scholarly journals Hsa_circ_0008259 modulates miR-21-5p and PDCD4 expression to restrain osteosarcoma progression

Aging ◽  
2021 ◽  
Author(s):  
Kai Guan ◽  
Shizhang Liu ◽  
Keke Duan ◽  
Xiaoxia Zhang ◽  
Huitong Liu ◽  
...  
Keyword(s):  
Pdcd4 Expression

scholarly journals LncRNA-GAS5 regulates PDCD4 expression and mediates myocardial infarction-induced cardiomyocytes apoptosis via targeting MiR-21

Cell Cycle ◽  
2020 ◽  
Vol 19 (11) ◽  
pp. 1363-1377 ◽  
Author(s):  
Xing-Hu Zhou ◽  
Hong-Xia Chai ◽  
Ming Bai ◽  
Zheng Zhang
Keyword(s):  
Myocardial Infarction ◽  
Pdcd4 Expression ◽  
Lncrna Gas5

scholarly journals Circ_0003266 sponges miR-503-5p to suppress colorectal cancer progression via regulating PDCD4 expression

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Caihong Wen ◽  
Xiaoqing Feng ◽  
Honggang Yuan ◽  
Yong Gong ◽  
Guangsheng Wang
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Progression ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Pdcd4 Expression ◽  
Novel Target

Abstract Background Circular RNAs (circRNAs) feature prominently in tumor progression. However, the biological function and molecular mechanism of circ_0003266 in colorectal cancer (CRC) require further investigation. Methods Circ_0003266 expression in 46 pairs CRC tissues / adjacent tissues, and CRC cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR); after circ_0003266 was overexpressed or knocked down in CRC cells, cell proliferation, apoptosis, migration, and invasion were evaluated by the cell counting kit-8 (CCK-8), flow cytometry, and Transwell assays, respectively; the interaction among circ_0003266, miR-503-5p, and programmed cell death 4 (PDCD4) was confirmed using bioinformatics analysis and dual-luciferase reporter assay; PDCD4 protein expression in CRC cells was quantified using Western blot. Results Circ_0003266 was significantly lowly expressed in CRC tissues and cell lines. Circ_0003266 overexpression markedly repressed CRC cell proliferation, migration, and invasion, and accelerated the cell apoptosis, but its overexpression promoted the malignant phenotypes of CRC cells. PDCD4 was a direct target of miR-503-5p and circ_0003266 promoted PDCD4 expression by competitively sponging miR-503-5p. Conclusion Circ_0003266 suppresses the CRC progression via sponging miR-503-5p and regulating PDCD4 expressions, which suggests that circ_0003266 may serve as a novel target for the treatment of CRC.

scholarly journals Clinical Significance of PDCD4 in Melanoma by Subcellular Expression and in Tumor-Associated Immune Cells

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1049
Author(s):  
Thuy T. Tran ◽  
Chetan K. Rane ◽  
Christopher R. Zito ◽  
Sarah A. Weiss ◽  
Shlomit Jessel ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Brain Metastasis ◽  
Immune Cell ◽  
Tissue Microarrays ◽  
Pleckstrin Homology Domain ◽  
Neoplastic Progression ◽  
Melanoma Brain Metastasis ◽  
Pdcd4 Expression ◽  
Programmed Cell Death 4 ◽  
And Function

Little is known about the subcellular localization and function of programmed cell death 4 (PDCD4) in melanoma. Our past studies suggest PDCD4 interacts with Pleckstrin Homology Domain Containing A5 (PLEKHA5) to influence melanoma brain metastasis outcomes, as high intracranial PDCD4 expression leads to improved survival. We aimed to define the subcellular distribution of PDCD4 in melanoma and in the tumor microenvironment during neoplastic progression and its impact on clinical outcomes. We analyzed multiple tissue microarrays with well-annotated clinicopathological variables using quantitative immunofluorescence and evaluated single-cell RNA-sequencing on a brain metastasis sample to characterize PDCD4+ immune cell subsets. We demonstrate differences in PDCD4 expression during neoplastic progression, with high tumor and stromal PDCD4 levels associated with improved survival in primary melanomas and in intracranial metastases, but not in extracranial metastatic disease. While the expression of PDCD4 is well-documented on CD8+ T cells and natural killer cells, we show that it is also found on B cells and mast cells. PDCD4 expression in the tumor microenvironment is associated with increased immune cell infiltration. Further studies are needed to define the interaction of PDCD4 and PLEKHA5 and to evaluate the utility of this pathway as a therapeutic target in melanoma brain metastasis.

scholarly journals PDCD4–MAPK–NF-κB Positive Loop Simultaneously Promotes Microglia Activation and Neuron Apoptosis During Neuroinflammation

2021 ◽  
Author(s):  
Quan Chen ◽  
Hongjian Lu ◽  
Chengwei Duan ◽  
Xiangyang Zhu ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Inflammatory Diseases ◽  
Damage Model ◽  
Pdcd4 Expression ◽  
Proapoptotic Protein ◽  
Inflammatory Activation ◽  
Elevated Expression ◽  
The Central Nervous System ◽  
Signaling Activation

