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Objectives Circular RNAs (circRNAs) are RNA transcripts that belong to non‐coding RNAs (ncRNAs), whose implication in human cancers has been recently demonstrated. However, the specific role of multiple circRNAs in breast cancer remains unidentified. Materials and methods Microarray analysis and bioinformatics analysis were applied to select circRNA and miRNA, respectively. The loop structure of circ‐TFF1 was confirmed using RNase R treatment, divergent primer PCR and Sanger sequencing. qRT‐PCR and Western blot were employed for gene expressions. In vitro and in vivo experiments were conducted to assess the function of circ‐TFF1 in biological processes in breast cancer cells. FISH and subcellular separation indicated circ‐TFF1 cellular distribution. Luciferase reporter and RIP assays and Pearson's correlation analysis were performed to evaluate relationships between genes. Results Circ‐TFF1 and TFF1 were both upregulated and positively associated with each other in breast cancer. Knockdown of circ‐TFF1 hindered breast cancer cell proliferation, migration, invasion and EMT in vitro and controlled tumour growth in vivo. Circ‐TFF1 acted as a ceRNA of TFF1 by sponging miR‐326, and its contribution to breast cancer progression was mediated by miR‐326/TFF1 axis. Conclusions Circ‐TFF1 is a facilitator in breast cancer relying on TFF1 by absorbing miR‐326, providing a novel promising target for BC treatment.

The research exhibited the critical role of circ_0000518 in BC. Circ_0000518 accelerated BC progression via elevating FGFR1 expression by sponging miR‐326. The findings highlighted the prospect of circ_0000518 as a new target for BC treatment.

Atherosclerosis can result in multiple cardiovascular diseases. Circular RNAs (CircRNAs) have been reported as significant non‐coding RNAs in atherosclerosis progression. Dysfunction of vascular smooth muscle cells (VSMCs) is involved in atherosclerosis. However, up to now, the effect of circ_0002984 in atherosclerosis is still unknown. Currently, we aimed to investigate the function of circ_0002984 in VSMCs incubated by oxidized low‐density lipoprotein (ox‐LDL). Firstly, our findings indicated that the expression levels of circ_0002984 were significantly up‐regulated in the serum of atherosclerosis patients and ox‐LDL‐incubated VSMCs. Loss of circ_0002984 suppressed VSMC viability, cell cycle distribution and migration capacity. Then, we carried out ELISA assay to determine TNF‐α and IL‐6 levels. The data implied that lack of circ_0002984 obviously repressed ox‐LDL–stimulated VSMC inflammation. Meanwhile, miR‐326‐3p, which was predicted as a target of circ_0002984, was obviously down‐regulated in VSMCs treated by ox‐LDL. Additionally, after overexpression circ_0002984 in VSMCs, a decrease in miR‐326‐3p was observed. Subsequently, miR‐326‐3p was demonstrated to target vesicle‐associated membrane protein 3 (VAMP3). Therefore, we hypothesized that circ_0002984 could modulate expression of VAMP3 through sponging miR‐326‐3p. Furthermore, we confirmed that up‐regulation of miR‐326‐3p rescued the circ_0002984 overexpressing‐mediated effects on VMSC viability, migration and inflammation. Additionally, miR‐326‐3p inhibitor‐mediated functions on VSMCs were reversed by knockdown of VAMP3. In conclusion, circ_0002984 mediated cell proliferation, migration and inflammation through modulating miR‐326‐3p and VAMP3 in VSMCs, which suggested that circ_0002984 might hold great promise as a therapeutic strategy for atherosclerosis.

