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Condition: Mitochondrial Disease
Cancer: Adenocarcinoma

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Total 10 results found since Jan 2013.

TIMELESS promotes the proliferation and migration of lung adenocarcinoma cells by activating EGFR through AMPK and SPHK1 regulation
CONCLUSIONS: Our study revealed that siTIM could inhibited EGFR activation through activating AMPK and inhibiting SPHK1 expression, as well as influencing mitochondrial function and alter the ATP level; TIM's high expression in LUAD is an important factor and a potential key target in LUAD.PMID:37433364 | DOI:10.1016/j.ejphar.2023.175883
Source: European Journal of Pharmacology - July 11, 2023 Category: Drugs & Pharmacology Authors: Houqing Yin Zequn Wang Dan Wang Muhadaisi Nuer Mengyuan Han Peng Ren Shanwu Ma Chutong Lin Jingjing Chen Haocheng Xian Dongmei Ai Xuejun Li Shaohua Ma Zhiqiang Lin Yan Pan Source Type: research

Prognostic significance of IMMT expression in surgically ‐resected lung adenocarcinoma
ConclusionHere, we first demonstrated that high ‐IMMT expression is related to some clinicopathological parameters, and that its expression is an independent prognostic predictor of poorer survival in patients with lung adenocarcinoma; further studies are required to clarify the biological function of IMMT in lung adenocarcinoma. However, resul ts suggest that this protein could be a novel prognostic indicator and therapeutic target.
Source: Thoracic Cancer - October 2, 2019 Category: Cancer & Oncology Authors: Yasuhiro Hiyoshi, Yuichi Sato, Masaaki Ichinoe, Ryo Nagashio, Daisuke Hagiuda, Makoto Kobayashi, Seiichiro Kusuhara, Satoshi Igawa, Kazu Shiomi, Naoki Goshima, Yoshiki Murakumo, Makoto Saegusa, Yukitoshi Satoh, Noriyuki Masuda, Katsuhiko Nao Tags: ORIGINAL ARTICLE Source Type: research

Sanguinarine Induces Apoptosis Pathway in Multiple Myeloma Cell Lines via Inhibition of the JaK2/STAT3 Signaling
In this study, we aimed to investigate the potential anti-proliferative and pro-apoptotic activities of SNG in a panel of MM cell lines (U266, IM9, MM1S, and RPMI-8226). SNG treatment of MM cells resulted in a dose-dependent decrease in cell viability through mitochondrial membrane potential loss and activation of caspase 3, 9, and cleavage of PARP. Pre-treatment of MM cells with a universal caspase inhibitor, Z-VAD-FMK, prevented SNG mediated loss of cell viability, apoptosis, and caspase activation, confirming that SNG-mediated apoptosis is caspase-dependent. The SNG-mediated apoptosis appears to be resulted from suppres...
Source: Frontiers in Oncology - April 16, 2019 Category: Cancer & Oncology Source Type: research

Genetic Regulation of Liver Metabolites and Transcripts Linking to Biochemical-Clinical Parameters
Conclusion In summary, this study is the first to combine metabolomics, transcriptomics, and genome-wide association studies in a porcine model. Our results improve understanding of the genetic regulation of metabolites which link to transcripts and finally biochemical-clinical parameters. Further, high-performance profiling of metabolites as intermediate phenotypes is a potentially powerful approach to uncover how genetic variation affects metabolic and health status. Our results advance knowledge in areas of biomedical and agricultural interest and identify potential correlates of biomarkers, SNPs-metabolites, SNPs-tran...
Source: Frontiers in Genetics - April 16, 2019 Category: Genetics & Stem Cells Source Type: research

lncRNA ZEB1-AS1 Mediates Oxidative Low-Density Lipoprotein-Mediated Endothelial Cells Injury by Post-transcriptional Stabilization of NOD2
Conclusion We report the discovery that ZEB1-AS1 functionally participates in ox-LDL-induced ECs injury via LRPPRC-mediated stabilization of NOD2. Uncovering the precise role of ZEB1-AS1/LRPPRC/NOD2 pathway in the progression of ox-LDL-induced ECs death and AS will not only increase our knowledge of ox-LDL-induced AS, but also enable the development of novel therapeutic strategies to overcome oxidation product-induced diseases. Author Contributions XX and CL designed and mainly did the study. CM, ZD, and YD helped and did the study. Conflict of Interest Statement The authors declare that the research was conducted in ...
Source: Frontiers in Pharmacology - April 15, 2019 Category: Drugs & Pharmacology Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Autophagy is involved in recombinant Newcastle disease virus (rL-RVG)-induced cell death of stomach adenocarcinoma cells in vitro.
Abstract Oncolytic viruses can kill malignant cells while sparing normal cells. Multiple pathways are involved in this action. The antitumor effects of viral infection on SGC-7901 and AGS cells were investigated. We measured endoplasmic reticulum stress and autophagy caused by the recombinant avirulent Newcastle disease virus (NDV) LaSota strain expressing the rabies virus glycoprotein (rL-RVG) and the NDV wild-type strain. The dose-response curves were analyzed using the MTT assay. The expression of RVG was detected by western blotting, RT-PCR and immunofluorescence analyses. Cell death and autophagy were observe...
Source: International Journal of Oncology - June 9, 2015 Category: Cancer & Oncology Authors: Bu XF, Wang MB, Zhang ZJ, Zhao YH, Li M, Yan YL Tags: Int J Oncol Source Type: research