scholarly journals Evaluating the Remote Control of Programmed Cell Death, with or without a Compensatory Cell Proliferation

2018 ◽  
Vol 14 (13) ◽  
pp. 1800-1812 ◽  
Author(s):  
Xixi Dou ◽  
Lichan Chen ◽  
Mingjuan Lei ◽  
Lucas Zellmer ◽  
Qingwen Jia ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Remote Control ◽  
Programmed Cell Death

scholarly journals Receptor Tyrosine Kinases: Role in Cancer Progression

2006 ◽  
Vol 13 (5) ◽  
pp. 191-193
Author(s):  
V. Sangwan ◽  
M. Park
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Progression ◽  
Tyrosine Kinases ◽  
Normal Tissue ◽  
Receptor Tyrosine Kinases ◽  
Tight Control ◽  
Tissue Patterning

Tight control of cell proliferation and morphogenesis in conjunction with programmed cell death (apoptosis) is required to ensure normal tissue patterning. [...]

Suppression of cell proliferation and programmed cell death by dexamethasone during postnatal lung development

2002 ◽  
Vol 282 (3) ◽  
pp. L477-L483 ◽  
Author(s):  
Cédric Luyet ◽  
Peter H. Burri ◽  
Johannes C. Schittny
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Lung Development ◽  
Structural Changes ◽  
Tissue Transglutaminase ◽  
Lung Parenchyma ◽  
Lung Maturation ◽  
Morphological Criteria ◽  
Postnatal Lung Development

Prematurely born babies are often treated with glucocorticoids. We studied the consequences of an early postnatal and short dexamethasone treatment (0.1–0.01 μg/g, days 1–4) on lung development in rats, focusing on its influence on peaks of cell proliferation around day 4 and of programmed cell death at days 19–21. By morphological criteria, we observed a dexamethasone-induced premature maturation of the septa ( day 4), followed by a transient septal immatureness and delayed alveolarization leading to complete rescue of the structural changes. The numbers of proliferating (anti-Ki67) and dying cells (TdT-mediated dUTP nick end labeling) were determined and compared with controls. In dexamethasone-treated animals, both the peak of cell proliferation and the peak of programmed cell death were reduced to baseline, whereas the expression of tissue transglutaminase (transglutaminase-C), another marker for postnatal lung maturation, was not significantly altered. We hypothesize that a short neonatal course of dexamethasone leads to severe but transient structural changes of the lung parenchyma and influences the balance between cell proliferation and cell death even in later stages of lung maturation.

scholarly journals miR-103 Functions as a Tumor Suppressor by Directly Targeting Programmed Cell Death 10 in NSCLC

2018 ◽  
Vol 26 (4) ◽  
pp. 519-528 ◽  
Author(s):  
Dong Yang ◽  
Jian-Jun Wang ◽  
Jin-Song Li ◽  
Qian-Yu Xu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Tumor Size ◽  
Apoptotic Cell ◽  
A549 Cells ◽  
Invasion And Migration ◽  
Metastatic Capacity ◽  
And Migration

Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. Absence of miR-103 has recently been identified to be associated with metastatic capacity of primary lung tumors. However, the exact role of miR-103 in NSCLC and the molecular mechanism are unclear. In the present study, we showed that miR-103 expression was reduced in NSCLC tissues and cells. miR-103 expression was negatively correlated with tumor size and stage. The overall survival was longer in patients with higher miR-103 level than in those with lower miR-103 expression. miR-103 inhibited cell proliferation in A549 cells, decreased tumor weight and volume, and prolonged survival of tumor-implanted nude mice. miR-103 increased apoptotic cell death in A549 cells. Furthermore, miR-103 decreased the invasion and migration abilities in A549 cells, as evidenced by Transwell and wound healing results. Downregulation of miR-103 significantly reduced the level of programmed cell death 10 (PDCD10). We found a significant decrease in the relative luciferase activity of the reporter gene in A549 cells cotransfected with the miR-103 mimic and pGL3-PDCD10 WT 3′-UTR, but not pGL3-PDCD10 mut 3′-UTR. We showed that overexpression of PDCD10 significantly inhibited miR-103-induced inhibition of cell proliferation, increased apoptosis, and decreased invasion and migration in A549 cells. Moreover, we found that PDCD10 expression was increased in NSCLC tissues and cells. PDCD10 expression was positively correlated with tumor size and stage. Overexpression of PDCD10 increased cell proliferation and inhibited apoptosis in A549 cells. The data demonstrated that dysregulation of the miR-103/PDCD10 signal may be a novel therapeutic target for the treatment of NSCLC.

