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Circular RNA (circRNA) is a crucial regulator in multiple human diseases, including osteoporosis (OP). However, the function of numerous circRNAs remains unclear. This study aimed to explore the role and mechanism of circ_0019693 in bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation and osteogenesis-coupled angiogenesis. The expression of circ_0019693, miR-942-5p and purkinje cell protein 4 (PCP4) was measured using quantitative real-time PCR (qPCR) or Western blot. Osteogenic differentiation was monitored according to the protein levels of RUNX family transcription factor 2 (RUNX2), osteopontin (OPN) and osteocalcin (OCN) by Western blot analysis, and the activity of alkaline phosphatase (ALP). Angiogenesis was evaluated by tube formation assay. The targeting relationship between miR-942-5p and circ_0019693 or PCP4 was identified using pull-down, dual-luciferase reporter, and RNA immunoprecipitation assays. Circ_0019693 was downregulated in serum samples and bone tissues from OP patients relative to normal subjects. Circ_0019693 expression was enhanced in the stages of BMSC osteogenic differentiation. Circ_0019693 overexpression enhanced the activity of ALP and the expression of RUNX2, OPN and OCN, and its overexpression also promoted angiogenesis. However, circ_0019693 knockdown played the opposite effects. MiR-942-5p was ensured to be a target of circ_0019693, and miR-942-5p enrichment reversed the effects of circ_0019693. In addition, PCP4 was a target of miR-942-5p, and miR-942-5p inhibitor-promoted BMSC osteogenic differentiation and angiogenesis were partly repressed by PCP4 knockdown. In conclusion, circ_0019693 promotes BMSC osteogenic differentiation osteogenesis-coupled angiogenesis via regulating miR-942-5p-targeted PCP4, thus blocking the development of OP.

Osteosarcoma (OS) is a common malignant bone cancer threatening children and young adults. Emerging evidence indicates that long non-coding RNAs (lncRNAs) play crucial roles in the progression of OS. Herein, we want to clarify the roles of lncRNA human leukocyte antigen complex group 11 (HCG11) in OS. Our data revealed that HCG11 expression is decreased in OS, which is a result of transcriptional repression of YY1. Low HCG11 level is closely associated with larger tumor size and shorter overall survival of OS patients. HCG11 negatively regulates cell proliferation, cell cycle, DNA replication in vitro and tumor growth in vivo. HCG11 can raise p27 Kip1 expression via binding to miR-942-5p and IGF2BP2, and p27 Kip1 acts as a key effector for HCG11 exerting biological functions. In conclusion, HCG11 is downregulated in OS, and restrains OS growth both in vitro and in vivo by raising p27 Kip1 expression via binding to miR-942-5p and IGF2BP2.

Objective Although attention deficit hyperactivity disorder (ADHD) is a disease with high genetic transition, our knowledge about the mechanism of the disease is limited. In this study, it was aimed to evaluate the levels of miR-132-3p and miR-942-5p that are associated with the dopamine carrier protein gene (DAT1) and dopamine receptor 5 (DRD5) genes, which have been shown to play a role in the development of ADHD. Methods According to the Diagnostic and Statistical Manual of Mental Disorders 5th edition, 50 children diagnosed with ADHD and 48 healthy controls were included in the study. Affective Disorders and Schizophrenia Interview Schedule-Now and Lifetime Version-Turkish Adaptation was used to evaluate ADHD and the diagnoses accompanying ADHD. Quantitative Real-Time Polymerase Chain Reaction was used to evaluate miR-132-3p and miR-942-5p expression levels. Results It was observed that miR-132-3p level (p = 0.001) was significantly higher with children with ADHD compared to the control group, and the level of miR-942-5p (p = 0.181) was higher in ADHD but did not reach statistically significant level. Conclusion In our study, we found that the increase in the miR-132-3p levels of children with ADHD may be a therapeutic target of the disease.

