Programmed Cell Death 4 (Neoplastic Transformation Inhibitor) Proteine (PDCD4)

Human Programmed Cell Death 4 (Neoplastic Transformation Inhibitor) (PDCD4) Interaktionspartner

1. Study established that upregulation of miR-96 in glioblastoma multiforme (GBM) cells confers radioresistance via targeting PDCD4, which might be a potential therapeutic target for GBM.

2. This study revealed a dynamic regulatory relationship between PDCD4 and critical factors for EMT, establishing a broad, functional role for PDCD4 in laryngeal carcinoma, which may be propagated by the STAT3-miR-21 pathway.

3. the localization of Pdcd4 to the cytoplasm may be responsible for the suppression of the target mRNA translation and apoptosis.

4. PDCD4 and PTEN were the functional targets of miR-21.

5. Various studies support evidence that PDCD4, is a novel tumor suppressor gene, and is downregulated or even absent in colorectal cancer (CRC) and suppresses CRC deterioration. [review]

6. In the high malignant group the PDCD4 mRNA and PDCD5 mRNA expressions were significantly decreased compared with the low malignant group and the control group. PDCD4 mRNA and PDCD5 mRNA expressions are promising targets for the diagnosis and treatment of glioma.

7. miR-21 may promote salivary adenoid cystic carcinoma progression via PDCD4 and PTEN down-regulation and Bcl-2 up-regulation.

8. The expression of PDCD4 is decreased in cervical cancer tissues, compared to miR-150 which is increased.

9. Our study demonstrated that lncRNA-XIST, which acts as a miRNA sponge, impedes miR-21-5p to maintain the expression of PDCD4, which contributes to the progression of osteosarcoma (OS). Our findings suggest that the newly identified XIST/miR-21-5p/PDCD4 axis could be a potential biomarker or therapeutic target for OS.

10. miR206 promoted the onset of SANFH by inducing apoptosis and suppressed the proliferation of osteoblasts, which was dependent on the inhibition of PDCD4.

11. Results found PDCD4 as a target gene of miR-93 and miR-93 could down-regulate the expression of PDCD4 by directly targeting its 3'-UTR. The re-expression of PDCD4 could attenuate the hepatocellular carcinoma (HCC) cell invasion and migration induced by miR-93, while the knockdown of PDCD4 would promote HCC cell migration and invasion via the EMT pathway.

12. Reduced expression of PDCD4 was found in decidual and chorionic tissues, and peripheral blood mononuclear cells from patients with missed abortion.

13. miR503 promotes tumour growth and invasion by directly targeting PDCD4.

14. A novel mechanism of Pdcd4 action as a translation inhibitor and tumor suppressor has been proposed.

15. Taken together, this study highlights an important role for miR-23a/b as oncomiRs in gastric cancer through the inhibition of PDCD4 translation. These findings may shed new light on the molecular mechanism of gastric carcinogenesis and provide a new avenue for gastric cancer treatment.

16. lncRNA CASC9 functions as an oncogene by negatively regulating PDCD4 expression through recruiting EZH2 and subsequently altering H3K27me3 level. Our study implicates lncRNA CASC9 as a valuable biomarker for ESCC diagnosis and prognosis.

17. Exosomes derived from cisplatin-resistant OSCC cells transferred miR-21 to oral squamous cell carcinoma (OSCC) parental cells and induced cisplatin resistance by targeting phosphatase and tensin homolog (PTEN) and programmed cell death 4 (PDCD4).

18. These results indicate that the ROS-STAT3-miR-21-PDCD4 signaling axis plays an important role in arsenic -induced carcinogenesis.

19. PDCD4 is expressed in the cytoplasm of glandular epithelium of control endometrium and varied during the cycle changes of endometrium. Compared with the proliferative phase of control endometrium, PDCD4 expression was down-regulated in proliferative phase of eutopic or ectopic endometrium. There was no cyclic variation of PDCD4 expression in eutopic endometrium of adenomyosis patients due to progesterone resistance.

20. Study confirmed that PDCD4 was downregulated in non-small cell lung cancer (NSCLC). PDCD4 is a functional target for miR-155 at both transcriptional and post-transcriptional levels.