Zinc finger protein RP-8, the Bombyx mori ortholog of programmed cell death 2, regulates cell proliferation

2020 ◽  
Vol 104 ◽  
pp. 103542 ◽  
Author(s):  
Muhammad Nadeem Abbas ◽  
Hanghua Liang ◽  
Saima Kausar ◽  
Zhen Dong ◽  
Hongjuan Cui
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Bombyx Mori ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein

Serum bile acids, programmed cell death and cell proliferation in the mucosa of patients with colorectal adenomas

2005 ◽  
Vol 37 (7) ◽  
pp. 509-514 ◽  
Author(s):  
M. Fracchia ◽  
G. Galatola ◽  
I. Sarotto ◽  
V. Guraldo ◽  
M. Perona ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Bile Acids ◽  
Colorectal Adenomas ◽  
Serum Bile Acids

scholarly journals Obinutuzumab (GA101) Significantly Inhibits Cell Proliferation and Induces Programmed Cell Death in Primary Mediastinal B-Cell Lymphoma (PMBL): Obinutuzumab May be a Future Targeted Agent for the Treatment of PMBL

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4492-4492
Author(s):  
Changhong Yin ◽  
Sanghoon Lee ◽  
Timmy O'Connell ◽  
Janet Ayello ◽  
Carmella van de Ven ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
B Cell ◽  
Signaling Pathways ◽  
Expression Profiling ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Targeted Agent

Abstract BACKGROUND: Primary Mediastinal large B-cell lymphoma (PMBL) is a rare form of Non Hodgkin Lymphoma (NHL) representing 2% of mature B-cell non-Hodgkin lymphoma in patients less than 18 years of age (Lones/Cairo et al, JCO 2000; Burkhardt et al, BJH 2005). PMBL has histological features somewhere between Diffuse Large B-Cell Lymphoma (DLBCL) and classical HL (cHL) (Abramson et al, Blood 2005). Gene expression studies suggested that the molecular signature of PMBL had a striking resemblance to the expression profile of cHL (Rosenwald et al, JEM 2003). We have recently reported that a significant decrease in EFS among children and adolescent PMBL patients compared with other stage III non-PMBL pediatric DLBCL patients following FAB/LMB 96 therapy, suggesting that children and adolescent with PMBL required alternative treatment strategies (Gerrard/Cairo et al, Blood 2013). PMBL has been demonstrated to have an over-activated NF-kB pathway by gene expression profiling (Rosenwald et al, JEM 2003). Since over 95% of PMBL express CD20, targeting the CD20 receptor with a CD20 antibody is of high clinical interest. Obinutuzumab (GA101) is novel glycoengineered anti-CD20 targeted monoclonal antibody recognizing a unique CD20 type II epitope and it has been demonstrated to have greater efficacy in reducing tumor size, inducing remission and improving survival in other B-NHL xenograft models (Mössner et al, Blood 2010). Obinutuzumab has been recently approved by FDA for first line treatment of chronic lymphocytic leukemia (CLL) in combination with chlorambucil. OBJECTIVES: We hypothesize that obinutuzumab may be a future potential targeted agent for the treatment of PMBL, and therefore, we investigated whether obinutuzumab treatment results in significant changes in signaling pathways, genes expression, programmed cell death and cell proliferation in PMBL. METHODS: Karpas-1106P cells (DSMZ) were treated with obinutuzumab (generously provided by Dr. Klein, Roche) at every 24 hours (1-100ug/ml). qRT-PCR, western blot, MTS, Caspase 3/7 assay (Promega) and FACS analysis were performed. The BeadChip array (Illumina, HumanHT-12) was used for gene expression profiling. RESULTS: There was a significant decrease of cell proliferation in obinutuzumab-treated Karpas cells with 10ug/ml (0.69 ± 0.025, p<0.005) vs control (1.00 ± 0.000) at 48 hours. Concomitantly, there was a significant increase in programmed cell death in 10ug/ml obinutuzumab treated Karpas (37.80 ± 10.096, p<0.05) vs control (1.19 ± 0.762) at 48 hours. We also observed a significant decrease of CD20 expression (0.74± 0.010, p<0.05) with 10ug/ml obinutuzumab treatment at 48 hours. A total of 133 differentially expressed genes were identified by gene expression profiling (>1.5-fold, 0.57%) and 77.5% of genes including apoptosis related genes (CASP2 and PAK2) and MAPK signaling pathways (RASA1 and JUN) and EGR1 were upregulated and 22.5% of genes including ID3, GRAP and RAB6B were downregulated in obinutuzumab treated Karpas vs control (Fig 1). There were significant decreases of p-STAT6 (0.72± 0.011, p=0.01), p-Akt (0.69± 0.011, p<0.05), p-ikBα (0.70± 0.017, p<0.05) and p-Erk (0.56± 0.019, p<0.05) with 10ug/ml obinutuzumab treatment at 48 hours (Fig 2). Additionally, There were significant down-regulation of mRNA expression of Bcl-xL (0.91±0.011, p<0.04) and Bax (0.66±0.022, p<0.02) vs control. CONCLUSIONS: We observed that obinutuzumab significantly inhibited cell proliferation and induced programmed cell death and downregulated downstream of PI3k/Akt and NF-kB signaling pathways. Gene expression analysis indicated obinutuzumab induced changes in the expression of genes in Karpas that were involved in apoptosis and signaling pathways including CASP2, EGR1 and ID3. Future studies 1) will investigate the efficacy of combination therapies to enhance programmed cell death, and 2) will assess the proteomic signature induced by obinutuzumab in obinutuzumab sensitive and resistant PMBL, and furthermore, 3) will focus on the in vivo effects of obinutuzumab in a NOD/SCID PMBL xenograft mouse model. Obinutuzumab may be a future potential targeted agent for the adjuvant treatment of PMBL lymphoma. Disclosures No relevant conflicts of interest to declare.

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