Circ_0004913 sponges miR-1290 and regulates FOXC1 to inhibit the proliferation of hepatocellular carcinoma

Abstract

Background: Circular RNA (circRNA), an novel type of non-coding RNA, could interact with miRNA and protein molecules to regulate the occurrence and progression of hepatocellular carcinoma (HCC). However, little is known about the pathogenesis of circ_0004913 in HCC. Materials: Through the GEO (Gene Expression Omnibus database) to find dysfunctional circRNAs in HCC, and circ_0004913 was selected as the research object. Quantitative reverse transcription PCR (qRT-PCR) was used to detect the expression level of circ_0067934 in HCC tissues and cells. CCK-8, Edu and flow cytometry assays were used to determine the malignant behavior of transfected HCC cells. Mechanistically, RNA immunoprecipitation and dualluciferase reporter gene assay were performed to explore the relation between circ_0067934, miR-1290 and FOXC1 (Forkhead box C1) in HCC. Results: The expression of circ_0004913 was down-regulated in HCC tissues and cell lines, while the overexpression of circ_0004913 attenuates the malignant behavior of HCC cells. Bioinformatics predicted that circ_0004913 interacts with miR-1290, which targeted FOXC1 mRNA. In fact, miR-1290 promoted the malignant behavior of HCC cells, while FOXC1 had the opposite effect. In addition, circ_0004913 overexpression enhanced FOXC1 expression by reducing miR-1290 expression, thereby inhibiting the proliferation of HCC cells. Conclusions: Circ_0004913 / miR-1290 / FOXC1 regulatory axis could inhibit the progress of HCC. Our findings may provide potential new targets for the diagnosis and treatment of HCC.

Prognostic and clinical value of circPRKCI expression in diverse human cancers

“…This study contributed to the development of circRNAs as diagnostic or therapeutic targets across cancer types. [44,45] The Cancer Genome Atlas (TCGA) Proliferation, migration, and invasion [25] Proliferation, colony formation, migration, invasion, and EMT [24] Proliferation, migration, and invasion [36] Proliferation, colony formation, cell cycle, and radiosensitivity [37] Proliferation, migration, and invasion [41] Proliferation, invasion, and apoptosis [29] Proliferation and apoptosis [38] Proliferation, migration, invasion, and apoptosis [39] Proliferation, migration, and invasion [32] Proliferation, invasion, migration, and glycolysis [40] Proliferation and invasion [19] Proliferation, migration, invasion, apoptosis, and EMT [34] Proliferation and colony formation [17] Proliferation, migration, and cell cycle [26] Proliferation and migration [21] Proliferation, metastasis, and glycolysis [20] Proliferation, migration, invasion, and apoptosis [31] BC: Bladder cancer; CC: Cervical cancer; ceRNA: Competing endogenous RNA; EC: Esophageal cancer; EMT: Epithelial-mesenchymal transition; GC: Gastric cancer; HCC: Hepatocellular carcinoma; LC: Lung cancer; LSCC: Laryngeal squamous cell cancer; LUAC: Lung adenocarcinoma; miRNA: MicroRNA; mRNA: Messenger RNA; PTC: Papillary thyroid cancer; TC: Thyroid cancer; -: Not available. analysis of PRKCI genes demonstrated amplification in more than 20% of clinical squamous cell carcinoma samples, correlated with decreased OS.…”

“…We found that circPRKCI could regulate progression in various cancers via ceRNA mechanism. [31,38] Only a few studies reported that circPRKCI modulates cancer progression via interacting with RBPs. For example, circPRKCI can bind to FXR1 protein competitively and block the formation of FXR1/PRKCI complex, thereby reducing cell invasion and drug resistance of NSCLC.…”

“…[24,36] Importantly, circPRKCI promoted proliferation, colony formation, and cell cycle progres- sion and decreased radiosensitivity by sponging miR-186-5p to upregulate PARP9 expression. [37] Moreover, the circPRKCI/miR-1290/FOXC1 axis, [38] circPRKCI/miR-545/AKT3 axis, [39] circPRKCI/miR-1324/FZD5 axis, [32] and circPRKCI/miR-1294, miR-186-5p/FOXK1 axis [40] promoted proliferation, migration, invasion, and glycolysis and inhibited apoptosis in HCC. Besides, circPRKCI was found to be upregulated in papillary thyroid cancer tissues and promoted proliferation, metastasis, and glycolysis via the miR-335/E2F3 axis, [20] and increased proliferation, migration, invasion and inhibited apoptosis via miR-1304/CXCR1 in thyroid cancer.…”

The potential role of miR‐1290 in cancer progression, diagnosis, prognosis, and treatment: An oncomiR or onco‐suppressor microRNA?

“…Consequently, the inhibitory effect of miR-1290 on Forkhead box C1 (FOXC1) is removing, and the expression of FOXC1 increased. 83 The expression of cir-cBRAF is downregulated in tissue and cell line of glioma, and its dysregulation is correlated with tumor size, WHO grade, and low survival rate of patients. CircBRAF could serve as a molecular sponge for miR-1290 to elevate the expression of miR-1290 target genes.…”