Circular RNA has been reported to be a new noncoding RNA which plays important roles in tumor progression. One of the most common functions of circular RNA is to regulate microRNA expression by acting as a microRNA sponge. However, the circular RNA expression profile and function remain mostly unclear in gastric cancer. In the study, we explored the expression and function of circCOL1A1 (hsa_circ_0044556) in gastric cancer. We performed RT-PCR with divergent primers, mRNA stability assay, and RNase R digestion assay to characterize circCOL1A1 in gastric cancer cell lines. qRT-PCR was applied to detect the level of circCOL1A1 in both gastric cancer cell lines and tissues. Gain- and loss-of-function studies were carried out to detect the influence of circCOL1A1 on gastric cancer cells by performing CCK8, migration, and invasion assays. The regulation of the downstream genes was identified by qRT-PCR, western blot assay, dual luciferase assay, and RNA pull-down assay. The results showed that circCOL1A1 was highly expressed in both gastric cancer cells and tissues. Silence of circCOL1A1 inhibited the proliferation, migration, and invasion of gastric cancer cells. circCOL1A1 regulated the expression of miR-145 by acting as a microRNA sponge, and the influence of circCOL1A1 could be abrogated by miR-145 mimics. Our research shows that miR-145 plays its functions through targeting and regulating RABL3. Inhibition of circCOL1A1/miR-145/RABL3 could effectively suppress gastric cancer cell proliferation, migration, and invasion. circCOL1A1 also promote the transformation of M1 into M2 macrophage. Our study identified circCOL1A1 as a novel oncogenic circRNA and will provide more information for gastric cancer therapy.
Recently, increasing numbers of non-coding RNA have been uncovered in research. As a new class of non-coding RNA, circular RNA has been identified to be involved in various diseases including many cancers. The circular RNA ciRS-7 is reported to play critical roles in tumorigenesis. However, the role of ciRS-7 in hepatocellular carcinoma (HCC) remains unclear. In this study, we investigated the expression and function of ciRS-7 in HCC cells and cancer tissues. CCK8 was applied to detect the influence of ciRS-7 on proliferation. Wound heal assay and invasion assay were used to identify the effects on migration and invasion. Quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blot, RNA pull-down, and luciferase reporter assay were used to investigate the downstream targets of ciRS-7. The results showed that ciRS-7 was highly expressed in both hepatocellular carcinoma cells and tissues. Overexpression of ciRS-7 could promote the proliferation, migration, and invasion of HCC. Further study showed that ciRS-7 regulated the miR-944 level through acting as a microRNA sponge. q-RT-PCR, Western blot, RNA pull-down and dual luciferase activity assays showed that miR-944 targeted and regulated the expression of NOX4. Furthermore, the tumor-promoting effect of ciRS-7 could be blocked by inhibition of miR-944/NOX4. Our study demonstrated that ciRS-7 enhanced the proliferation, migration, and invasion of HCC through miR-944/NOX4 pathway. ciRS-7 could be a promising therapeutic target for HCC.
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