scholarly journals The endoplasmic reticulum mitochondrial calcium cross talk is downregulated in malignant pleural mesothelioma cells and plays a critical role in apoptosis inhibition

Oncotarget ◽  
2015 ◽  
Vol 6 (27) ◽  
pp. 23427-23444 ◽  
Author(s):  
Simone Patergnani ◽  
Carlotta Giorgi ◽  
Stefania Maniero ◽  
Sonia Missiroli ◽  
Pio Maniscalco ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Malignant Pleural Mesothelioma ◽  
Cross Talk ◽  
Critical Role ◽  
Mitochondrial Calcium ◽  
Pleural Mesothelioma ◽  
Apoptosis Inhibition

scholarly journals Critical role of the Ror-family of receptor tyrosine kinases in invasion and proliferation of malignant pleural mesothelioma cells

2018 ◽  
Vol 23 (7) ◽  
pp. 606-613 ◽  
Author(s):  
Takeshi Saji ◽  
Michiru Nishita ◽  
Hiroyuki Ogawa ◽  
Takefumi Doi ◽  
Yasuhiro Sakai ◽  
...  
Keyword(s):  
Malignant Pleural Mesothelioma ◽  
Tyrosine Kinases ◽  
Receptor Tyrosine Kinases ◽  
Critical Role ◽  
Pleural Mesothelioma

scholarly journals Identification of Overexpressed Genes in Malignant Pleural Mesothelioma

2021 ◽  
Vol 22 (5) ◽  
pp. 2738
Author(s):  
Federica Morani ◽  
Luisa Bisceglia ◽  
Giulia Rosini ◽  
Luciano Mutti ◽  
Ombretta Melaiu ◽  
...  
Keyword(s):  
Cell Lines ◽  
Malignant Pleural Mesothelioma ◽  
Gene List ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Mitotic Cell ◽  
Functional Enrichment ◽  
Pleural Mesothelioma ◽  
Apoptosis Inhibition ◽  
Tcga Dataset

Malignant pleural mesothelioma (MPM) is a fatal tumor lacking effective therapies. The characterization of overexpressed genes could constitute a strategy for identifying drivers of tumor progression as targets for novel therapies. Thus, we performed an integrated gene-expression analysis on RNAseq data of 85 MPM patients from TCGA dataset and reference samples from the GEO. The gene list was further refined by using published studies, a functional enrichment analysis, and the correlation between expression and patients’ overall survival. Three molecular signatures defined by 15 genes were detected. Seven genes were involved in cell adhesion and extracellular matrix organization, with the others in control of the mitotic cell division or apoptosis inhibition. Using Western blot analyses, we found that ADAMTS1, PODXL, CIT, KIF23, MAD2L1, TNNT1, and TRAF2 were overexpressed in a limited number of cell lines. On the other hand, interestingly, CTHRC1, E-selectin, SPARC, UHRF1, PRSS23, BAG2, and MDK were abundantly expressed in over 50% of the six MPM cell lines analyzed. Thus, these proteins are candidates as drivers for sustaining the tumorigenic process. More studies with small-molecule inhibitors or silencing RNAs are fully justified and need to be undertaken to better evaluate the cancer-driving role of the targets herewith identified.

scholarly journals Endoplasmic Reticulum Stress Signaling as a Therapeutic Target in Malignant Pleural Mesothelioma

Cancers ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 1502 ◽  
Author(s):  
Xu ◽  
Yang ◽  
Yang ◽  
Berezowska ◽  
Gao ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Malignant Pleural Mesothelioma ◽  
Treatment Options ◽  
Pleural Mesothelioma ◽  
Unfolded Protein ◽  
Proteotoxic Stress ◽  
Tcga Dataset ◽  
Protein Response

Malignant pleural mesothelioma (MPM) is a lethal cancer with limited treatment options. No targeted therapy has emerged yet. Here, we performed an integrated molecular characterization of patient tumors in the TCGA dataset, and discovered that endoplasmic reticulum (ER) stress and the adaptive unfolded protein response (UPR) signaling are characteristically deregulated in MPM. Consequently, pharmacological perturbation of ER stress/UPR axis by HA15, an agent that induces persistent proteotoxic stress in the ER, selectively suppresses the viability of MPM cells including those refractory to standard chemotherapy. Mechanically, HA15 augments the already high basal level of ER stress in MPM cells, embarks pro-apoptotic malfunctional UPR and autophagy, which eventually induces cell death in MPM. Importantly, HA15 exerts anti-MPM effectiveness in a mouse model of patient-derived xenografts (PDX) without eliciting overt toxicity when compared to chemotherapy. Our results revealed that programs orchestrating ER stress/UPR signaling represent therapeutic vulnerabilities in MPM and validate HA15 as a promising agent to treat patients with MPM, naïve or resistant to chemotherapy.

83-OR: Pancreatic Exocrine to Endocrine Cell Cross Talk Mediates Endoplasmic Reticulum Stress and Beta-Cell Dysfunction in MODY8

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 83-OR
Author(s):  
SEVIM KAHRAMAN ◽  
DANIELLE DIEGISSER ◽  
BENTE B. JOHANSSON ◽  
ANDERS MOLVEN ◽  
ROHIT KULKARNI
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Beta Cell ◽  
Cross Talk ◽  
Endocrine Cell ◽  
Beta Cell Dysfunction ◽  
Cell Dysfunction ◽  
Pancreatic Exocrine
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