Medulloblastoma (MB) is a malignant pediatric brain tumor, and we reveal a new regulatory molecular axis critical for MB progression. Low expression of miR‐326 and its host gene β‐arrestin1 (ARRB1) promotes tumor growth enhancing the E2F1 pro‐survival function. High levels of EZH2 are responsible for the presence of H3K27me3 that controls miR‐326 and ARRB1 through a bivalent domain. Restoration of miR‐326 and re‐expression of ARRB1 reverse E2F1 function into pro‐apoptotic activity. Persistent mortality rates of medulloblastoma (MB) and severe side effects of the current therapies require the definition of the molecular mechanisms that contribute to tumor progression. Using cultured MB cancer stem cells and xenograft tumors generated in mice, we show that low expression of miR‐326 and its host gene β‐arrestin1 (ARRB1) promotes tumor growth enhancing the E2F1 pro‐survival function. Our models revealed that miR‐326 and ARRB1 are controlled by a bivalent domain, since the H3K27me3 repressive mark is found at their regulatory region together with the activation‐associated H3K4me3 mark. High levels of EZH2, a feature of MB, are responsible for the presence of H3K27me3. Ectopic expression of miR‐326 and ARRB1 provides hints into how their low levels regulate E2F1 activity. MiR‐326 targets E2F1 mRNA, thereby reducing its protein levels; ARRB1, triggering E2F1 acetylation, reverses its function into pro‐apoptotic activity. Similar to miR‐326 and ARRB1 overexpression, we also show that EZH2 inhibition restores miR‐326/ARRB1 expression, limiting E2F1 pro‐proliferative activity. Our results reveal a new regulatory molecular axis critical for MB progression.

Osteosarcoma (OS) is a malignant bone cancer lacking of effective treatment target when the metastasis occurred. This study investigated the implication of MicroRNA‐326 in OS proliferation and metastasis to provide the clue for the treatment of metastatic OS. This study knocked down SP1 in MG63 and 143B cells and then performed Microarray assay to find the expression of miRNAs that were influenced by SP1. MTT, EdU, wound‐healing and cell invasion assays were performed to evaluated cell proliferation and invasion. OS metastasis to lung was detected in a nude mice model. ChIP assay and DAPA were applied to determine the regulatory effect of SP1 and histone deacetylase 1 (HDAC) complex on miR‐326 expression. Human OS tissues showed lowly expressed miR‐326 but highly expressed Sp1 and HDAC. Sp1 recruited HDAC1 to miR‐326 gene promoter, which caused the histone deacetylation and subsequent transcriptional inhibition of miR‐326 gene. miR‐326 deficiency induced the stimulation of SMO/Hedgehog pathway and promoted the proliferation and invasion of 143B and MG63 cells as well as the growth and metastasis in nude mice. SP1/HDAC1 caused the transcriptional inhibition of miR‐326 gene by promoting histone deacetylation; miR‐326 deficiency conversely stimulated SMO/Hedgehog pathway that was responsible for the proliferation and metastasis of OS.

Background Many long noncoding RNAs (lncRNAs) are the key regulators for cancer progression, including breast cancer (BC). RUSC1 antisense 1 (RUSC1‐AS1) has been found to be highly expressed in BC, but its role and potential molecular mechanism in BC remain to be further elucidated. Methods Quantitative reverse transcription‐polymerase chain reaction (RT‐PCR) was utilized to measure RUSC1‐AS1, microRNA (miR)‐326 and X‐ray repair cross‐complementing group 5 (XRCC5) expression. Cell proliferation, metastasis, cell cycle, apoptosis and angiogenesis were determined by cell counting kit‐8, colony formation, transwell, flow cytometry and tube formation assays. Protein expression was detected by western blot analysis. The targeted relationship between miR‐326 and RUSC1‐AS1 or XRCC5 was validated using dual‐luciferase reporter assay and RIP assay. Xenograft models were constructed to uncover the effect of RUSC1‐AS1 on BC tumorigenesis. Results RUSC1‐AS1 was upregulated in BC, and its downregulation suppressed BC proliferation, metastasis, cell cycle, angiogenesis, and tumor growth. MiR‐326 was confirmed to be sponged by RUSC1‐AS1, and its inhibitor reversed the regulation of RUSC1‐AS1 silencing on BC progression. XRCC5 could be targeted by miR‐326. Overexpression of XRCC5 reversed the inhibitory impacts of miR‐326 on BC progression. Conclusion RUSC1‐AS1 could serve as a sponge of miR‐326 to promote BC progression by targeting XRCC5, suggesting that RUSC1‐AS1 might be a target for BC treatment. LncRNA RUSC1‐AS1 promoted BC cell proliferation, metastasis, cell cycle, angiogenesis, and suppressed apoptosis through targeting the miR‐326/XRCC5 axis.

