MicroRNA-1271-5p suppresses the proliferation, invasion and migration of oral squamous cell carcinoma by inhibiting F13A1 expression

被引:0
|
作者
Xu, Pei [1 ]
Wang, Jia [1 ]
Tao, Ye [1 ]
Zhang, Chen [1 ]
Xia, Yan [1 ]
机构
[1] Anhui Med Coll, Sch Stomatol, 632 Furong Rd, Hefei 230601, Anhui, Peoples R China
关键词
Oral squamous cell carcinoma; miR-1271-5p; PI3K; AKT pathway; Progression; COAGULATION-FACTOR; CANCER GROWTH; LUNG-CANCER; FACTOR-XIII; BIOMARKERS; PROMOTES; GENE;
D O I
10.1007/s13273-023-00381-y
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
BackgroundMiR-1271-5p and coagulation factor XIII A (F13A1) are reported to be associated with the malignant progression of various types of cancers. The aim of this present research study was to delineate miR-1271-5p and F13A1 functional significance on oral squamous cell carcinoma (OSCC) progression.MethodsMiR-1271-5p and F13A1 expression levels were determined via RT-qPCR and western blot, their overexpression or knockdown effects on OSCC cells were assessed through various in vitro assays, including colony formation, wound healing, transwell and flow cytometry, and their mutual relationship were investigated using an online software and validated confirmed by additional in vitro experiments. Further, mechanistic assays were performed to determine their influence on the PI3K/AKT pathway.ResultsOur results indicated downregulation of miR-1271-5p and upregulation of F13A1 in the investigated OSCC cell lines. In addition, upon overexpressing miR-1271-5p or knocking down F13A1, the cell proliferation, migration and invasion were suppressed and apoptotic rate was enhanced. Further investigations showed that the growth and invasive capabilities of OSCC cells were limited by miR-1271-5p through the downregulation of F13A1 mediated PI3K/AKT pathway.ConclusionMiR-1271-5p could suppress OSCC progression by influencing F13A1 expression to inhibit the PI3K/AKT signaling, indicating the promising potential of targeting miR-1271-5p as a novel approach for treating OSCC.
引用
收藏
页码:797 / 806
页数:10
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