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"Thor."
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LncRNA THOR promotes endometrial cancer progression through the AKT and ERK signaling pathways
The long noncoding RNA (lncRNA)
THOR
is highly conserved and expressed in various human cancer tissues, although its potential role and underlying mechanism in endometrial cancer (EC) remain unknown. This study aims to explore
THOR
’s biological function and molecular mechanism in EC progression.
THOR
expression in EC tissues and cell lines was detected by quantitative reverse transcription PCR (qRT-PCR) and in situ hybridization (ISH).
THOR
expression based on The Cancer Genome Atlas (TCGA) and clinical sample analyses was significantly higher in EC tissues than normal tissues, and higher
THOR
levels were closely associated with poor overall survival in EC. Additionally, a positive correlation between ISH-detected
THOR
expression and pathological grade was observed. CCK-8, colony formation, and transwell migration and invasion assays revealed that
THOR
significantly enhances the proliferation, migration, and invasion abilities of EC cells. Moreover, IGF2BP1 protein expression and ERK and AKT protein phosphorylation levels in EC cells increased significantly with
THOR
overexpression in EC cells. In conclusion, our findings suggest that
THOR
promotes EC cell growth and invasion, and IGF2BP1-mediated AKT and ERK signaling pathways activation might be involved. Clinically,
THOR
is significantly expressed in EC, and high
THOR
expression correlates with poor prognosis, making it a potential prognostic marker for EC.
Journal Article
Thor
This book explores the fascinating drama, love stories, and destruction in the myths surrounding Thor, the Norse god of thunder and lightning.
Book
Exploring genetic and epigenetic alterations in hTERT gene in colorectal cancer
Introduction: Colorectal cancer (CRC) is a heterogeneous and multifactorial malignancy driven by a series of genetic and epigenetic alterations. In this field, telomere/telomerase dysfunction contributes to CRC carcinogenesis by impairing genomic stability and cellular replication. Objective: This study aimed to evaluate genetic and epigenetic alterations in CRC by examining mutation rates in the human telomerase reverse transcriptase (hTERT) promoter region, relative telomere length (RTL), hTERT gene expression, and DNA methylation in the TERT hypermethylated oncological region (THOR). Methods: A total of 45 CRC and 34 adjacent normal tissue samples from Moroccan patients were analyzed using molecular approaches, such as Sanger sequencing, quantitative PCR (qPCR), reverse transcription qPCR (RT-qPCR), and methylation-specific PCR (MSP). Results: No mutations in the hTERT promoter region were identified. However, hypermethylation in the THOR region was reported in 82.2% of CRC samples and 79.4% of adjacent normal tissues. High hTERT expression was detected in 50% of CRC patients. In addition, telomere length was significantly shorter (p=0.002) in cancerous tissues (1.41 [1.36 - 1.43]) compared to normal mucosa (1.559 [1.46 - 1.63]), with an RTL ratio less than 1 (0.90 [0.86 - 0.95]). No significant differences were found between clinicopathological features and hTERT expression, THOR methylation, or RTL, except for a significant correlation between THOR hypermethylation and smaller tumor size (p=0.017) and between THOR methylation and RTL in CRC tissues (p=0.034). Conclusion: These results suggest that telomere lengthening is crucial for CRC initiation and progression, and cancer cells tend to shorten telomeres to maintain the chromosomal instability (CIN) required for tumor progression. Further research is needed to elucidate the mechanisms underlying telomere shortening in CRC and understand the role of telomerase/telomere complex in CRC initiation and progression, which could provide new diagnostic, prognostic, and therapeutic targets.
Journal Article
Thor : epic collection. Worldengine
Visionary writer Warren Ellis and superstar artist Mike Deodato Jr. unite to change everything for a Thunder God forsaken by his father and left mortal in Manhattan. Death is coming for Thor - and Ragnarok may not be far behind! But can he find solace - and renewed vigor - in the arms of the Enchantress? And together, can they save the World Tree, Yggdrasil? Then, William Messner-Loebs takes over with Deodato in bringing an epic chapter of Asgard's saga to a close! Thor joins Captain America and his Avengers comrades in battle with the Zodiac before facing the climactic twilight of the gods alongside his hammer brother Red Norvell! Prepare to bid farewell to a legend!
