MiR-1301-3p Inhibits Epithelial-Mesenchymal Transition via Targeting RhoA in Pancreatic Cancer.
Xinxue ZhangZhangyong RenJunming XuQing ChenJun MaZhe LiuJiantao KouZhao XinRen LangQiang HePublished in: Journal of oncology (2022)
Micro(mi)RNAs play an essential role in the epithelial-mesenchymal transition (EMT) process in human cancers. This study aimed to uncover the regulatory mechanism of miR-1301-3p on EMT in pancreatic cancer (PC). The miRNA profilings from Gene Expression Omnibus data sets (GSE31568, GSE41372, and GSE32688) demonstrated the downregulation of miR-1301-3p in PC tissues, which was validated with 72 paired PC tissue samples through qRT-PCR detection. The low level of miR-1301-3p was associated with a poor prognosis for PC patients from the PC cohort of The Cancer Genome Atlas and the validation cohort. Gene Ontology analyses indicated that the target genes of miR-1301-3p were involved in cell cycle and adherent junction regulation. In vitro assays revealed that miR-1301-3p suppressed the proliferation and migration abilities of PC cells. Western blotting and luciferase reporter assays suggested that miR-1301-3p inhibited RhoA expression by targeting its 3'-untranslated region; RhoA upregulated N-cadherin and vimentin levels; however, it downregulated the E-cadherin level. In conclusion, our study showed that miR-1301-3p could serve as a prognostic biomarker for PC and suppress PC cell malignancy by targeting the RhoA-induced EMT process.
Keyphrases
- epithelial mesenchymal transition
- poor prognosis
- cell cycle
- gene expression
- transforming growth factor
- long non coding rna
- signaling pathway
- single cell
- genome wide
- cell proliferation
- end stage renal disease
- newly diagnosed
- dna methylation
- high throughput
- chronic kidney disease
- south africa
- prognostic factors
- stem cells
- big data
- electronic health record
- copy number
- cell therapy
- young adults
- oxidative stress
- mesenchymal stem cells
- peritoneal dialysis
- high glucose
- real time pcr
- quantum dots
- artificial intelligence
- cell migration
- label free
- childhood cancer
- cell adhesion