Coding of Glioblastoma Progression and Therapy Resistance through Long Noncoding RNAs

Zottel, Alja; Šamec, Neja; Paska, Alja Videtič; Jovčevska, Ivana

doi:10.3390/cancers12071842

Cited by 32 publications

(26 citation statements)

References 142 publications

(183 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…75 Upregulated H19 promotes TMZ resistance in U251 and M059J glioma cell lines as studied by Jia et al 76 The study has reported that the resistant cells have higher H19 expression than do non-resistant cells, and silencing of H19 resulted in downregulation of EMT markers and Wnt/b-catenin markers. 58,76 Taurine upregulated gene 1 (TUG1)…”

Section: H19 Imprinted Maternally Expressed Transcript (H19)mentioning

confidence: 99%

LncRNAs associated with glioblastoma: From transcriptional noise to novel regulators with a promising role in therapeutics

Yadav

Pal

Rubstov

et al. 2021

Molecular Therapy - Nucleic Acids

View full text Add to dashboard Cite

Glioblastoma multiforme (GBM) is the most widespread and aggressive subtype of glioma in adult patients. Numerous long non-coding RNAs (lncRNAs) are deregulated or differentially expressed in GBM. These lncRNAs possess unique regulatory functions in GBM cells, ranging from high invasion/ migration to recurrence. This review outlines the present status of specific involvement of lncRNAs in GBM pathogenesis, with a focus on their association with key molecular and cellular regulatory mechanisms. Also, we highlighted the potential of different novel RNA-based strategies that may be beneficial for therapeutic purposes. lncRNAsDepending on the genomic location and with respect to neighboring protein-coding genes, lncRNAs can be sense, antisense, intronic, intergenic, and bidirectional. Sense and antisense are transcribed in the same or opposite direction of protein-coding gene strands. Bidirectional lncRNAs are transcribed in the opposite direction of their neighboring protein-coding gene (<1 kb away). Intronic lncRNAs are transcribed completely from the introns of the protein-coding gene, while intergenic lncRNAs are transcribed from different genomic locations. 10 The activity of lncRNAs depends on its subcellular localization, allowing division of lncRNAs into nuclear or cytoplasmic subgroups. 11 A gene transcriptional status can be regulated by transcriptional interference and chromatin remodeling acquired from lncRNA located in the nuclear region. 12,13 In contrast, lncRNAs that are exported to the cytoplasm serve as mediators for RNA processing and can affect mRNA stability or regulate protein function. 14 lncRNAs can interact with RNA, proteins, and DNA via different modes of molecular mechanisms such as signaling, decoy, guide, scaffold, and miRNA sponge. lncRNAs can function as a signaling molecule for any biological condition and are capable of regulating the expression of genes concerning a specific response; as a decoy

show abstract

Section: H19 Imprinted Maternally Expressed Transcript (H19)mentioning

confidence: 99%

LncRNAs associated with glioblastoma: From transcriptional noise to novel regulators with a promising role in therapeutics

Yadav

Pal

Rubstov

et al. 2021

Molecular Therapy - Nucleic Acids

View full text Add to dashboard Cite

show abstract

“…In recent years, LncRNA has attracted more and more attentions. Studies have shown that lncRNA plays a key role in regulating gene expression such as chromatin modification, transcription and post-transcriptional processing, and its abnormal expression is related to many physiological and pathological processes, such as embryonic development, cell proliferation and differentiation, steatosis, oxidative stress, endoplasmic reticulum stress, etc [ 19 , 20 ]. One of the first investigations of lncRNAs in NAFLD fibrosis demonstrated that MEG3 expression was decreased in livers from CCl4-treated mice compared to oil-fed control mice, and Meg3 expression diminished concordantly with the progression of fibrosis [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA-Gm9795 promotes inflammation in non-alcoholic steatohepatitis via NF-$$\kappa {}$$B/JNK pathway by endoplasmic reticulum stress

