NEAT1/miR-101-dependent Up-regulation of DNA-PKcs Enhances Malignant Behaviors of Pancreatic Ductal Adenocarcinoma Cells

Hu, Hao; Chen, Wuqiang; Zhang, Shuo; Xue, Yuzheng; He, Youzhao; Gu, Yuanlong

doi:10.7150/jca.58824

Cited by 4 publications

(4 citation statements)

References 34 publications

(62 reference statements)

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“…The contribution of NEAT1 to cancer progression has also been studied in other cancers, including cervical cancer [ 77 ], cholangiocarcinoma [ 78 ], endometrial cancer [ 79 ], esophageal carcinoma [ 80 ], gallbladder cancer [ 81 ], glioblastoma [ 82 ], Hodgkin’s lymphoma [ 83 ], laryngeal carcinoma [ 84 ], melanoma [ 85 ], multiple myeloma [ 11 ], nasopharyngeal carcinoma [ 86 ], osteosarcoma [ 87 ], pancreatic carcinoma [ 88 ], retinoblastoma [ 89 ], thyroid cancer [ 90 ], and tongue carcinoma [ 91 ]. In those cancers, NEAT1 plays a pro-proliferative role and promotes the progression of cancer by upregulating the expression of some oncogenes or downregulating the expression of some tumor suppressor genes.…”

Section: Neat1 Sponges Micrornas and Stabilizes Mrnasmentioning

confidence: 99%

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Zhang

et al. 2022

Cancers

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As one of the best-studied long noncoding RNAs, nuclear paraspeckle assembly transcript 1 (NEAT1) plays a pivotal role in the progression of cancers. NEAT1, especially its isoform NEAT1-1, facilitates the growth and metastasis of various cancers, excluding acute promyelocytic leukemia. NEAT1 can be elevated via transcriptional activation or stability alteration in cancers changing the aggressive phenotype of cancer cells. NEAT1 can also be secreted from other cells and be delivered to cancer cells through exosomes. Hence, elucidating the molecular interaction of NEAT1 may shed light on the future treatment of cancer. Herein, we review the molecular function of NEAT1 in cancer progression, and explain how NEAT1 interacts with RNAs, proteins, and DNA promoter regions to upregulate tumorigenic factors.

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Section: Neat1 Sponges Micrornas and Stabilizes Mrnasmentioning

confidence: 99%

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Zhang

et al. 2022

Cancers

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“…In addition, it is well known that lncRNA NEAT1 acts as a ceRNA of miRNA to inhibit miRNA expression, eventually leading to the elevated expression of target gene [ 27 ]. The current study also exhibited that lncRNA NEAT1 could competitively bind to miR-491-5p to induce PCa cell proliferation, migration, and gemcitabine resistance.…”

Section: Discussionmentioning

confidence: 99%

“…NEAT1 is a transcriptional mediator for multiple genes implicated in pancreatic carcinogenesis [ 26 ] via a competing endogenous RNA (ceRNA) mechanism interacting with miRNAs. Prior findings have suggested that NEAT1/miR-101-dependent release of DNA-PKcs augments the malignant behaviors of pancreatic ductal adenocarcinoma cells [ 27 ]. Whereas, how the effect of NEAT1 was delivered to cancer cells remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Extracellular Vesicle-Loaded Oncogenic lncRNA NEAT1 from Adipose-Derived Mesenchymal Stem Cells Confers Gemcitabine Resistance in Pancreatic Cancer via miR-491-5p/Snail/SOCS3 Axis

