LncRNA FGF14‐AS2 represses growth of prostate carcinoma cells via modulating miR‐96‐5p/AJAP1 axis

ObjectiveThis investigation devoted to lncRNA FGF14 antisense RNA 2 (FGF14‐AS2) in prostate carcinoma progression.MethodsThe levels of lncRNA FGF14‐AS2, miR‐96‐5p, and Adherens junction‐associated protein‐1 (AJAP1) in prostate carcinoma were tested by Western blot and qRT‐PCR. How these two genes interacted was confirmed by RNA immunoprecipitation and dualluciferase gene methods. The effect of FGF14‐AS2/miR‐96‐5p/AJAP1 axis in prostate carcinoma progression was determined by MTT, Transwell, and nude mice tumor model.ResultsFGF14‐AS2 was a downregulated lncRNA in prostate carcinoma tissue and cells. FGF14‐AS2 could restrain miR‐96‐5p expression while miR‐96‐5p hampered AJAP1. FGF14‐AS2 could effectively decrease the biological behaviors of prostate carcinoma cells, while knock‐down of FGF14‐AS2 triggered opposite results. Moreover, miR‐96‐5p mimic presented a cancer promoter role in prostate carcinoma cells. AJAP1 expression level could affect levels of proteins related to epithelial‐mesenchymal transition. In vivo experiment suggested that overexpressing FGF14‐AS2 could reverse the promotion of silenced AJAP1 on prostate carcinoma cell metastasis, thus to inhibit tumor growth.ConclusionlncRNA FGF14‐AS2 was a downregulated lncRNA in prostate carcinoma and influenced cell proliferation and metastasis. The influence relied on modulating miR‐96‐5p and its target gene AJAP1.     

LncRNA PITPNA‐AS1/miR‐223‐3p/PTN axis regulates malignant progression and stemness in lung squamous cell carcinoma

BackgroundLong noncoding RNAs (lncRNAs) are a kind of molecule that cannot code proteins, and their expression is dysregulated in diversified cancers. LncRNA PITPNA‐AS1 has been shown to act as a tumor promoter in a variety of malignancies, but its function and regulatory mechanisms in lung squamous cell carcinoma (LUSC) are yet unknown.MethodsThe mRNA and protein expression of genes were examined by RT‐qPCR, western blot, and IHC assay. The cell proliferation, migration, invasion, and stemness were detected through CCK‐8, colony formation, Transwell and spheroid formation assays. The CD44⁺ and CD166⁺‐positive cells were detected through flow cytometry. The binding ability among genes through luciferase reporter and RNA pull‐down assays. The tumor growth was detected through in vivo nude mice assay.ResultsThe lncRNA PITPNA‐AS1 had increased expression in LUSC and was linked to a poor prognosis. In LUSC, PITPNA‐AS1 also enhanced cell proliferation, migration, invasion, and stemness. This mechanistic investigation showed that PITPNA‐AS1 absorbed miR‐223‐3p and that miR‐223‐3p targeted PTN. MiR‐223‐3p inhibition or PTN overexpression might reverse the inhibitory effects of PITPNA‐AS1 suppression on LUSC progression, as demonstrated by rescue experiments. In addition, the PITPNA‐AS1/miR‐223‐3p/PTN axis accelerated tumor development in vivo.ConclusionsIt is the first time we investigated the potential role and ceRNA regulatory mechanism of PITPNA‐AS1 in LUSC. The data disclosed that PITPNA‐AS1 upregulated PTN through sponging miR‐223‐3p to enhance the onset and progression of LUSC. These findings suggested the ceRNA axis may serve as a promising therapeutic biomarker for LUSC patients.     

Circ_0000463 contributes to the progression and glutamine metabolism of non‐small‐cell lung cancer by targeting miR‐924/SLC1A5 signaling

