Long non-coding RNA CCAT2 as a therapeutic target in colorectal cancer

Foßelteder, Johannes; Calin, George A.; Pichler, Martin

doi:10.1080/14728222.2018.1541453

Cited by 21 publications

(15 citation statements)

References 15 publications

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“…The group of ncRNAs can be divided into subgroups, including the approximately 20-nt long microRNAs (miRNAs), [3,4], Piwi-interacting RNAs (piRNAs) [5], small-interfering RNAs (siRNAs) [6], circular RNAs [7], and long non-coding RNAs (lncRNAs) which are typically >200 nt long [8]. While miRNAs and their significance in cellular regulation were discovered in 1993 [9,10], within the past few years, lncRNAs have emerged as interesting molecules [11,12]. Since then, lncRNAs have been found to be involved in a variety of biological processes, including gene expression regulation, subcellular architecture, and protein complex stabilization [13,14], as well as in physiology and pathophysiology [15,16,17].…”

Section: Introductionmentioning

confidence: 99%

The Implications of the Long Non-Coding RNA NEAT1 in Non-Cancerous Diseases

Prinz

Kapeller

Pichler

et al. 2019

IJMS

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Long non-coding RNAs (lncRNAs) are involved in a variety of biological and cellular processes as well as in physiologic and pathophysiologic events. This review summarizes recent literature about the role of the lncRNA nuclear enriched abundant transcript 1 (NEAT1) in non-cancerous diseases with a special focus on viral infections and neurodegenerative diseases. In contrast to its role as competing endogenous RNA (ceRNA) in carcinogenesis, NEAT1’s function in non-cancerous diseases predominantly focuses on paraspeckle-mediated effects on gene expression. This involves processes such as nuclear retention of mRNAs or sequestration of paraspeckle proteins from specific promoters, resulting in transcriptional induction or repression of genes involved in regulating the immune system or neurodegenerative processes. NEAT1 expression is aberrantly—mostly upregulated—in non-cancerous pathological conditions, indicating that it could serve as potential prognostic biomarker. Additional studies are needed to elucidate NEAT1’s capability to be a therapeutic target for non-cancerous diseases.

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Section: Introductionmentioning

confidence: 99%

The Implications of the Long Non-Coding RNA NEAT1 in Non-Cancerous Diseases

Prinz

Kapeller

Pichler

et al. 2019

IJMS

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“…When significant lncRNAs and circular RNAs that interact with the miRNA hubs of the FRM mRNA-mRNA-miRNA network were explored, a single lncRNA (CCAT2) was identified to interact with hsa-miR-17-5p, and hsa-miR-20a-5p ( Figure 3b) and four circular RNAs (hsa_circ_0000627, hsa_circ_0007533, hsa_circ_0104480, and hsa_circ_0104481) were identified to interact with hsa-miR-335 ( Figure 3c). This implies that CCAT2, which is a downstream target in the Wnt signaling, highly expressed in COAD patient samples and showed a positive correlation with metastatic progression and a negative correlation with the overall survival rates [16,45,56], showed interactions with two significant miRNA hubs of the FRM network. Though the physiological role of recently discovered circRNAs is still unexplored, elucidation of the circRNAs that were identified in the present study as associated with FSS-driven and ROS-mediated COAD metastasis, particularly those that showed differential expression in COAD, may provide novel therapeutic strategies.…”

Section: Generation Of Various Interaction Network Of the Selected Rmentioning

confidence: 96%

Non-coding RNAs in fluid shear stress-driven and reactive oxygen species-mediated colon cancer metastasis

