The role of Pdcd4 in tumour suppression and protein translation

Wang, Qing; Yang, Huiling

doi:10.1111/boc.201800014

Cited by 84 publications

(78 citation statements)

References 71 publications

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“…Programmed cell death protein 4 (PDCD4) is a tumor suppressor responsible for the inhibition of cell growth, tumor invasion, metastasis, or induction of apoptosis [213]. It is localized in the nucleus of proliferating cells and binds to the eukaryotic initiation factor-4A (eIF4A) or eukaryotic translation initiation factor 4 G (eIF4G), inhibiting translation [214,215]. PDCD4 controls the inhibition of cancer invasion by regulating the expression of mitogen-activated protein 4 kinases 1 or urokinase plasminogen activator receptor [216].…”

Section: Downregulation Of Programmed Cell Death Proteinmentioning

confidence: 99%

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Baj

Korona-Głowniak

Forma

et al. 2020

Cells

124

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Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world's population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial-mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial-mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.

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Section: Downregulation Of Programmed Cell Death Proteinmentioning

confidence: 99%

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Baj

Korona-Głowniak

Forma

et al. 2020

Cells

124

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“…However, an interaction with eIF4A and with eIF2β has been shown for DAP5, an ITAF of the eIF4G family that regulates several cellular IRESs of genes involved in apoptosis as well as its own IRES [77]. Another ITAF acting via eIF4A interaction is the tumor suppressor Pdcd4 [65]. Its interaction with eIF4A was demonstrated by crystal structure and mutation analysis, whereas it also interacts directly with the IRES.…”

Section: Interaction With Translation Initiation Factorsmentioning

confidence: 99%

IRES Trans-Acting Factors, Key Actors of the Stress Response

Godet¹,

David²,

Hantelys³

et al. 2019

Preprint

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The cellular stress response corresponds to the molecular changes that cell undergoes in response to various environmental stimuli. It induces drastic changes in the regulation of gene expression, at transcriptional and post-transcriptional levels. Actually, translation is strongly affected with a blockade of the classical cap-dependent mechanism, whereas alternative mechanisms are activated to support translation of specific mRNAs. One of the major mechanisms involved in stress-activated translation is the internal ribosome entry site (IRES)-driven initiation. IRESs, first discovered in viral mRNAs, are present in cellular mRNAs coding for master regulators of cell responses, whose expression must be tightly controlled. IRESs allow translation of these mRNAs in response to different stresses, including DNA damage, amino-acid starvation, hypoxia or endoplasmic reticulum stress, as well as to physiological stimuli such as cell differentiation or synapse network formation. Importantly, cellular mRNA IRESs are regulated by IRES trans-acting factor (ITAFs), exerting their action by at least nine different mechanisms. This review presents an update of the reported ITAFs regulating cellular mRNA translation and of the different mechanisms allowing them to control translation initiation in specific conditions. The impact of ITAFs on coordinated expression of mRNA families and consequences in cell physiology and diseases are also highlighted.

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“…PDCD4 was for several years mainly known as a tumour suppressor gene and potential target for anticancer therapies (Lankat-Buttgereit and Goke, 2009;Wang and Yang, 2018). Recent reports show that PDCD4 is response to inflammatory stimuli and can regulate inflammation (Cohen and Prince, 2013;van den Bosch et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…production PDCD4 is well known as a tumour suppressor and potential target of anticancer therapies (Lankat-Buttgereit and Goke, 2009;Wang and Yang, 2018) and also responds to inflammatory stimuli (Cohen and Prince, 2013;van den Bosch et al, 2014). In glioblastoma cells, PDCD4 inhibits IL-6 production via attenuation of AP-1 transcription (Dikshit et al, 2013).…”

Section: Pdcd4 Inhibits Mdsc Expansion In Mice Bm Cells Via Down-regumentioning

confidence: 99%

Lung Tumour Cell-derived Exosomes Promote the Expansion of MDSC Through miR-21a/PDCD4/IL-6/STAT3 Pathway

Zhang

et al. 2019

Preprint

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The percentage of MDSC population in peripheral blood is significantly increased in lung cancer patients. The accumulation of MDSC contributes to the development of a tumourassociated immune suppressive environment. But the mechanism mediating MDSC accumulation in lung cancer patients is elusive. We found that exosomes from Lewis lung cancer cells (LLC-Exo) can be taken up by the mice bone marrow cells and then promote MDSC expansion, which enhance tumour growth. Mechanistically, during the induction of MDSC from the bone marrow cells, miR-21a from LLC-Exo can stimulate BM cells to produce more IL-6 by inhibiting pdcd4 expression post-transcriptionally. Autocrine IL-6 induces tyrosine 705(Y705) of STAT3 to be phosphorylated during MDSC expansion.LLC-Exo with miR-21a deletion lost its ability to stimulate IL-6 production, STAT3 activation and MDSC expansion. These results demonstrate that lung cancer cell-derived exosomes promote functional MDSC expansion through activation of miR-21a/PDCD4/IL-6/STAT3 pathway.

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The role of Pdcd4 in tumour suppression and protein translation

Cited by 84 publications

References 71 publications

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

IRES Trans-Acting Factors, Key Actors of the Stress Response

Lung Tumour Cell-derived Exosomes Promote the Expansion of MDSC Through miR-21a/PDCD4/IL-6/STAT3 Pathway

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