Abstract
ObjectiveMiR-1224 has been reported to exhibit abnormal expression in several tumors. However, the expressing pattern and roles of miR-1224 in gastric cancer (GC) remain unclear. Our current research aimed to explore the potential involvement of miR-1224 in the GC progression.Materials and MethodsThe expression of miR-1224 was examined in tissue samples of 128 GC patients and cell lines by RT-PCR. Besides, the associations of miR-1224 expressions with clinicopathologic features and prognosis of GC patients were analyzed. Then, the possible influences of miR-1224 on cell proliferation and cell migration were determined. Afterward, the molecular target of miR-1224 was identified using bioinformatics assays and confirmed experimentally. Finally, RT-PCR and Western blot assays were performed to investigate the effect of the abnormal miR-1224 expression on the EMT and Wnt/β-catenin pathway.ResultsmiR-1224 was lowly expressed in the GC specimens and cell lines due to T classification and TNM stage. Survival assays demonstrated that GC patients with low expressions of miR-1224 possessed poor overall survivals. Moreover, in vitro and in vivo assays revealed that the overexpression of miR-1224 inhibited cell proliferation, migration, and invasion in GC cells. SATB homeobox 1 (SATB1) was verified as a direct target of miR-1224 in GC. Furthermore, β-catenin and c-myc were significantly inhibited in miR-1224-overexpression cells.ConclusionsOur findings highlight the potential of miR-1224 as a therapeutic target and novel biomarker for GC patients
Highlights
Gastric cancer (GC) is a malignant tumor originating from the glandular epithelium of the gastric mucosa [1, 2]
Survival assays demonstrated that GC patients with low expressions of miR-1224 possessed poor overall survivals
Our findings highlight the potential of miR-1224 as a therapeutic target and novel biomarker for GC patients
Summary
Gastric cancer (GC) is a malignant tumor originating from the glandular epithelium of the gastric mucosa [1, 2]. It is estimated that approximately 1 million new cases of GC are diagnosed per year worldwide [3]. The survival rate in five years for GC has not improved significantly over the past several decades despite the improvements in surgery, radiotherapy, and chemotherapy [6,7,8]. Cancer metastasis and local tumor recurrence have been major reasons for death among GC patients [9]. The molecular mechanisms of metastasis and local tumor recurrence has not been unveiled, though increasing efforts have been made to solve it [10]. Investigating the molecular events underlying GC progression would contribute to the development of novel strategies for the clinical management of patients with this tumor
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