KrishnaPriya

Banerjee

Karunagaran

et al. 2020

Preprint

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BackgroundColon adenocarcinoma (COAD) is the third most common cancer in the world. Fluid shear stress (FSS) and intracellular reactive oxygen species (ROS) levels are known to mediate COAD metastasis. The present work was performed to explore the role of regulatory non-coding RNA molecules associated with FSS and ROS in COAD metastasis.MethodsThe interactions between the mRNAs associated with FSS and ROS, the corresponding miRNAs, lncRNAs and circRNAs in COAD metastasis were used to generate the mRNA-miRNA-lncRNA-circRNA network. The expression levels of the RNAs in the network were also considered besides the identification of RNA hubs and modules. Further, functional enrichment and survival analysis of the significant miRNAs together with the OncoPrint as well as survival analysis of the selected mRNAs were performed. Subsequently, their functional role was also corroborated with existing literature.ResultsTen significant miRNA hubs were identified, out of which hsa-miR-17-5p and hsa-miR-20a-5p were found to interact with a lncRNA, CCAT2 and hsa-miR-335 was found to interact with four circRNAs. 60% of the FSS and ROS associated mRNAs and 90% of the top 10 miRNA-enriched pathways that emerged from the functional analysis were reported to be involved in COAD metastasis. 15 significant miRNAs were identified in ten different modules suggesting their importance in FSS and ROS mediated COAD metastasis. Finally, ten miRNAs and three mRNAs associated with FSS and/or ROS were identified as significant overall survival markers; 33 mRNAs were also identified as metastasis-free survival markers whereas 15 mRNAs showed >10% gene alterations in TCGA-COAD data and hence emerged as significant molecular markers in the process.ConclusionWe hypothesize that the biologically significant RNAs identified in this integrated analysis may provide valuable insights to understand the molecular mechanism of the FSS driven and ROS mediated COAD metastasis and to design efficient treatment strategies.

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“…lncRNAs are a class of non-protein coding RNAs that are more than 200 nucleotides in length [21]. In cancer, over the last decade lncRNAs were successfully established as regulators of tumor growth, progression and therapy resistance and are considered as potential therapeutic targets [22][23][24][25][26]. Additionally, their utility as diagnostic and prognostic biomarkers has been suggested [27].…”

Section: Introductionmentioning

confidence: 99%

Long-Noncoding RNA (lncRNA) in the Regulation of Hypoxia-Inducible Factor (HIF) in Cancer

Barth

Prinz

Teppan

et al. 2020

ncRNA

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Hypoxia is dangerous for oxygen-dependent cells, therefore, physiological adaption to cellular hypoxic conditions is essential. The transcription factor hypoxia-inducible factor (HIF) is the main regulator of hypoxic metabolic adaption reducing oxygen consumption and is regulated by gradual von Hippel-Lindau (VHL)-dependent proteasomal degradation. Beyond physiology, hypoxia is frequently encountered within solid tumors and first drugs are in clinical trials to tackle this pathway in cancer. Besides hypoxia, cancer cells may promote HIF expression under normoxic conditions by altering various upstream regulators, cumulating in HIF upregulation and enhanced glycolysis and angiogenesis, altogether promoting tumor proliferation and progression. Therefore, understanding the underlying molecular mechanisms is crucial to discover potential future therapeutic targets to evolve cancer therapy. Long non-coding RNAs (lncRNA) are a class of non-protein coding RNA molecules with a length of over 200 nucleotides. They participate in cancer development and progression and might act as either oncogenic or tumor suppressive factors. Additionally, a growing body of evidence supports the role of lncRNAs in the hypoxic and normoxic regulation of HIF and its subunits HIF-1α and HIF-2α in cancer. This review provides a comprehensive update and overview of lncRNAs as regulators of HIFs expression and activation and discusses and highlights potential involved pathways.

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Long non-coding RNA CCAT2 as a therapeutic target in colorectal cancer

Cited by 21 publications

References 15 publications

The Implications of the Long Non-Coding RNA NEAT1 in Non-Cancerous Diseases

The Implications of the Long Non-Coding RNA NEAT1 in Non-Cancerous Diseases

Non-coding RNAs in fluid shear stress-driven and reactive oxygen species-mediated colon cancer metastasis

Long-Noncoding RNA (lncRNA) in the Regulation of Hypoxia-Inducible Factor (HIF) in Cancer

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