Zhao

et al. 2021

J Transl Med

View full text Add to dashboard Cite

Background Non-alcoholic steatohepatitis (NASH) is a key stage in leading development of non-alcoholic simple fatty liver (NAFL) into cirrhosis and even liver cancer. This study aimed at exploring the lncRNAs expression profile in NASH and the biological function of a novel LncRNA-gm9795. Methods Microarray analysis was performed to compare the expression profiles of lncRNAs in the liver of NASH, NAFLD and normal mice (5 mice for each group). Methionine-choline-deficient Medium (MCD) with Lipopolysaccharide (LPS) or palmitic acid (PA)were used to built NASH cell models. The role and mechanism of LncRNA-gm9795 in NASH were explored by knocking down or over-expressing its expression. Results A total of 381 lncRNAs were found to be not only highly expressed in NAFLD, but also is going to go even higher in NASH. A novel LncRNA-gm9795 was significantly highly expressed in liver tissues of NASH animal models and NASH cell models. By staining with Nile red, we found that gm9795 did not affect the fat accumulation of NASH. However, gm9795 in NASH cell models significantly promoted the expression of TNF $$\alpha {}$$ α , IL-6, IL-1$$\beta {}$$ β , the important inflammatory mediators in NASH. At the same time, we found that gm9795 upregulated the key molecules in endoplasmic reticulum stress (ERS), while NF-$$\kappa {}$$ κ B/JNK pathways were also activated. When ERS activator Thapsigargin (TG) was introduced in cells with Ggm9757 si-RNA, NF-$$\kappa {}$$ κ B and JNK pathways were activated. Conversely, ERS inhibitor Tauroursodeoxycholic acid (TUDCA) inhibited NF-kB and JNK pathways in cells with gm9795 overexpression plasmid. Conclusion LncRNA-gm9795 promotes inflammatory response in NASH through NF-kB and JNK pathways by ERS, which might provide theoretical basis for revealing the pathogenesis of NASH and discovering new therapeutic targets

show abstract

“…In recent years, LncRNA has attracted more and more attentions. Studies have shown that lncRNA plays a key role in regulating gene expression such as chromatin modification, transcription and post-transcriptional processing, and its abnormal expression is related to many physiological and pathological processes, such as embryonic development, cell proliferation and differentiation, steatosis, oxidative stress, endoplasmic reticulum stress, etc [14,15]. One of the first investigations of lncRNAs in NAFLD fibrosis demonstrated that MEG3 expression was decreased in livers from CCl4-treated mice compared to oil-fed control mice, and Meg3 expression diminished concordantly with the progression of fibrosis [16].…”

Section: Discussionmentioning

confidence: 99%

Gm9795 Promotes Inflammation in Non-Alcoholic Steatohepatitis via NF-κB/JNK Pathway by Endoplasmic Reticulum Stress

Ye¹,

Zhao²,

Xu³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Non-alcoholic steatohepatitis (NASH) is a key stage in leading development of non-alcoholic simple fatty liver (NAFL) into cirrhosis and even liver cancer. This study aimed at exploring the lncRNA expression profifile in NASH and the biological function of a novel LncRNA-gm9795. Methods: Microarray analysis was performed to compare the expression profifiles of lncRNAs in the liver of NASH, NAFLD and normal mice. Methionine-choline-deficient Medium(MCD) with Lipopolysaccharide(LPS) or palmitic acid（PA）were used to built NASH cell models.The role and mechanism of LncRNA-gm9795 in NASH were explored by knocking down or over-expressing its expression. Results: A total of 381 lncRNAs were found to be not only highly expressed in NAFLD, but also is going to go even higher in NASH. A novel LncRNA-Gm9795 was significantly highly expressed in liver tissues of NASH animal models and NASH cell models. By staining with Nile red, we found that Gm9795 did not affect the fat accumulation of NASH. However, Gm9795 in NASH cell models significantly promoted the expression of TNFα, IL-6, IL-1β, the important inflammatory mediators in NASH. At the same time, we found that Gm9795 upregulated the key molecules in endoplasmic reticulum stress (ERS), while NF-κB/JNK pathways were also activated. When ERS activator Thapsigargin(TG) was introduced in cells with Gm9757 si-RNA, NF-κB and JNK pathways were activated. Conversely, ERS inhibitor Tauroursodeoxycholic(TUDCA) acid inhibited NF-kB and JNK pathways in cells with Gm9795 overexpression plasmid. Conclusion: LncRNA-gm9795 promotes inflammatory response in NASH through NF-kB and JNK pathways by ERS, which might provide theoretical basis for revealing the pathogenesis of NASH and discovering new therapeutic targets

show abstract

Coding of Glioblastoma Progression and Therapy Resistance through Long Noncoding RNAs

Cited by 32 publications

References 142 publications

LncRNAs associated with glioblastoma: From transcriptional noise to novel regulators with a promising role in therapeutics

LncRNAs associated with glioblastoma: From transcriptional noise to novel regulators with a promising role in therapeutics

LncRNA-Gm9795 promotes inflammation in non-alcoholic steatohepatitis via NF-$$\kappa {}$$B/JNK pathway by endoplasmic reticulum stress

Gm9795 Promotes Inflammation in Non-Alcoholic Steatohepatitis via NF-κB/JNK Pathway by Endoplasmic Reticulum Stress

Contact Info

Product

Resources

About