[Retracted] MicroRNA‑19a promotes nasopharyngeal carcinoma by targeting transforming growth factor β receptor 2

Ma, Fang; Wang, Zhiyuan; Wang, Jingjing; Liu, Xianling; Hu, Chunhong

doi:10.3892/etm.2021.10523

Cited by 1 publication

(1 citation statement)

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“…Studies have shown that miRNAs can play a key role in the development and progression of tumors as tumor suppressors, which indicates that miRNAs may be used as biomarkers for cancer diagnosis and treatment [ 11 ]. Moreover, it has been found that various miRNAs were involved in NPC, such as miR-663b and miR-19a, which are involved in the occurrence and development of NPC [ 12 , 13 ]. MiR-136-5p was evidenced to be regulated in many cancers, including hepatocellular carcinoma [ 14 ] and renal cell carcinoma [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1

Yan

Zhou

2023

Anti-Cancer Drugs

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Nasopharyngeal carcinoma (NPC) is a malignant tumor caused by nasopharyngeal epithelium. Long non-coding RNAs (lncRNAs) and microRNAs have been identified as vital regulators in many tumors, including NPC. This study aimed to explain the biological roles and relevant mechanisms of lncRNA FOXP4-AS1 (FOXP4-AS1) in NPC. The levels of lncRNA FOXP4-AS1, miR-136-5p and MAPK1 in C666-1 and NP69 cells were analyzed by quantitative reverse transcription PCR (qRT-PCR). C666-1 cells viability, migration and invasion were evaluated by MTT and Transwell assay, respectively. The target gene of miR-136-5p predicted by TargetScan was further verified using dual luciferase reporter assay. Moreover, qRT-PCR and Western blot were adopted to assess epithelial–mesenchymal transition (EMT)-related gene expression, including E-cadherin and N-cadherin. We found that lncRNA FOXP4-AS1 was upregulated, while miR-136-5p was low-expressed in C666-1 cells, as opposed to NP69. Knockdown of FOXP4-AS1 notably suppressed C666-1 cell growth, inhibited cell migration and invasion. We also observed that E-cadherin expression was fortified and N-cadherin level was decreased in C666-1 cells after FOXP4-AS1-siRNA transfection. However, all these findings were eliminated in C666-1 cells after miR-136-5p inhibitor treatment. We also found miR-136-5p directly targeted MAPK1 and correlated inversely with MAPK1 expression in C666-1 cells. Further investigation suggested that MAPK1-plasmid reversed the effects of miR-136-5p mimic on cells viability, migration, invasion and EMT. To conclude, our data revealed that lncRNA FOXP4-AS1 knockdown alleviated metastasis and EMT in NPC via miR-136-5p/MAPK1, indicating that lncRNA FOXP4-AS1 may be a valuable therapeutic target for NPC diagnosis and treatment.

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