BackgroundCircular RNAs (circRNAs) have shown pivotal regulatory roles in the pathology of non‐small cell lung cancer (NSCLC). However, the role of circ_0000463 in NSCLC progression and its associated molecular mechanism remain to be illustrated.MethodsCell proliferation ability was analyzed by colony formation assay and 5‐ethynyl‐2’‐deoxyuridine (EdU) assay. Cell migration and invasion abilities were assessed by scratch test and transwell invasion assay. Flow cytometry was employed to analyze cell apoptotic rate. The interaction between microRNA‐924 (miR‐924) and circ_0000463 or solute carrier family 1 member 5 (SLC1A5) was confirmed by dual‐luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The uptake of glutamine and the production of glutamate and α‐ketoglutarate were analyzed using their corresponding kits. Xenograft model in vivo was established to analyze the role of circ_0000463 in tumor growth.ResultsCirc_0000463 expression was elevated in NSCLC tissues and cell lines. Circ_0000463 knockdown suppressed the proliferation, migration, and invasion and promoted the apoptosis of NSCLC cells. Circ_0000463 acted as a molecular sponge for miR‐924, and circ_0000463 interference‐mediated anti‐tumor effects were largely reversed by the silence of miR‐924 in NSCLC cells. miR‐924 interacted with the 3’ untranslated region (3’UTR) of SLC1A5, and SLC1A5 overexpression largely overturned miR‐924 overexpression‐mediated anti‐tumor effects in NSCLC cells. Moreover, circ_0000463 absence suppressed the glutamine metabolism of NSCLC cells by targeting miR‐924/SLC1A5 axis. Circ_0000463 knockdown suppressed xenograft tumor growth in vivo.ConclusionCirc_0000463 absence suppressed the malignant behaviors and glutamine metabolism of NSCLC cells through mediating miR‐924/SLC1A5 axis.     

Circ_SAR1A regulates the malignant behavior of lung cancer cells via the miR‐21‐5p/TXNIP axis

BackgroundLung cancer is one of the most common malignancies globally and a significant component of cancer‐related deaths. The lack of early diagnosis accounts for detecting approximately 75% of cancer patients at an intermediate to an advanced stage, with a low 5‐year survival rate. Therefore, a more comprehensive understanding of the molecular mechanisms of lung cancer development is necessary to find reliable and effective therapeutic and diagnostic biomarkers.Methodscirc_SAR1A, miR‐21‐5p, and TXNIP in lung cancer tissues, animal xenografts, and cell lines were validated by qRT‐PCR and western blotting analyses. RNase R digestion and nuclear/cytoplasm fractionation experiments were utilized to determine the stability and localization of circ_SAR1A in lung cancer cells. The binding between miR‐21‐5p and circ_SAR1A or TXNIP was confirmed by luciferase reporter, RNA pull‐down, Spearman''s correlation, and rescue assays. CCK‐8, colony formation, flow cytometry, Transwell, and western blotting were utilized to illustrate the malignant behavior of lung cancer cells.Resultscirc_SAR1A and TXNIP were down‐regulated while miR‐21‐5p was up‐regulated in lung cancer samples and cells. circ_SAR1A was located predominantly in the cytoplasm; it inhibited lung cancer growth in vitro and in vivo by sponging to miR‐21‐5p. miR‐21‐5p silencing suppressed lung cancer malignancy by targeting TXNIP.Conclusionscirc_SAR1A is a critical negative regulator of lung carcinogenesis. circ_SAR1A/miR‐21‐5p/TXNIP attenuation inhibited lung cancer progression, presenting an ideal diagnostic and a potential therapeutic target.     

Hsa_circ_0007142 contributes to cisplatin resistance in esophageal squamous cell carcinoma via miR‐494‐3p/LASP1 axis

BackgroundChemoresistance is one of the major obstacles for tumor treatment. Circular RNAs (circRNAs) have been confirmed to play vital roles in chemoresistance of cancer, including esophageal squamous cell carcinoma (ESCC). We investigated the roles and mechanisms of circ_0007142 in cisplatin (DDP) resistance of ESCC.MethodsQuantitative real‐time polymerase chain reaction (qRT‐PCR) was conducted to determine the levels of circ_0007142, DOCK1 mRNA, microRNA‐494‐3p (miR‐494‐3p) and LIM And SH3 Protein 1 (LASP1) mRNA. RNase R assay was conducted to analyze the characteristic of circ_0007142. Cell Counting Kit‐8 (CCK‐8) assay was performed to evaluate IC50 of DDP. Flow cytometry analysis, 5‐ethynyl‐2’‐deoxyuridine (EdU) assay and transwell assay were carried out to examine cell apoptosis, proliferation and invasion, respectively. Dual‐luciferase reporter assay was employed to verify the association between miR‐494‐3p and circ_0007142 or LASP1. Murine xenograft assay was conducted to investigate the role of circ_0007142 in DDP resistant in vivo. The protein level of LASP1 in tumors was measured by Immunohistochemistry (IHC) analysis.ResultsCirc_0007142 was upregulated in DDP‐resistant ESCC tissues and cells. Circ_0007142 knockdown improved DDP sensitivity, induced cell apoptosis and hampered cell proliferation and invasion in DDP‐resistant ESCC cells. Circ_0007142 functioned as the sponge for miR‐494‐3p and miR‐494‐3p inhibition reversed the impacts of circ_0007142 knockdown on DDP resistance, cell apoptosis, proliferation, and invasion. LASP1 was a target of miR‐494‐3p, and the effects on DDP resistance, cell apoptosis, growth, and invasion mediated by LASP1 downregulation were rescued by miR‐494‐3p inhibition. Moreover, circ_0007142 knockdown enhanced DDP sensitivity in vivo.ConclusionCirc_0007142 improved DDP resistance of ESCC by upregulating LASP1 via sponging miR‐494‐3p.     

