scholarly journals Down-regulation of programmed cell death 4 leads to epithelial to mesenchymal transition and promotes metastasis in mice

2013 ◽  
Vol 49 (7) ◽  
pp. 1761-1770 ◽  
Author(s):  
Qing Wang ◽  
Jiang Zhu ◽  
Yong Zhang ◽  
Zhenxiao Sun ◽  
Xiaoling Guo ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Epithelial To Mesenchymal Transition ◽  
Down Regulation ◽  
Mesenchymal Transition ◽  
Programmed Cell Death 4

scholarly journals miR-21 Promotes Fibrogenic Epithelial-to-Mesenchymal Transition of Epicardial Mesothelial Cells Involving Programmed Cell Death 4 and Sprouty-1

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e56280 ◽  
Author(s):  
Hasse Brønnum ◽  
Ditte C. Andersen ◽  
Mikael Schneider ◽  
Maria B. Sandberg ◽  
Tilde Eskildsen ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Epithelial To Mesenchymal Transition ◽  
Mesothelial Cells ◽  
Mesenchymal Transition ◽  
Programmed Cell Death 4

scholarly journals Fibrinogen-like protein 1 (FGL1): the next immune checkpoint target

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Wenjing Qian ◽  
Mingfang Zhao ◽  
Ruoyu Wang ◽  
Heming Li
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Checkpoint ◽  
Epithelial To Mesenchymal Transition ◽  
Immune Escape ◽  
De Novo ◽  
Lymphocyte Activation ◽  
Response Prediction ◽  
Immune Checkpoint Blockade ◽  
Mesenchymal Transition

AbstractImmune checkpoint therapy has achieved significant efficacy by blocking inhibitory pathways to release the function of T lymphocytes. In the clinic, anti-programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) monoclonal antibodies (mAbs) have progressed to first-line monotherapies in certain tumor types. However, the efficacy of anti-PD-1/PD-L1 mAbs is still limited due to toxic side effects and de novo or adaptive resistance. Moreover, other immune checkpoint target and biomarkers for therapeutic response prediction are still lacking; as a biomarker, the PD-L1 (CD274, B7-H1) expression level is not as accurate as required. Hence, it is necessary to seek more representative predictive molecules and potential target molecules for immune checkpoint therapy. Fibrinogen-like protein 1 (FGL1) is a proliferation- and metabolism-related protein secreted by the liver. Multiple studies have confirmed that FGL1 is a newly emerging checkpoint ligand of lymphocyte activation gene 3 (LAG3), emphasizing the potential of targeting FGL1/LAG3 as the next generation of immune checkpoint therapy. In this review, we summarize the substantial regulation mechanisms of FGL1 in physiological and pathological conditions, especially tumor epithelial to mesenchymal transition, immune escape and immune checkpoint blockade resistance, to provide insights for targeting FGL1 in cancer treatment.

scholarly journals MiR-21 over-expression and Programmed Cell Death 4 down-regulation features malignant pleural mesothelioma

Oncotarget ◽  
2018 ◽  
Vol 9 (25) ◽  
pp. 17300-17308 ◽  
Author(s):  
Lorenzo Nicolè ◽  
Rocco Cappellesso ◽  
Tiziana Sanavia ◽  
Vincenza Guzzardo ◽  
Ambrogio Fassina
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Malignant Pleural Mesothelioma ◽  
Pleural Mesothelioma ◽  
Down Regulation ◽  
Over Expression ◽  
Programmed Cell Death 4

scholarly journals Programmed cell death 4 and BCR-ABL fusion gene expression are negatively correlated in chronic myeloid leukemia

2016 ◽  
Vol 12 (4) ◽  
pp. 2976-2981 ◽  
Author(s):  
Xia Zhang ◽  
Riming Liu ◽  
Baohua Huang ◽  
Xiaolu Zhang ◽  
Weijuan Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Chronic Myeloid Leukemia ◽  
Programmed Cell Death ◽  
Myeloid Leukemia ◽  
Fusion Gene ◽  
Programmed Cell Death 4

scholarly journals Retraction: Linc00472 suppresses breast cancer progression and enhances doxorubicin sensitivity through regulation of miR-141 and programmed cell death 4

RSC Advances ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 5895-5895
Author(s):  
Laura Fisher
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Programmed Cell Death 4

Retraction of ‘Linc00472 suppresses breast cancer progression and enhances doxorubicin sensitivity through regulation of miR-141 and programmed cell death 4’ by Pengwei Lu et al., RSC Adv., 2018, 8, 8455–8468, DOI: 10.1039/C8RA00296G

scholarly journals Programmed cell death 4 (PDCD4) expression during multistep Barrett's carcinogenesis

2010 ◽  
Vol 63 (8) ◽  
pp. 692-696 ◽  
Author(s):  
Matteo Fassan ◽  
Marco Pizzi ◽  
Giorgio Battaglia ◽  
Luciano Giacomelli ◽  
Paola Parente ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Intestinal Metaplasia ◽  
Negative Regulator ◽  
Pcr Analysis ◽  
Low Grade ◽  
Cytoplasmic Staining ◽  
Programmed Cell Death 4 ◽  
Columnar Metaplasia

AimTo test the contribution of programmed cell death 4 (PDCD4) tumour suppressor gene in Barrett's carcinogenesis.MethodsPDCD4 immunohistochemical expression was assessed in 88 biopsy samples obtained from histologically proven long-segment Barrett's mucosa (BM; 25 non-intestinal columnar metaplasia, 25 intestinal metaplasia (IM), 16 low-grade intraepithelial neoplasia (LG-IEN), 12 high-grade IEN (HG-IEN) and 10 Barrett's adenocarcinoma (BAc)). As controls, 25 additional samples of native oesophageal mucosa (N) were obtained from patients with dyspepsia. To further support the data, the expression levels of miR-21, an important PDCD4 expression regulator, in 14 N, 5 HG-IEN and 11 BAc samples were determined by quantitative real-time PCR analysis.ResultsPDCD4 immunostaining decreased progressively and significantly with the progression of the phenotypic changes occurring during Barrett's carcinogenesis (p<0.001). Normal basal squamous epithelial layers featured strong PDCD4 nuclear immunoreaction (mostly coexisting with weak–moderate cytoplasmic staining). Non-intestinal columnar metaplasia and intestinal metaplasia preserved a strong nuclear immunostaining; conversely, a significant decrease in PDCD4 nuclear expression was seen in dysplastic (LG-IEN and HG-IEN) and neoplastic lesions. Weak–moderate cytoplasmic immunostaining was evident in cases of LG-IEN, while HG-IEN and BAc samples showed weak cytoplasmic or no protein expression. As expected, miR-21 expression was significantly upregulated in HG-IEN and BAc samples, consistently with PDCD4 dysregulation.ConclusionsThese data support a significant role for PDCD4 downregulation in the progression of BM to BAc, and confirm miR-21 as a negative regulator of PDCD4 in vivo. Further efforts are needed to validate PDCD4 as a potential prognostic marker in patients with Barrett's oesophagus.

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