Chao Yu,* Deguan Li,* Qiang Yan, Yigao Wang, Xiaodong Yang, Shangxin Zhang, Yonghong Zhang, Zhen Zhang Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, People’s Republic of China*These authors contributed equally to this workCorrespondence: Zhen ZhangDepartment of General Surgery, The First Affiliated Hospital of Anhui Medical University, No. 218, Jixi Road, Shushan District, Hefei, Anhui, 230022, People’s Republic of ChinaTel +86-055162923887Email zlkgep@163.comBackground: Colorectal cancer (CRC) is one of the most common aggressive neoplasms worldwide. Circular RNAs (circRNAs) have been involved in the biological process of CRC. This study aimed to explore the effects of circ_0005927 on CRC progression and underneath mechanism.Materials and Methods: The expression of circ_0005927, microRNA-942-5p (miR-942-5p) and basic leucine zipper ATF-like transcription factor 2 (BATF2) was detected by quantitative real time polymerase chain reaction (qRT-PCR). The protein expression of BATF2 was determined by Western blot. The effects among circ_0005927, miR-942-5p and BATF2 on cell colony-forming ability, apoptosis and migratory and invasive abilities were revealed by cell colony formation, flow apoptosis and transwell assays, respectively. The associated relationship between miR-942-5p and circ_0005927 or BATF2 was predicted by Circinteractome or TargetScan online database, and identified by dual-luciferase reporter or RNA immunoprecipitation (RIP) assay. The impacts of circ_0005927 overexpression on tumor growth in vivo were investigated by in vivo tumor formation assay.Results: Circ_0005927 expression and the mRNA and protein expression of BATF2 were dramatically downregulated, while miR-942-5p expression was obviously upregulated in CRC tissues or cells compared with control groups. Circ_0005927 overexpression repressed cell colony-forming ability, migration and invasion, whereas induced cell apoptosis in CRC; however, these impacts were hindered by miR-942-5p mimic or BATF2 knockdown. Furthermore, circ_0005927 was a sponge of miR-942-5p, and miR-942-5p bound to BATF2. In addition, circ_0005927 overexpression repressed tumor growth in vivo.Conclusion: Circ_0005927 suppressed cell colony-forming ability, migration and invasion, and promoted cell apoptosis by sponging miR-942-5p to induce BATF2 in CRC. The possible mechanism provides a theoretical basis for the study of circRNA-directed therapy for CRC.Keywords: circular RNA, circ_0005927, miR-942-5p, BATF2, CRC

Haining Wang,1 Xiule Lin,1 Jilin Li,2 Guoning Zeng,1 Tan Xu1 1Department of Cardiovascular Medicine, The First Affiliated Hospital of Shantou University Medical College, Cardiac Care Unit (CCU), Shantou, Guangdong Province, 515041, People’s Republic of China; 2Department of Cardiovascular Medicine, The Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong Province, 515000, People’s Republic of ChinaCorrespondence: Haining WangDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Shantou University Medical College, CCU, Shantou City, Guangdong Province, 515041, People’s Republic of ChinaTel +86-(0754)88258290Email wg1424@163.comJilin LiDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong Province, 515000, People’s Republic of ChinaEmail xnjgbezpruec18@163.comBackground: Long non-coding RNAs (LncRNAs) play important roles in doxorubicin (DOX)-induced apoptosis of cardiomyocytes. However, the function of lncRNA SOX2-OT is unclear. This study was carried out to investigate the function of SOX2-OT in doxorubicin-induced cardiomyocyte apoptosis.Methods: qRT-PCR and immunoblotting were used to detect the expression levels of SOX2-OT, miR-942-5p and death protein-5 (DP5) in DOX-treated primary cardiomyocytes and rat models. The relationship among miR-942-5p, SOX2-OT, and DP5 was explored by luciferase reporter assay. The effects of SOX2-OT, miR-942-5p and DP5 on doxorubicin-induced cardiomyocyte apoptosis were evaluated by Annexin V-FITC/PI method and caspase-3 activity assay. The effect of SOX2-OT on cardiomyocyte apoptosis was analyzed by TUNEL staining and echocardiography.Results: SOX2-OT and DP5 were highly expressed, while miR-942-5p was down-regulated in DOX-treated primary cardiomyocytes and rat model. SOX2-OT can upregulate DP5 as a sponge of miR-942-5p, which was a direct target of miR-942-5p. In addition, miR-942-5p reversed the protective effect of knockdown of SOX2-OT on cardiomyocytes by inhibiting the expression of DP5 in vitro and in vivo.Conclusion: Knockdown of SOX2-OT down-regulated DP5 via sponging miR-942-5p and inhibiting DOX-induced apoptosis of primary cardiomyocytes.Keywords: lncRNA SOX2-OT, miR-942-5p, DP5, cardiomyocyte, apoptosis

