Open AccessHsa_circ_0023642 promotes proliferation, invasion, and migration of gastric cancer by sponging microRNA‐223
Author(s) -
Zhang Yi,
Xia Lei,
Wu Jing,
Xu Xinyu,
Li Gang
Publication year - 2020
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.23428
Subject(s) - downregulation and upregulation , microrna , gene silencing , cancer , carcinogenesis , cancer research , chemistry , cish , microbiology and biotechnology , biology , in situ hybridization , messenger rna , gene , biochemistry , genetics
Background Circular RNAs (circRNAs) have a closed‐loop structure and are associated with various cellular biological processes, including carcinogenesis and cancer development. However, our knowledge of circRNAs in gastric cancer (GC) remains limited. Thus, this study aimed to investigate the role and underlying molecular mechanisms of hsa_circ_0023642 in GC. Materials and methods Bioinformatic analysis revealed that hsa_circ_0023642 was upregulated in GC. Chromogenic in situ hybridization (CISH) chips was used to explore the relationship between the expression of hsa_circ_0023642 and the malignant degree, clinical stage, and prognosis of patients with GC. The role of hsa_circ_0023642 in GC was assessed in vitro, and biotin‐coupled RNA pull‐down was conducted to evaluate the interaction in between hsa_circ_0023642 and miR‐223. Results The current study showed that hsa_circ_0023642 was upregulated in GC and presented a high positive correlation with the malignant progression of GC. In addition, in vitro experiments showed that the silencing of hsa_circ_0023642 in GC cell lines MKN‐45 and SGC‐7901 significantly reduced the proliferation, invasion, and migration of GC cells. We confirmed that hsa_circ_0023642 could serve as a sponge of miR‐223, subsequently promoting GC progression. Conclusion This study shows that the upregulation of hsa_circ_0023642 affects the malignant progression, clinical stage, and prognosis of GC which provides a new molecular target for the therapy of GC.