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Hepatocellular carcinoma (HCC) is one of the most common cancers with high prevalence and mortality, and it has brought huge economic and health burden for the world. It is urgent to found novel targets for HCC diagnosis and clinical intervention. Circular RNA (circRNA) has been reported to participate in many cancer progressions including HCC, suggesting that circRNA might paly essential role in HCC initiation and progression. Our study aims to found that potential circRNA participates in HCC development and its underlying molecular mechanisms. We obtained three pairs of HCC tissues and its adjacent normal tissues data from GEO DataSets. MTT, cell colony, EdU, wound‐healing, transwell invasion and mouse xenograft model assays were used to demonstrate the biological functions of circCAMSAP1 in HCC progression. Furthermore, we conducted bioinformatics analysis, AGO2‐RIP, RNA pull‐down and luciferase reporter assays to assess the association of circCAMSAP1‐miR‐1294‐GRAMD1A axis in HCC cells. The expression of circCAMSAP1 was up‐regulated in HCC tissues compared with its adjacent normal tissues. Up‐regulation of circCAMSAP1 promoted HCC biological functions both in vitro and in vivo. The promotive effects of circCAMSAP1 on HCC progression function through miR‐1294/GRAMD1A pathway. CircCAMSAP1 was up‐regulated in HCC tissues, and circCAMSAP1 up‐regulated GRAMD1A expression to promote HCC proliferation, migration and invasion through miR‐1294. CircCAMSAP1 might be a potential prognosis and therapeutic target for HCC.

Background Circular RNAs (circRNAs) have been found to render pivotal effects in gastric cancer (GC). However, the effect of hsa_circ_0043691 in GC still needs to be further unveiled. Methods The contents of hsa_circ_0043691, miR‐1294, and pre‐leukemia transcription factor 3 (PBX3) were examined using qRT‐PCR or Western blot assay. In vitro colony formation, transwell, wound healing, flow cytometry, tube formation assays, glutaminolysis corresponding kit and in vivo Xenograft mice model were utilized to evaluate cell functions. The relationship between miR‐1294 and hsa_circ_0043691 or PBX3 was further verified. Results The levels of hsa_circ_0043691 and PBX3 were upregulated, whereas miR‐1294 expression was diminished in GC tissues and cells. Hsa_circ_0043691 deficiency significantly inhibited GC cell progression and glutaminolysis metabolism. Mechanistically, hsa_circ_0043691 was directly bound to miR‐1294 to modulate PBX3 expression. Besides, silencing of hsa_circ_0043691 impeded tumor growth in vivo. Conclusion Hsa_circ_0043691 knockdown repressed GC malignant phenotypes by miR‐1294/PBX3 axis, which exhibited a novel therapeutic target for GC treatment. Hsa_circ_0043691 promotes GC malignant phenotypes by targeting miR‐1294/PBX3 axis.

Previous studies have proved circFN1 is highly expressed in acute myeloid leukemia (AML) patients and AML cell lines. This study aims to investigate the impact of circFN1 on AML and its mechanism. Via real‐time quantitative PCR to detect circFN1, miR‐1294, ARHGEF10L expressions in clinical plasma samples and AML cell lines, AML cells were cultured in vitro and transfected with si‐circFN1, pcDNA3.1‐circFN1, and si‐ARHGEF10L, respectively, or co‐transfected pcDNA3.1‐circFN1 + miR‐1294 mimic and pcDNA3.1‐circFN1 + si‐ARHGEF10L. Using dual luciferase reporter experiment to detect the relationship between circFN1 and miR‐1294, as well as miR‐1294 and ARHGEF10L. CCK‐8 was used to detect cell proliferation, Transwell to cell invasion, TUNEL staining and flow cytometry to detect cell apoptosis, RT‐qPCR to circFN1 RNA, miR‐1294, and ARHGEF10L expression levels in HL‐60 cells, and western blot to ARHGEF10L protein expression level in HL‐60 cells. We found highly expressed circFN1 and ARHGEF10L, as well as low‐expressed miR‐1294 in AML patients and AML cell lines. In contrast to si‐NC group, si‐circFN1 group could signally inhibit HL‐60 cell proliferation and migration, but promote cell apoptosis; compared with mimic NC group, miR‐1294 mimic group could visually inhibit HL‐60 cell proliferation and migration, but promote cell apoptosis. miR‐1294 was the target of circFN1, and ARHGEF10L was the target of miR‐1294. Over‐expressing miR‐1294 or silencing ARHGEF10L could signally inhibit circFN1 promoting HL‐60 cell proliferation and migration and repressing cell apoptosis. circFN1 promotes proliferation and invasion of AML cell and represses cell apoptosis via regulating miR‐1294/ARHGEF10L axis, which provides new insight for molecular targeted‐treatment for AML.