Hsa_circRNA_0001971 contributes to oral squamous cell carcinoma progression via miR‐186‐5p/Fibronectin type III domain containing 3B axis

BackgroundCircular RNAs (circRNAs) are closely associated with the progression of oral squamous cell carcinoma (OSCC). circRNA_0001971 has been proved to accelerate the OSCC development. Here, we aim to identify the new molecular mechanism of hsa_circRNA_0001971 (circRNA_0001971) in OSCC.MethodsThe levels of circRNA_0001971, miR‐186‐5p, and fibronectin type III domain containing 3B (FNDC3B) in tissues and cells were verified by qRT‐PCR or Western blotting. The interaction between circRNA_0001971, miR‐186‐5p, and FNDC3B was identified by bioinformatics analysis, luciferase assay, and RIP assay. The effect of circRNA_0001971/miR‐186‐5p/FNDC3B axis on OSCC cell proliferation, migration, and invasion by cell functional experiments including CCK8, wound healing, and transwell assays.ResultsOur study displayed that circRNA_0001971 and FNDC3B were elevated in OSCC, whereas miR‐186‐5p was declined in OSCC. Silencing circRNA_0001971 attenuated the malignancy of OSCC cells by suppressing proliferation, migration, and invasion. In OSCC cells, circRNA_0001971 sponged miR‐186‐5p to enhance FNDC3B. Due to the interaction between circRNA_0001971, miR‐186‐5p, and FNDC3B, FNDC3B overexpression relieved the negative function of silencing circRNA_0001971 in OSCC cells.ConclusionOverall, our study discovered that circRNA_0001971 was a tumor promoter in OSCC progression by targeting miR‐186‐5p/FNDC3B axis.     

The role of AURKA/miR‐199b‐3p in hepatocellular carcinoma cells

BackgroundPrevious studies proved that AURKA functions as an oncogene in several cancers. This article aimed to probe the miRNA‐induced regulatory mechanism of AURKA in hepatocellular carcinoma (HCC).MethodsDifferentially expressed genes in TCGA‐LIHC dataset were screened by bioinformatics methods. Levels of miR‐199b‐3p and AURKA mRNA were examined by qRT‐PCR. Western blot was utilized to evaluate protein levels of AURKA, p‐AKT, and AKT. Dual‐luciferase assay was introduced to explore their interaction. MTT, colony formation, scratch healing, transwell, and flow cytometry assays were introduced into cell proliferation, migration, invasion, and apoptosis assessment. The impact of miR‐199b‐3p/AURKA axis on HCC tumor growth was determined in a tumor xenograft model.ResultsWe found that AURKA was highly expressed in HCC and was coupled to poor prognosis of HCC. As manifested by cellular assays, compared to the normal cells HL‐7702, AURKA presented notably high expression in HCC cell lines. Overexpressed AURKA evidently impelled the proliferation, colony formation, migration, and invasion of HCC cells while suppressing apoptosis. The regulatory gene upstream of AURKA was predicted to be miR‐199b‐3p by bioinformatics method, and there was a markedly negative correlation between the two. Overexpressed miR‐199b‐3p constrained HCC cell proliferation, migration, and invasion while fostering apoptosis, which could be counteracted by upregulating AURKA. MiR‐199b‐3p repressed the tumor growth in vivo by targeting AURKA and affected PI3K/AKT signaling pathway.ConclusionTo summarize, this study implied the regulatory mechanism of miR‐199b‐3p/AURKA axis in HCC, and supplied optional therapeutic targets for HCC patients.     