Background Breast cancer (BC) is a heterogeneous malignant tumor that threatens the health of women worldwide. Hsa_circRNA_0000518 (circ_0000518) has been revealed to be upregulated in BC tissues. However, the role and mechanism of circ_0000518 in BC are indistinct. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) was implemented to detect the levels of circ_0000518, microRNA (miR)‐326, and fibroblast growth factor receptor 1 (FGFR1) mRNA in BC tissues and cells. Cell counting kit‐8 (CCK‐8), colony formation, flow cytometry, and transwell assays were executed to estimate BC cell proliferation, cell cycle progression, apoptosis, migration, and invasion. The relationship between circ_0000518 or FGFR1 and miR‐326 was verified by dual‐luciferase reporter and/or RNA immunoprecipitation (RIP) assays. The role of circ_0000518 in vivo was confirmed by xenograft assay. Results Circ_0000518 and FGFR1 were upregulated while miR‐326 was downregulated in BC tissues and cells. Circ_0000518 silencing impeded tumor growth in vivo and induced cell cycle arrest, apoptosis, cured proliferation, colony formation, migration, and invasion of BC cells in vitro. Circ_0000518 regulated FGFR1 expression via competitively binding to miR‐326 in BC cells. MiR‐326 inhibitor reversed the inhibitory influence of circ_0000518 knockdown on the malignant behaviors of BC cells. FGFR1 overexpression abolished miR‐326 mimic‐mediated influence on the malignant behaviors of BC cells. Conclusions Circ_0000518 facilitated BC development via regulation of the miR‐326/FGFR1 axis, suggesting that circ_0000518 might be a promising target for BC treatment. The research exhibited the critical role of circ_0000518 in BC. Circ_0000518 accelerated BC progression via elevating FGFR1 expression by sponging miR‐326. The findings highlighted the prospect of circ_0000518 as a new target for BC treatment.

Pancreatic cancer (PC) is a common malignant cancer characterized by high mortality and poor prognosis. LINC00690 was involved in the occurrence and progression of PC, but the underlying mechanisms require further investigation. The goal of this study was to figure out how LINC00960 mediates glycolysis in PC. LINC00960, miR‐326‐3p, and Tuftelin 1 (TUFT1) expression levels were detected in PC cell lines. LINC00960 and TUFT1 expression levels were increased in PC cells when compared with normal pancreatic cells, whereas miR‐326‐3p expression levels were decreased. The expression levels of LINC00690 affected glycolysis in PC, and inhibition of LINC00960 inhibited tumor growth in vivo. LINC00690 targeted and suppressed the expression of miR‐326‐3p. MiR‐326‐3p bound to TUFT1, and miR‐326‐3p inhibited AKT–mTOR pathway activation via TUFT1. In conclusion, the depletion of LINC00960 repressed cell proliferation and glycolysis in PC by mediating the miR‐326‐3p/TUFT1/AKT–mTOR axis. Thus, we present a novel mechanism underlying the progression of PC that suggests LINC00960 is a potential therapeutic target for this cancer.

As a common chronic respiratory disease, the incidence of asthma is increasing in recent years worldwide. Airway remodeling is the primary pathological basis of refractory asthma, but the studies about the underlying mechanism of airway remodeling was a lack. In the study, we aimed to investigate the effects and mechanisms of miR‐326 on airway remodeling in airway smooth muscle cells (ASMCs). The results showed that transforming growth factor‐β1 (TGF‐β1) accelerated matrix protein deposition by increasing the expression levels of collagen I and fibronectin, and promoted proliferative ability of ASMCs. However, miR‐326 was significantly downregulated in TGF‐β1‐treated ASMCs. MiR‐326 mimics robustly decreased the collagen I and fibronectin levels and inhibited cell proliferation of TGF‐β1‐treated ASMCs. Luciferase assay investigated that tumor necrosis factor superfamily member 14 (TNFSF14) was a direct target of miR‐326. The expression of TNFSF14 was negatively regulated by miR‐326. Moreover, exogenous TNFSF14 effectively reversed the inhibitory effects of miR‐326 overexpression on the expression levels of collagen I and fibronectin, and promoted cell proliferation of TGF‐β1‐treated ASMCs. In conclusion, miR‐326 suppressed matrix protein deposition and cell proliferation of TGF‐β1‐treated ASMCs via inhibiting TNFSF14. MiR‐326 might be a promising novel therapeutic target for asthma.