Zhao

et al. 2023

Stem Cells International

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It is becoming increasingly evident that key mechanisms of mesenchymal stem cell (MSC) efficacy appear to associate with paracrine activities, and the delivery of cargos through extracellular vesicles (EVs) controls the mechanistic actions of MSCs. Thus, this study clarified a possible mechanism by which EV-encapsulated NEAT1 from adipose-derived mesenchymal stem cells (ADSCs) might mediate gemcitabine resistance in pancreatic cancer (PCa). Microarray profile suggested a differentially expressed lncRNA NEAT1 in PCa, and we determined its expression in PCa cells. NEAT1 was found to be upregulated in PCa. The binding affinity among NEAT1, miR-491-5p, and Snail was identified through bioinformatic analysis and experimental validation. NEAT1 competitively bound to miR-491-5p to elevate Snail expression and diminish SOCS3 expression. PCa cells were cocultured with EVs extracted from ADSCs, followed by assessment of malignant phenotypes, tumorigenesis, and gemcitabine resistance of PCa cells using gain- or loss-of-function experiments. ADSC-derived EVs carrying NEAT1 promoted PCa cell proliferation, migration, and gemcitabine resistance in vitro and enhanced tumorigenicity in vivo by inhibiting miR-491-5p and SOCS3 and upregulating Snail. Collectively, the findings from our study found a new potential strategy for gemcitabine resistance in PCa by illustrating the mechanistic insights of oncogenic ADSC-derived EVs-loaded NEAT1 via regulating the miR-491-5p/Snail/SOCS3 axis.

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“… 14 LncRNA serves as a competitive endogenous RNA (ceRNA) of a specific miRNA and inhibits the expression of this target miRNA. 15 , 16 The evidence can be clearly seen in the publication of Perez-Hernandez et al, which enumerates that miR-146a is relative to albuminuria in patients with EH. 17 Luo et al illustrate this view evidently by the documentation that the expression of miR-10a-5p and miR-497-5p is lessened in 98 patients with EH.…”

Section: Introductionmentioning

confidence: 98%

LncRNA FENDRR Servers as a Possible Marker of Essential Hypertension and Regulates Human Umbilical Vein Endothelial Cells Dysfunction via miR-423-5p/Nox4 Axis

Zhao¹,

Wang²,

Liu³

et al. 2022

IJGM

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Purpose Essential hypertension (EH) is an intricate non-communicable infirmity and lncRNAs are validated as essential mediators in EH. The study aimed to propose the expression pattern of FENDRR and miR-423-5p, substantiate the potential mechanism of FENDRR/miR-423-5p/Nox4 axis in EH. Patients and Methods The expression of FENDRR and miR-423-5p was evaluated by qRT-PCR and the clinical significance was explored by the ROC curve. Pearson correlation indicated the relationship between FENDRR and miR-423-5p. The function of FENDRR and miR-423-5p on HUVECs was clarified by CCK-8 assay, Transwell assay, and flow cytometry. Western blot was used to assess the relative protein expression of Nox4. Results FENDRR was highly expressed and miR-423-5p was lowly expressed in EH patients and a negative correlation between them was determined. FENDRR might serve as a predictive diagnosis in differentiating EH patients. Knockdown of FENDRR or overexpression of miR-423-5p showed expansionary effects in cell proliferation, cell migration, and inhibiting cell apoptosis. Meanwhile, miR-423-5p was determined as a target of FENDRR and mediated the function of FENDRR on HUVECs. Moreover, Nox4 is a down-streaming target gene of miR-423-5p. The protein expression of Nox4 was regulated by the alternation of miR-423-5p expression. Conclusion FENDRR played an energetic role in EH and contributed to HUVECs dysfunction by restricting cell proliferation, suppressing cell migration, and accelerating cell apoptosis by manipulating the miR-423-5p/Nox4 axis.

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NEAT1/miR-101-dependent Up-regulation of DNA-PKcs Enhances Malignant Behaviors of Pancreatic Ductal Adenocarcinoma Cells

Cited by 4 publications

References 34 publications

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Molecular Interactions of the Long Noncoding RNA NEAT1 in Cancer

Extracellular Vesicle-Loaded Oncogenic lncRNA NEAT1 from Adipose-Derived Mesenchymal Stem Cells Confers Gemcitabine Resistance in Pancreatic Cancer via miR-491-5p/Snail/SOCS3 Axis

LncRNA FENDRR Servers as a Possible Marker of Essential Hypertension and Regulates Human Umbilical Vein Endothelial Cells Dysfunction via miR-423-5p/Nox4 Axis

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