Abstract Neuroinflammation and neuron injury are common features of the central nervous system (CNS) diseases. It is of great significance to identify their shared regulatory mechanisms and explore the potential therapeutic targets. Programmed cell death factor 4 (PDCD4), an apoptosis-related molecule, extensively participates in tumorigenesis and inflammatory diseases, but its expression and biological function during CNS neuroinflammation remain unclear. In the present study, utilizing the lipopolysaccharide (LPS)-induced neuroinflammation model in mice, we reported an elevated expression of PDCD4 both in injured neurons and activated microglia of the inflamed brain. A similar change in PDCD4 expression was observed in vitro in the microglial activation model. Silencing PDCD4 by shRNA significantly inhibited the phosphorylation of MAPKs (p38, ERK, and JNK), prevented the phosphorylation and nuclear translocation of NF-κB p65, and thus attenuated the LPS-induced microglial inflammatory activation. Interestingly, LPS also required the MAPK/NF-κB signaling activation to boost PDCD4 expression in microglia, indicating the presence of a positive loop. Moreover, a persistent elevation of PDCD4 expression was detected in the H2O2-induced neuronal oxidative damage model. Knocking down PDCD4 significantly inhibited the expression of proapoptotic protein BAX, suggesting the proapoptotic activity of PDCD4 in neurons. Taken together, our data indicated that PDCD4 may serve as a hub regulatory molecule that simultaneously promotes the microglial inflammatory activation and the oxidative stress-induced neuronal apoptosis within CNS. The microglial PDCD4–MAPK–NF-κB positive feedback loop may exaggerate the vicious cycle of neuroinflammation and neuronal injury and thus may become a potential therapeutic target for neuroinflammatory diseases.

scholarly journals PDCD4 expression in coronary atherosclerosis rat models and its mechanism

2019 ◽  
Author(s):  
Yuhong Gao ◽  
Hongmei Li ◽  
Yanchun Zhou ◽  
Hongmei Lv ◽  
Yanping Chen
Keyword(s):  
Coronary Atherosclerosis ◽  
Rat Models ◽  
Pdcd4 Expression

Amplification of the miR-181c/d cluster is inversely correlated with PDCD4 expression in gastric cancer

2014 ◽  
Vol 59 (19) ◽  
pp. 2240-2248 ◽  
Author(s):  
Yuanming Pan ◽  
Rui Xing ◽  
Juan An ◽  
Jiantao Cui ◽  
Wenmei Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Pdcd4 Expression

p38 MAPK Signaling Mediates Retinoic Acid-Induced Expression of a Novel Tumor Suppressor Protein Programmed Cell Death 4 (PDCD4) in Acute Promyelocytic Leukemia Cells.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1942-1942
Author(s):  
Ugur Akar ◽  
Bulent Ozpolat ◽  
Nancy Colburn ◽  
Gabriel Lopez-Berestein
Keyword(s):  
Retinoic Acid ◽  
Cell Differentiation ◽  
P38 Mapk ◽  
Myeloid Cell ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Granulocytic Differentiation ◽  
P38 Inhibitor ◽  
Pdcd4 Expression ◽  
Mitogen Activated Protein

Abstract Programmed-cell-death-4 (PDCD4) is a novel tumor suppressor protein that suppresses tumor promoter-induced neoplastic transformation. PDCD4 specifically inhibits the helicase activity of eukaryotic translation initiation factor 4A (eIF4A) and translation initiation and cap-dependent mRNA translation in vitro and in vivo. Loss or underexpression of PDCD4 is associated with carcinogenesis and chemoresistance in solid tumors. The role and regulation of PDCD4 in the the hematopoietic system and myeloid leukemia cells are not known. We previously reported that ATRA induces translational suppression through multiple posttranscriptional mechanisms during terminal cell differentiation (Harris et al, Blood, 104 (5) 2004). Therefore, in this study, we investigated the expression and regulation of PDCD4 during myeloid cell differentiation. All-trans-retinoic acid (ATRA) induces terminal differentiation in acute myeloid leukemia (AML) and promyelocytic (APL) cells, a well established model for myeloid cell differentiation. We found that treatment of HL60 (M2 type AML) and NB4 APL (M3 type AML) cells with ATRA (1 mM) induced PDCD4 protein and mRNA expression during granulocytic differentiation detected by western blot and RT-PCR analysis, respectively. We also demonstrated that inhibition of PDCD4 by siRNA reduced granulocytic differentiation induced by ATRA, suggesting that PDCD4 plays a role in granuliocytic differentiation. To determine mechanisms regulating PDCD4 we investigated the role of pP38 MAPK (Mitogen activated protein kinase) in reugulation of PDCD4 expression. ATRA induced PDCD4 expression correlated with activation of p38 MAPK (Mitogen Activated Protein Kinase) pathway in NB4 cells. To test the hypothesis that p38 MAPK signaling pathway mediates retinoic acid induced PDCD4 expression we treated cells with a specific p38 MAPK inhibitor, SB203580, ATRA or combination with ATRA. We observed that p38 inhibitor inhibited ATRA-induced expression of PDCD4 in NB4 cells. Basal level of PDCD4 expression was also markedly downregulated in the presence of p38 inhibitor when compared to untreated control cells, suggesting that p38 pathway is involved in ATRA-dependent and independent PDCD4 expression. Currently we are investigating whether inhibition of p38 by small interfering RNA (siRNA) will prevent expression of ATRA induced PDCD4 in APL cells. We are also trying to identify whether ATF2 transcription factor, a downstream of p38, is involved in PDCD4 expression. p38-mediated induction of PDCD4 pathway reveals a novel mechanism of PDCD4 regulation and ATRA action, providing a new insight into understanding terminal differentiation of myeloid cells. Better understanding the role of PDCD4 and posttranscriptional control of gene expression may offer targets for the differentiation therapy and chemo preventive strategies.

Loss of PDCD4 expression in human lung cancer correlates with tumour progression and prognosis

2003 ◽  
Vol 200 (5) ◽  
pp. 640-646 ◽  
Author(s):  
Yuan Chen ◽  
Thomas Knösel ◽  
Glen Kristiansen ◽  
Agnieszka Pietas ◽  
Mitchell E Garber ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Tumour Progression ◽  
Human Lung Cancer ◽  
Pdcd4 Expression
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