Long noncoding RNAs (lncRNAs) act as essential regulators in cancer tumorigenesis. Our study aimed to explore the underlying mechanism of lncRNA human leukocyte antigen complex group 11 (HCG11) in cervical cancer (CC) progression. Long noncoding RNA HCG11 was downregulated in CC. Functional assays demonstrated that lncRNA HCG11 inhibited CC cell proliferation and invasion. Then, we confirmed that lncRNA HCG11 could directly bind to miR‐942‐5p. Moreover, inhibition of miR‐942‐5p suppressed the growth and invasion of CC cells, and growth factor‐independent transcription repressor 1 (GFI1) gene was the target gene of miR‐942‐5p. Long noncoding RNA HCG11 increased the expression of GFI1 and suppressed cell proliferation and invasion by acting as a miR‐942‐5p sponge. Finally, the overexpression of lncRNA HCG11 suppressed the proliferation and metastasis of CC cells in vivo., Long noncoding RNA human leukocyte antigen complex group 11 (HCG11) was downregulated in cervical cancer (CC). Long noncoding RNA HCG11 inhibited growth and invasion in CC by sponging miR‐942‐5p and targeting growth factor‐independent transcription repressor 1. The overexpression of lncRNA HCG11 suppressed the proliferation and invasion of CC cells in vivo.

Background Micro (mi)RNAs are small noncoding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression. This study investigated host miRNA activity in the innate immune response to Cryptosporidium parvum infection. Methods In vitro infection model adopts HCT-8 human ileocecal adenocarcinoma cells infected with C. parvum. The expression of miR-942-5p was estimated using quantitative real-time polymerase chain reaction (qPCR). The TLRs-NF-κB signaling was confirmed by qPCR, western blotting, TLR4- and TLR2-specific short-interfering (si)RNA, and NF-κB inhibition. Results HCT-8 cells express all known toll-like receptors (TLRs). Cryptosporidium parvum infection of cultured HCT-8 cells upregulated TLR2 and TLR4, and downstream TLR effectors, including NF-κB and suppressed IκBα (nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha). The expression of miR-942-5p was significantly upregulated at 4, 8, 12 and 24 h post-infection, and especially at 8 hpi. The results of TLR4- and TLR2-specific siRNA and NF-κB inhibition showed that upregulation of miR-942-5p was promoted by p65 subunit-dependent TLR2/TLR4-NF-κB pathway signaling. Conclusions miR-942-5p of HCT-8 cells was significantly upregulated after C. parvum infection, especially at 8 hpi, in response to a p65-dependent TLR2/TLR4-NF-κB signaling. TLR4 appeared to play a dominant role.

Background Resistance to gefitinib remains a major obstacle for the successful treatment of non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutations. In this paper, we studied the precise actions of circular RNA (circRNA) microtubule actin crosslinking factor 1 (circ_MACF1) in gefitinib resistance. Methods We established gefitinib-resistant NSCLC cells (PC9/GR and A549/GR). The levels of circ_MACF1, microRNA (miR)-942-5p, and transforming growth factor beta receptor 2 (TGFBR2) were gauged by quantitative real-time PCR (qRT-PCR) or western blot. Subcellular fractionation and Ribonuclease R (RNase R) assays were done to characterize circ_MACF1. Cell survival, proliferation, colony formation, apoptosis, migration, and invasion were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 5-Ethynyl-2’-Deoxyuridine (EdU), colony formation, flow cytometry, and transwell assays, respectively. Dual-luciferase reporter assays were used to verify the direct relationship between miR-942-5p and circ_MACF1 or TGFBR2. The xenograft assays were used to assess the role of circ_MACF1 in vivo. Results Circ_MACF1 was down-regulated in A549/GR and PC9/GR cells. Overexpression of circ_MACF1 repressed proliferation, migration, invasion, and promoted apoptosis and gefitinib sensitivity of A549/GR and PC9/GR cells in vitro, as well as inhibited tumor growth under gefitinib in vivo. Circ_MACF1 directly targeted miR-942-5p, and miR-942-5p mediated the regulatory effects of circ_MACF1. TGFBR2 was identified as a direct and functional target of miR-942-5p. Circ_MACF1 modulated TGFBR2 expression through miR-942-5p. Conclusion Our findings demonstrated that circ_MACF1 regulated cell functional behaviors and gefitinib sensitivity of A549/GR and PC9/GR cells at least partially by targeting miR-942-5p to induce TGFBR2 expression.

