDM2). We aimed to ascertain that β-sitosterol (SI), which is one of the several phytosterols found mostly in foods, would regulate TSLP-induced mast cell proliferation. The results showed that SI significantly decreased the proliferation of human mast cell line (HMC-1) cells promoted by TSLP. SI significantly decreased the mRNA expression of Ki-67 in the TSLP-treated HMC-1 cells. SI significantly suppressed the production and mRNA expression of interleukin-13 in the TSLP-treated HMC-1 cells. Furthermore, SI downregulated the expression of MDM2 and phosphorylation of STAT6, whereas it upregulated the expression of p53, activation of caspase-3, and cleavage of poly ADP-ribose polymerase in the TSLP-treated HMC-1 cells. Results of this study suggest that SI may be a potential therapeutic agent for mast cell-mediated allergic diseases.

Sign in / Sign up

Export Citation Format

Share Document