Mouse (Murine) Programmed Cell Death 4 (Neoplastic Transformation Inhibitor) (PDCD4) Interaktionspartner

1. These skeletal effects were attributed to inhibition of bone resorption and osteoclast function by miR-21 deficiency through miR-21 targeting programmed cell death 4 (PDCD4), despite the existence of RANKL. As far as we know, this is the first in vivo evidence of a pro-osteoclastic microRNA.

2. MEG3 functions as a competing endogenous RNAs (ceRNAs) and competes with PDCD4 mRNA for directly binding to miR-21, which mediates ischemic neuronal death.

3. In colorectal cancer tissues, the Sin1 protein but not mRNA was significantly upregulated while Pdcd4 protein was downregulated, suggesting that loss of Pdcd4 might correlate with Sin1 protein level but not mRNA level in colorectal cancer.

4. -induced expression of PDCD4 is associated with increased beta cell death.

5. miR-155 not only directly inhibited SOCS1 expression, but also increased the expression of p-STAT and PDCD4, as well as the production of proinflammation mediators IL-6 and TNF-alpha in atherogenesis

6. our data suggest that Pdcd4 as a crucial regulator in SGs induced by ox-LDL or HFD maybe a potential target for mitigating SG-associated stress responses in obesity and related diseases.

7. Pdcd4 deficiency attenuates atherosclerosis in hyperlipidemic mice in part through the upregulation of the anti-inflammatory cytokine IL-10.

8. PDCD4 Deficiency Aggravated Colitis and Colitis-associated Colorectal Cancer Via Promoting IL-6/STAT3 Pathway.

9. Study found that miR-16 was the direct regulatory element of PDCD4 and played a vital role in atherosclerosis by regulating PDCD4 and the downstream NF-kappaB and MAPK pathways.

10. Pdcd4 produces unfavorable influences on adipose-derived stem cells(ADSC) stemness, which contribute to adipose dysfunction, obesity and metabolic syndromes, thereby proposing Pdcd4 as a potential intervening target for regulating ADSC cells function.

11. PDCD4 serves as an important regulator of keratinocytes proliferation and contact inhibition in vitro.

12. In conclusion, miR-21 is sensitive to high-concentration glucose treatment in macrophages, and appears to have a protective effect in macrophage apoptosis induced by high concentrations of glucose via PDCD4.

13. atheroprotective unidirectional pulsatile shear stress affects the expression of PDCD4 in endothelial cells

14. we demonstrate that miR-21 regulates T-cell acute lymphoblastic leukemia cell survival via repression of the tumor suppressor Pdcd4.

15. Dual expression of shAkt1 and Pdcd4 effectively suppresses lung tumorigenesis

16. miR-21 is endowed with anti-apoptotic properties by suppressing the expression of PDCD4 gene and active caspase 3/8 fragments in the condition of renal IRI

17. sulforaphane protects PDCD4 downregulation posed by pro-inflammatory stimuli through modulating both transcription and proteolysis via controlling Akt1 and/or S6K1 activities in RAW 264.7 cells

18. these findings support the existence of a microRNA-21-responsive PDCD4/caspase-3 pathway in the pulmonary tissues that when active serves to promote endothelial apoptosis in vitro and pulmonary hypertension in vivo.

19. we demonstrated that the miR-21-PDCD4 signaling was involved in the cellular responses to UVB in a mouse epidermal cell line

20. during bacterial pneumonia IFNlambda promotes inflammation by inhibiting miR-21 regulation of PDCD4.

Zebrafish Programmed Cell Death 4 (Neoplastic Transformation Inhibitor) (PDCD4) Interaktionspartner

1. miR-21 plays a necessary role in cardiac valvulogenesis, in large part due to an obligatory downregulation of PDCD4

Pig (Porcine) Programmed Cell Death 4 (Neoplastic Transformation Inhibitor) (PDCD4) Interaktionspartner

1. TMZ pretreatment effectively reduced the myocardial damage caused by CME via inhibiting the PDCD4/NF-kappaB/ TNF-alpha pathway in cardiomyocytes.