Statistics show that the prognosis of cervical cancer (CC) is poor, and the death rate of CC in advanced stage has been rising in recent years. Increasing evidence has demonstrated that circular RNAs (circRNAs) serve as promising biomarkers in human cancers, including CC. The present study planned to find out the circRNA involved in CC and to explore its regulatory mechanism in CC. We discovered the new circRNA, circ-0033550, upregulated in CC. Its associated gene was AKT (also known as protein kinase B) serine/threonine kinase 1 (AKT1), so we renamed circ-0033550 as circ-AKT1. We confirmed the high expression of circ-AKT1 in CC samples and cell lines, as well as the circle structure of circ-AKT1. Functionally, gain- and loss-of-function experiments indicated that circ-AKT1 and AKT1 promoted CC cell proliferation and invasion. Moreover, circ-AKT1 and AKT1 were induced by transforming growth factor beta (TGF-β) and facilitated EMT (epithelial-mesenchymal transition) in CC. Mechanically, we illustrated that circ-AKT1 upregulated AKT1 by sponging miR-942-5p. Rescue assays confirmed the role of the circ-AKT1/miR-942-5p/AKT1 axis in CC progression. In vivo assays validated that circ-AKT1 promoted tumor growth in CC. Overall, circRNA-AKT1 sequestered miR-942-5p to upregulate AKT1 and promote CC progression, which may offer a new molecular target for the treatment improvement of CC.

Long noncoding RNAs (lncRNAs) have emerged as key regulators of cell differentiation and development. However, potential roles for lncRNAs in chondrogenic differentiation have remained poorly understood. Here we identify lncRNA ADAMTS9 antisense RNA 2, ADAMTS9-AS2, which controls the chondrogenic differentiation by acting as a competing endogenous RNA (ceRNA) in human mesenchymal stem cells (hMSCs). We screen out ADAMTS9-AS2 of undifferentiated and differentiated cells during chondrogenic differentiation by microarrays. Suppression or overexpression of lncRNA ADAMTS9-AS2 correlates with inhibition and promotion of hMSC chondrogenic differentiation, respectively. We find that ADAMTS9-AS2 can sponge miR-942-5p to regulate the expression of Scrg1, a transcription factor promoting chondrogenic gene expression. Finally, we confirm the function of ADAMTS9-AS2 to cartilage repair in the absence of transforming growth factor β (TGF-β) in vivo. In conclusion, ADAMTS9-AS2 plays an important role in chondrogenic differentiation as a ceRNA, so that it can be regarded as a therapy target for cartilage repair. Keywords: LncRNA ADAMTS9-AS2, MiR-942-5p, chondrogenesis, hMSCs, cartilage regeneration, chondrogenic differentiation, cartilage defect

Circular RNAs (circRNAs) play prominent roles in regulating the progression of cancers. This study is aimed to decipher the role of hsa_circ_0000730 in cervical cancer (CC).The differentially expressed circRNAs of CC were screened out from the Gene Expression Omnibus database. qRT‐PCR was used to detect circ_0000730 expression in CC tissues and cell lines, and the Kaplan–Meier curve was adopted to figure out the relationship between circ_000730 expression and the overall survival time of CC patients. BrdU assay and Tanswell assay were utilized to examine the proliferation, migration, and invasion of CC cells. Western blot was adopted to detect PTEN protein expression. Bioinformatics analysis and dual‐luciferase reporter assay were used to examine the target relationship between miR‐942‐5p and circ_0000730 or PTEN, respectively.Circ_0000730 was among the differentially expressed circRNAs in CC. Circ_0000730 was significantly down‐regulated in the cancer tissues of 50 CC patients and CC cell lines. Additionally, underexpression of circ_0000730 was associated with the shorter survival time of CC patients. Gain‐ and loss‐of‐function assays highlighted that circ_0000730 significantly inhibited the proliferation, migration, and invasion of CC cells. Mechanistically, miR‐942‐5p was identified as a downstream target of circ_0000730, and circ_0000730 could positively regulate PTEN expression via repressing miR‐942‐5p in CC cells.Circ_0000730 inhibits the proliferation, migration, and invasion of CC cells via regulating miR‐942‐5p/PTEN axis. Circ_0000730 probably acts as a tumor suppressor in CC, and it may be a candidate target for the treatment of CC.