Book
Long noncoding RNA THOR is highly expressed in colorectal cancer and predicts a poor prognosis
Aim: Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. This study aimed to investigate the role of long noncoding RNA THOR in CRC. Materials & methods: The expression of THOR in 103 cases of CRC tissues and four CRC cell lines was examined by quantitative real-time PCR. Cell counting kit-8 and colony formation assays were applied to detect cell proliferation, and flow cytometry was used for testing cell cycle and apoptosis of CRC. Results: We found that THOR was highly expressed in CRC and correlated with tumor node metastasis stage, histological subtype, tumor size and differentiation and survival in CRC patients. Meanwhile, knockdown of THOR significantly suppressed cell proliferation and cell cycle of CRC, whereas promoted cell apoptosis. Conclusion: Our findings suggest that THOR is an oncogenic long noncoding RNA in CRC and a potential prognostic biomarker for this cancer.
Journal Article
Thor : worthy origins
\"Among the lofty spires of Asgard, Young Thor is the strongest, brashest and most arrogant god of all. But his giant-slashing, troll-smashing days come to an abrupt end when he's tricked by his jealous brother Loki into a foolish attack. Cast down to Earth into the crippled mortal form of Dr. Donald Blake, follow the Thunder God's journey of self-discovery and a mortal man's awakening to the power within. Revisit the fantastical origin of the Son of Odin in this new graphic novel, which thrusts the tale of Thor into the modern age with thunderous results! In this epic saga of towering Frost Giants, belching maidens and massive battles, one hero must decide which identity is truly his - before both of the worlds he loves are destroyed!\" --Amazon.com.
Book
Rapamycin activation of 4E-BP prevents parkinsonian dopaminergic neuron loss
Here, Tain
et al
. describe the genetic interaction between 4E-BP, an inhibitor of translation, with Parkinson's disease–associated
park
and
Pink1
in
Drosophila
, where the manipulation of 4E-BP reduced the pathologic phenotypes, including degeneration of dopaminergic neurons, in
park
and
Pink1
mutant flies.
Mutations in
PINK1
and
PARK2
cause autosomal recessive parkinsonism, a neurodegenerative disorder that is characterized by the loss of dopaminergic neurons. To discover potential therapeutic pathways, we identified factors that genetically interact with
Drosophila park
and
Pink1
. We found that overexpression of the translation inhibitor
Thor
(4E-BP) can suppress all of the pathologic phenotypes, including degeneration of dopaminergic neurons in
Drosophila
. 4E-BP is activated
in vivo
by the TOR inhibitor rapamycin, which could potently suppress pathology in
Pink1
and
park
mutants. Rapamycin also ameliorated mitochondrial defects in cells from individuals with
PARK2
mutations. Recently, 4E-BP was shown to be inhibited by the most common cause of parkinsonism, dominant mutations in
LRRK2
. We also found that loss of the
Drosophila LRRK2
homolog activated 4E-BP and was also able to suppress
Pink1
and
park
pathology. Thus, in conjunction with recent findings, our results suggest that pharmacologic stimulation of 4E-BP activity may represent a viable therapeutic approach for multiple forms of parkinsonism.
Journal Article
Thor
\"Once just a powerful and arrogant royal from another realm, Thor became one of Earth's finest defenders. Join the action as this Super Hero battles for mankind in this complete origin story as told in Thor.\"-- Provided by publisher.
Book
A sensitivity study on the response of convection initiation to in situ soil moisture in the central United States
Soil moisture can affect precipitation, however there is significant debate about the sign and strength of land–atmosphere coupling. This may be due to the differences regarding the selection of data sources, the presence of atmospheric persistence, and the spatial and temporal scales of the analysis. This study is a sensitivity analysis that quantifies how each of these factors influences land–atmosphere coupling in the central United States from 2005 to 2007. Four different sources of soil moisture are used to represent soil moisture: in situ measurements and three satellite products. The Thunderstorm Observation by Radar (ThOR) algorithm is used to identify convective events. The results show that warm-season afternoon convection initiates preferentially over dry soil, if in situ measurements are used. However, when satellite data are used the sign and strength of the soil moisture-precipitation coupling varies depending on which satellite dataset is used. This demonstrates that evaluations of land–atmosphere coupling strength are sensitive to the source of soil moisture. Our results also show that accounting for atmospheric persistence tends to weaken apparent land–atmosphere coupling. Changing the spatial scale of the analysis can also influence the sign and coupling strength. Analyses that are performed at a coarser spatial resolution tend to indicate a wet preference because they do not capture the local negative feedbacks. This study demonstrates that contradictions in the literature regarding the sign and strength of soil moisture-precipitation feedbacks can be partly attributed to differences in datasets, methods and scale of the analysis.
Journal Article