TUG1 as a Therapy Target in Pancreatic Cancer

Liang, Haifeng; Cui, Zhaokun; Song, Qingping

doi:10.1007/s10620-020-06636-1

Cited by 5 publications

(3 citation statements)

References 5 publications

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“…Yang et al demonstrated that TUG1 affects tumor invasion and gemcitabine resistance in pancreatic cancer [ 46 ]. Liang et al demonstrated that TUG1 may be a potential target for the treatment of PAAD [ 47 ]. Taken together, TUG1/miR-144-3p/COL10A1axis was identified as potential regulatory pathways in PAAD.…”

Section: Discussionmentioning

confidence: 99%

“…For example, Qin and Zhao demonstrated that lncRNA TUG1 can promote the malignant progression of pancreatic cancer via the EMT pathway [45]. Yang et al demonstrated that TUG1 a ects tumor invasion and demonstrated that TUG1 may be a potential target for the treatment of PAAD [47]. Taken together, TUG1/miR-144-3p/COL10A1axis was identi ed as potential regulatory pathways in PAAD.…”

Section: Discussionmentioning

confidence: 99%

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Bioinformatics-Based Analysis: Noncoding RNA-Mediated COL10A1 Is Associated with Poor Prognosis and Immune Cell Infiltration in Pancreatic Cancer

Liu

Zhao

Guo

et al. 2022

Journal of Healthcare Engineering

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Background. Collagen type X alpha 1 (COL10A1) is a structural component of the extracellular matrix that is aberrantly expressed in a variety of cancer tissues. However, its role in pancreatic cancer progression is not well understood. Methods. The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and Gene Expression Profiling Interaction Analysis (GEPIA) data were employed to explore the expression of COL10A1 in normal and tumor tissues and its prognostic value in pancreatic adenocarcinoma. The clinical data of pancreatic cancer in TCGA were used to explore the relationship between COL10A1 and clinical features. Genes coexpressed with COL10A1 were explored using multiple databases and analyzed for functional enrichment. In addition, the lncRNA/miRNA/COL10A1 axis that may be involved in COL10A1 regulation in pancreatic cancer was explored by constructing a competitive endogenous RNA (ceRNA) regulatory axis. Finally, COL10A1 was analyzed for correlation with immune cell infiltration and various immune checkpoint molecules in pancreatic cancer. Results. It was found that the expression of COL10A1 was significantly increased in pancreatic cancer tissues. High expression of COL10A1 was related to the clinicopathological characteristics and the worse prognosis of pancreatic cancer patients. The TUG1/miR-144-3p/COL10A1 axis was identified as the most likely upstream noncoding RNA pathway for COL10A1 in pancreatic cancer. Besides, in pancreatic adenocarcinoma, the expression level of COL10A1 showed a significant positive correlation with tumor immune cell infiltration, biomarkers of immune cells, and expression of immune checkpoint molecules. Conclusion. COL10A1 is an early diagnostic marker, and its high expression correlates with immune infiltration in pancreatic cancer. The TUG1/miR-144-3p/COL10A1 axis was identified as the most likely upstream noncoding RNA pathway for COL10A1 in pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Bioinformatics-Based Analysis: Noncoding RNA-Mediated COL10A1 Is Associated with Poor Prognosis and Immune Cell Infiltration in Pancreatic Cancer

Liu

Zhao

Guo

et al. 2022

Journal of Healthcare Engineering

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“…LncRNA taurine upregulated gene 1 (TUG1), which is originally identified in the genomic screen of taurine-treated mouse retinal cells, is a nucleotide lncRNA sequence localized to chromosome 22q12.2 (137,138). Recent studies have been indicated that TUG1 is dysregulated in numerous human cancers and acts as an unfavorable predictor of survival for patients with cancer, such as renal cell carcinoma, ovarian cancer, bladder urothelial carcinoma, oral squamous cell carcinoma, esophageal squamous cell carcinoma, hepatocellular carcinoma, and intrahepatic cholangiocarcinoma (137,138). Zhao et al (139) revealed that TUG1 was essential for the migration and EMT in PC by serving as a ceRNA.…”

Section: Tug1/mir-382/ezh2mentioning

confidence: 99%

Long Noncoding Competing Endogenous RNA Networks in Pancreatic Cancer

et al. 2021

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Pancreatic cancer (PC) is a highly malignant disease characterized by insidious onset, rapid progress, and poor therapeutic effects. The molecular mechanisms associated with PC initiation and progression are largely insufficient, hampering the exploitation of novel diagnostic biomarkers and development of efficient therapeutic strategies. Emerging evidence recently reveals that noncoding RNAs (ncRNAs), including long ncRNAs (lncRNAs) and microRNAs (miRNAs), extensively participate in PC pathogenesis. Specifically, lncRNAs can function as competing endogenous RNAs (ceRNAs), competitively sequestering miRNAs, therefore modulating the expression levels of their downstream target genes. Such complex lncRNA/miRNA/mRNA networks, namely, ceRNA networks, play crucial roles in the biological processes of PC by regulating cell growth and survival, epithelial–mesenchymal transition and metastasis, cancer stem cell maintenance, metabolism, autophagy, chemoresistance, and angiogenesis. In this review, the emerging knowledge on the lncRNA-associated ceRNA networks involved in PC initiation and progression will be summarized, and the potentials of the competitive crosstalk as diagnostic, prognostic, and therapeutic targets will be comprehensively discussed.

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Analysis of the subcellular location of FAM230B and its interaction with premature miR-302b in osteosarcoma

Cheng

Wang

2022

J Bone Miner Metab

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TUG1 as a Therapy Target in Pancreatic Cancer

Cited by 5 publications

References 5 publications

Bioinformatics-Based Analysis: Noncoding RNA-Mediated COL10A1 Is Associated with Poor Prognosis and Immune Cell Infiltration in Pancreatic Cancer

Bioinformatics-Based Analysis: Noncoding RNA-Mediated COL10A1 Is Associated with Poor Prognosis and Immune Cell Infiltration in Pancreatic Cancer

Long Noncoding Competing Endogenous RNA Networks in Pancreatic Cancer

Analysis of the subcellular location of FAM230B and its interaction with premature miR-302b in osteosarcoma

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