Background circRNA hsa_circ_0018289‐mediated growth and metastasis of CC cells were investigated, as well as the mechanistic pathway. Methods Quantitative real‐time reverse transcription‐polymerase chain reaction (qRT‐PCR) was carried out to examine the expression of hsa_circ_0018289, microRNA (miR)‐1294, and isoprenylcysteine carboxyl methyltransferase (ICMT). CC cell proliferation, migration, and invasion were evaluated by 5‐ethynyl‐2’‐deoxyuridine (EdU) incorporation, colony formation, transwell assays, Western blot analysis of ICMT, and glycolysis‐associated proteins. Dual‐luciferase reporter or RNA pull‐down analysis of the target interaction between miR‐1294 and hsa_hsa_circ_0018289 or ICMT. Xenograft model assay was implemented to assess the role of hsa_circ_0018289 in vivo. Immunofluorescence (IHC) was employed to detect the level of Ki‐67. Results Hsa_circ_0018289 was elevated in CC tissues and cells, its deficiency could repress growth, metastasis, and glycolysis of CC cells in vitro, as well as hamper tumor growth in vivo. Hsa_circ_0018289 sponged miR‐1294 while miR‐1294 bound with ICMT, and the inhibition of miR‐1294 or addition of ICMT could partially relieve the effect caused by hsa_circ_0018289 depletion. Conclusion Hsa_circ_0018289 contributes to malignant development by regulating the miR‐1294/ICMT axis, affording novel insight into CC therapy. Schematic diagram of circ_0018289 regulating CC cell malignancy behavior.

Background Esophageal squamous cell carcinoma (ESCC) is a global cancer related to the sixth largest cause of death. Circular RNAs (circRNAs) have affected the progress of ESCC during recent years, but the mechanism is not completely clear. So here we probed the effects of hsa_circ_0096710 (circ_0096710) in ESCC. Methods Relative levels of circ_0096710, miR‐1294, and ADAM10 were quantified by the quantitative real‐time reverse transcription‐polymerase chain reaction in ESCC tissues. Western blot assessed ADAM10, PCNA, MMP2, VEGFA, and OCT4 protein levels. Cell proliferative capacity was assessed by cell counting and cell colony‐forming assays. Transwell assays assessed cell migration and invasion. Angiogenesis was detected by tube formation assays. Stemness of cancer cells was estimated by sphere formation assays. Dual‐luciferin reporter and RNA immunoprecipitation assays determined the targeting relationship between miR‐1294 and circ_0096710 or ADAM10. Results Relative levels of circ_0096710 and ADAM10 mRNA were upregulated in ESCC cells, yet miR‐1294 was downregulated. Circ_0096710 silencing repressed ESCC cell proliferation, migration, invasion, angiogenesis, and stem‐like properties. Moreover, circ_0096710 was an upstream target of miR‐1294, and miR‐1294 inhibition reversed the role of circ_0096710 downregulation in ESCC cells. Furthermore, ADAM10 was a downstream target of miR‐1294, and miR‐1294 overexpression suppressed ESCC cell proliferation, migration, invasion, angiogenesis, and stem‐like properties by targeting ADAM10. Meanwhile, circ_0096710 upgraded ADAM10 expression through sponging miR‐1294. Also, circ_0096710 downregulation restrained tumor growth in mouse models. Conclusion Circ_0096710 upregulates ADAM10 via mediating miR‐1294 expression so as to accelerate the occurrence of ESCC, suggesting that circ_0096710 may be a potential therapeutic target for ESCC. Schematic illustration of the mechanism by which circ_0096710 upregulates ADAM10 expression by interacting with miR‐1294, resulting in promoting esophageal squamous cell carcinoma (ESCC) cell proliferation, migration, invasion, angiogenesis, and stem‐like properties.