scholarly journals Silencing of Long Non-Coding RNA HOTAIR Alleviates Epithelial–Mesenchymal Transition in Pancreatic Cancer via the Wnt/β-Catenin Signaling Pathway

2021 ◽  
Vol Volume 13 ◽  
pp. 3247-3257
Author(s):  
Yinhua Tang ◽  
Guang Song ◽  
Hongcheng Liu ◽  
Shuang Yang ◽  
Xiaoyi Yu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals ALKBH5 Inhibits Pancreatic Cancer Motility by Decreasing Long Non-Coding RNA KCNK15-AS1 Methylation

2018 ◽  
Vol 48 (2) ◽  
pp. 838-846 ◽  
Author(s):  
Yuan He ◽  
Hao Hu ◽  
Yandong Wang ◽  
Hao Yuan ◽  
Zipeng Lu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
The Body ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cancer Pathogenesis ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna

Background/Aims: Mounting evidence suggests that epitranscriptional modifications regulate multiple cellular processes. N6-Methyladenosine (m6A), the most abundant reversible methylation of mRNA, has critical roles in cancer pathogenesis. However, the mechanisms and functions of long non-coding RNA (lncRNA) methylation remain unclear. Pancreatic cancer resulted in 411,600 deaths globally in 2015. By the time of pancreatic cancer diagnosis, metastasis has often occurred in other parts of the body. The present study sought to investigate lncRNA m6A modification and its roles in pancreatic cancer. Methods: Differential expression between cancer cells and matched normal cells was evaluated to identify candidate lncRNAs. The lncRNA KCNK15-AS1 was detected in cancer tissues and various pancreatic cells using RT-qPCR. KCNK15-AS1 was transfected into cells to explore its role in migration and invasion. Then, m6A RNA immunoprecipitation was performed to detect methylated KCNK15-AS1 in tissues and cells. Epithelial–mesenchymal transition (EMT) markers were used to evaluate KCNK15-AS1-mediated EMT processes. Results: KCNK15-AS1 was downregulated in pancreatic cancer tissues compared with paired adjacent normal tissues. KCNK15-AS1 inhibited migration and invasion in MIA PaCa-2 and BxPC-3 cells. Furthermore, total RNA methylation in cancer cells was significantly enriched relative to that in immortalized human pancreatic duct epithelial (HPDE6-C7) cells. In addition, the m6A eraser ALKBH5 was downregulated in cancer cells, which can demethylate KCNK15-AS1 and regulate KCNK15-AS1-mediated cell motility. Conclusion: Our results have revealed a novel mechanism by which ALKBH5 inhibits pancreatic cancer motility by demethylating lncRNA KCNK15-AS1, identifying a potential therapeutic target for pancreatic cancer.

scholarly journals Long non-coding RNA SNHG16 regulates cell behaviors through miR-542-3p/HNF4α axis via RAS/RAF/MEK/ERK signaling pathway in pediatric neuroblastoma cells

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Defeng Deng ◽  
Shuangjie Yang ◽  
Xiang Wang
Keyword(s):  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Neuroblastoma Cells ◽  
Erk Signaling ◽  
Mesenchymal Transition ◽  
Cell Behaviors ◽  
Non Coding Rna ◽  
Extracellular Signal ◽  
Long Non Coding Rna

Abstract Neuroblastoma (NB) is an extracranial solid tumor in children with complex mechanism. Increasing reports indicated that long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16) account for the pathogenesis of NB. Nevertheless, the precise functions of SNHG16 needed to be further exposed in NB progression. Our data revealed that SNHG16 and hepatocyte nuclear factor 4 α (HNF4α) were up-regulated, but miR-542-3p was down-regulated in NB. Knockdown of SNHG16 or HNF4α could impede cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) in vitro. Interestingly, the role of SNHG16 detetion in cell behaviors was rescued by HNF4α overexpression in NB cells. Mechanically, SNHG16 modulated the progression of tumor growth via miR-542-3p/HNF4α axis in NB. Also, SNHG16 knockdown inactivated rat sarcoma/effector of RAS/mitogen-activated extracellular signal-regulated kinase/extracellular regulated protein kinases (RAS/RAF/MEK/ERK) signaling pathway through HNF4α. Therefore, SNHG16/miR-542-3p/HNF4α axis modified NB progression via RAS/RAF/MEK/ERK signaling pathway, might highlight a novel therapeutic approach for NB.

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