Background: Atherosclerosis (AS) is a typical inflammatory vascular disease. Many reports corroborated that circular RNAs (circRNAs) is involved in AS progression. However, the potential function and possible mechanism of circ_0003204 in AS progression remain indistinct.Methods: Expression level analysis was performed using qRT-PCR and western blot. Cell viability and apoptosis were determined using Cell Counting Kit-8 (CCK-8), flow cytometry, and western blot assays. The status of oxidative stress and inflammation was determined via commercial detection kits and ELISA assay, respectively. The binding relationship was verified via dual-luciferase reporter and RNA immunoprecipitation assays.Results: ox-LDL increased circ_0003204 and HDAC9 levels and decreased miR-942-5p level. Silencing of circ_0003204 enhanced cell viability and inhibited cell apoptosis, oxidative stress and inflammation in ox-LDL-disposed HUVECs. In addition, circ_0003204 targeted miR-942-5p to regulate ox-LDL-resulted HUVECs injury. Also, miR-942-5p affected ox-LDL-triggered HUVECs injury by targeting HDAC9. Furthermore, circ_0003204 elevated HDAC9 expression via decoying miR-942-5p.Conclusion: circ_0003204 aggravated ox-LDL-induced HUVECs damage via modulating miR-942-5p/HDAC9 pathway.

Haining Wang,1 Xiule Lin,1 Jilin Li,2 Guoning Zeng,1 Tan Xu1 1Department of Cardiovascular Medicine, The First Affiliated Hospital of Shantou University Medical College, Cardiac Care Unit (CCU), Shantou, Guangdong Province, 515041, People’s Republic of China; 2Department of Cardiovascular Medicine, The Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong Province, 515000, People’s Republic of ChinaCorrespondence: Haining WangDepartment of Cardiovascular Medicine, The First Affiliated Hospital of Shantou University Medical College, CCU, Shantou City, Guangdong Province, 515041, People’s Republic of ChinaTel +86-(0754)88258290Email wg1424@163.comJilin LiDepartment of Cardiovascular Medicine, The Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong Province, 515000, People’s Republic of ChinaEmail xnjgbezpruec18@163.comBackground: Long non-coding RNAs (LncRNAs) play important roles in doxorubicin (DOX)-induced apoptosis of cardiomyocytes. However, the function of lncRNA SOX2-OT is unclear. This study was carried out to investigate the function of SOX2-OT in doxorubicin-induced cardiomyocyte apoptosis.Methods: qRT-PCR and immunoblotting were used to detect the expression levels of SOX2-OT, miR-942-5p and death protein-5 (DP5) in DOX-treated primary cardiomyocytes and rat models. The relationship among miR-942-5p, SOX2-OT, and DP5 was explored by luciferase reporter assay. The effects of SOX2-OT, miR-942-5p and DP5 on doxorubicin-induced cardiomyocyte apoptosis were evaluated by Annexin V-FITC/PI method and caspase-3 activity assay. The effect of SOX2-OT on cardiomyocyte apoptosis was analyzed by TUNEL staining and echocardiography.Results: SOX2-OT and DP5 were highly expressed, while miR-942-5p was down-regulated in DOX-treated primary cardiomyocytes and rat model. SOX2-OT can upregulate DP5 as a sponge of miR-942-5p, which was a direct target of miR-942-5p. In addition, miR-942-5p reversed the protective effect of knockdown of SOX2-OT on cardiomyocytes by inhibiting the expression of DP5 in vitro and in vivo.Conclusion: Knockdown of SOX2-OT down-regulated DP5 via sponging miR-942-5p and inhibiting DOX-induced apoptosis of primary cardiomyocytes.Keywords: lncRNA SOX2-OT, miR-942-5p, DP5, cardiomyocyte, apoptosis

Chao Yu,* Deguan Li,* Qiang Yan, Yigao Wang, Xiaodong Yang, Shangxin Zhang, Yonghong Zhang, Zhen Zhang Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, People’s Republic of China*These authors contributed equally to this workCorrespondence: Zhen ZhangDepartment of General Surgery, The First Affiliated Hospital of Anhui Medical University, No. 218, Jixi Road, Shushan District, Hefei, Anhui, 230022, People’s Republic of ChinaTel +86-055162923887Email zlkgep@163.comBackground: Colorectal cancer (CRC) is one of the most common aggressive neoplasms worldwide. Circular RNAs (circRNAs) have been involved in the biological process of CRC. This study aimed to explore the effects of circ_0005927 on CRC progression and underneath mechanism.Materials and Methods: The expression of circ_0005927, microRNA-942-5p (miR-942-5p) and basic leucine zipper ATF-like transcription factor 2 (BATF2) was detected by quantitative real time polymerase chain reaction (qRT-PCR). The protein expression of BATF2 was determined by Western blot. The effects among circ_0005927, miR-942-5p and BATF2 on cell colony-forming ability, apoptosis and migratory and invasive abilities were revealed by cell colony formation, flow apoptosis and transwell assays, respectively. The associated relationship between miR-942-5p and circ_0005927 or BATF2 was predicted by Circinteractome or TargetScan online database, and identified by dual-luciferase reporter or RNA immunoprecipitation (RIP) assay. The impacts of circ_0005927 overexpression on tumor growth in vivo were investigated by in vivo tumor formation assay.Results: Circ_0005927 expression and the mRNA and protein expression of BATF2 were dramatically downregulated, while miR-942-5p expression was obviously upregulated in CRC tissues or cells compared with control groups. Circ_0005927 overexpression repressed cell colony-forming ability, migration and invasion, whereas induced cell apoptosis in CRC; however, these impacts were hindered by miR-942-5p mimic or BATF2 knockdown. Furthermore, circ_0005927 was a sponge of miR-942-5p, and miR-942-5p bound to BATF2. In addition, circ_0005927 overexpression repressed tumor growth in vivo.Conclusion: Circ_0005927 suppressed cell colony-forming ability, migration and invasion, and promoted cell apoptosis by sponging miR-942-5p to induce BATF2 in CRC. The possible mechanism provides a theoretical basis for the study of circRNA-directed therapy for CRC.Keywords: circular RNA, circ_0005927, miR-942-5p, BATF2, CRC

Background Ovarian cancer (OC) is the gynecologic cancer with the highest mortality. Circular RNAs (circRNAs) play a vital role in the development and progression of cancer. This study aimed to explore the potential role of circ_0015756 in OC and its molecular mechanism. Methods The levels of circ_0015756, microRNA-942-5p (miR-942-5p) and Cullin 4B (CUL4B) were determined by quantitative real-time PCR (qRT-PCR) or Western blot assay. Cell proliferation, apoptosis, migration and invasion were assessed by Cell Counting Kit-8 (CCK-8), colony formation assay, flow cytometry and transwell assay. The levels of proliferation-related and metastasis-related proteins were measured by Western blot assay. The relationship between miR-942-5p and circ_0015756 or CUL4B was verified by dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. Xenograft assay was used to analyze tumor growth in vivo. Results Circ_0015756 and CUL4B levels were increased, while miR-942-5p level was decreased in OC tissues and cells. Depletion of circ_0015756 suppressed proliferation, migration and invasion and promoted apoptosis in OC cells. Down-regulation of circ_0015756 hindered OC cell progression via modulating miR-942-5p. Also, up-regulation of miR-942-5p impeded OC cell development by targeting CUL4B. Mechanistically, circ_0015756 up-regulated CUL4B via sponging miR-942-5p. Moreover, circ_0015756 silencing inhibited tumor growth in vivo. Conclusion Knockdown of circ_0015756 suppressed OC progression via regulating miR-942-5p/CUL4B axis, suggesting that circ_0015756 might be a potential therapeutic target for ovarian cancer.

Background MicroRNA 942-5p (miR-942-5p) has been reported to promote migration and invasion in non-small cell lung cancer (NSCLC), but the underlying mechanism is not completely understood. The interplay between long non-coding RNAs (lncRNAs) and miRNAs plays a crucial role in tumor progression. Methods In the present study, we performed bioinformatic and biochemical analyses to identify miR-942-5p-interacting lncRNAs. The function and clinical significance of the candidate lncRNA(s) in NSCLC were determined. Results We identified LIFR-AS1 as a pivotal miR-942-5p-interacting lncRNA. Overexpression of miR-942-5p caused a reduction of LIFR-AS1 in NSCLC cells. LIFR-AS1 showed the ability to sponge miR-942-5p, leading to derepression of ZNF471. Functionally, LIFR-AS1 overexpression inhibited NSCLC cell migration and invasion, whereas LIFR-AS1 silencing yielded an opposite effect. In vivo studies confirmed that LIFR-AS1 overexpression suppressed lung metastasis of NSCLC cells. Rescue experiments demonstrated that enforced expression of miR-942-5p or depletion of ZNF471 restored the migration and invasion capacity of LIFR-AS1-overexpressing cells. Moreover, overexpression of ZNF471 restrained NSCLC cell invasion. Clinically, LIFR-AS1 downregulation was significantly correlated with TNM stage, lymph node metastasis, and reduced overall survival in NSCLC patients. Conclusions we provide first evidence for the involvement of the LIFR-AS1/miR-942-5p/ZNF471 axis in NSCLC invasion and metastasis. LIFR-AS1 may represent a novel target for the treatment of NSCLC.