Hsa_circ_0005100 regulates tumorigenicity of colorectal carcinoma via miR‐145‐5p/ MACC1 axis

BackgroundCircular RNAs (circRNAs) are a kind of RNA molecules involved in the regulation of cancer progression, including colorectal carcinoma (CRC); nevertheless, their regulation mode is blurry. In the present work, we attempted to reveal the characteristics of hsa_hsa_circ_0005100 in CRC.MethodsDifferential expressions of hsa_circ_0005100, FMN2 mRNA, microRNA‐145‐5p (miR‐145‐5p), and MACC1 were indicated by qRT‐PCR and Western blot. The capacities of cell growth and motility were validated by the MTT assay, flow cytometry assay, EdU assay, colony formation assay, and transwell assay. Moreover, the targeted relationship of miR‐145‐5p and hsa_circ_0005100 or MACC1 was distinguished by dual‐luciferase reporter assay. The animal experiment was implemented to confirm the influence of hsa_circ_0005100 on tumorigenesis in vivo.ResultsHsa_circ_0005100 and MACC1 expression levels were increased, but miR‐145‐5p expression level was diminished in CRC. Hsa_circ_0005100 knockdown repressed cell proliferation, cell cycle, migration, and invasion, while expedited cell apoptosis in CRC cells. Furthermore, miR‐145‐5p was disclosed to block CRC via overturning MACC1. Hsa_circ_0005100 targeted miR‐145‐5p to modulate MACC1. Additionally, hsa_circ_0005100 knockdown also attenuated tumorigenesis in vivo.ConclusionHsa_circ_0005100 was a vital regulator in the development of CRC by miR‐145‐5p/MACC1 axis, which deepened the understanding of CRC pathogenesis from circRNA insights.     

Hsa_circ_0001806 promotes glycolysis and cell progression in hepatocellular carcinoma through miR‐125b/HK2

ObjectiveHepatocellular carcinoma (HCC) is one of the most common malignant tumours and a leading cause of cancer death. Circular RNA (circRNA) has been demonstrated to play an important role in regulating tumour development. The current study aims to explore the specific role of hsa_circ_0001806 during HCC progression.MethodsThe expression of hsa_circ_0001806 in HCC tissues and cells was measured through qRT‐PCR. Cell proliferation, apoptosis and migration were measured using CCK‐8 and Annexin V/PI staining kits, and Transwell assay. Bioinformatics prediction and dual‐luciferase reporter assay were adopted to explore the mechanism underlying the cell function of hsa_circ_0001806 in HCC cells. In addition, glycolysis was assessed by measuring the glucose uptake, lactate production and ATP level using a glucose assay kit, fluorometric lactate assay kit and ATP detection assay kit.ResultsHsa_circ_0001806 was up‐regulated in HCC tissues and cells and positively associated with the advanced TNM stage, metastasis and poor overall survival. The overexpression of hsa_circ_0001806 promoted HCC cell proliferation, migration and glycolysis and inhibited cell apoptosis, while the silence of hsa_circ_0001806 showed an opposite effect. Furthermore, hsa_circ_0001806 acted as a sponge of miR‐125b to up‐regulate hexokinase II (HK2) expression. In addition, the inhibition of miR‐125b and HK2 overexpression partly reversed the inhibitory effect of hsa_circ_0001806 silencing on HCC cell proliferation, migration and glycolysis.ConclusionThe inhibition of hsa_circ_0001806 suppressed HCC cell proliferation, migration and glycolysis through mediating miR‐125b/HK2 axis.     

LncRNA LIFR‐AS1 overexpression suppressed the progression of serous ovarian carcinoma

BackgroundSerous ovarian carcinoma (SOC) is a common malignant tumor in female reproductive system. Long noncoding RNA (lncRNA) LIFR‐AS1 is a tumor suppressor gene in colorectal cancer, but its effect and underlying mechanism in SOC are still unclear. Therefore, this study focuses on unveiling the regulatory mechanism of LIFR‐AS1 in SOC.MethodsThe relationship between LIFR‐AS1 expression and prognosis of SOC patients was analyzed by TCGA database and Starbase, and then, the LIFR‐AS1 expression in SOC tissues and cells was detected by quantitative real‐time PCR (qRT‐PCR) and in situ hybridization (ISH). Besides, the relationship between LIFR‐AS1 and clinical characteristics was analyzed. Also, the effects of LIFR‐AS1 on the biological behaviors of SOC cells were measured by Cell Counting Kit‐8, colony formation, and wound‐healing and Transwell assays, respectively. Western blot and qRT‐PCR were employed to determine the protein expressions of genes related to proliferation (PCNA), apoptosis (cleaved caspase‐3), epithelial‐mesenchymal transition (E‐cadherin, N‐cadherin, and Snail).ResultsLIFR‐AS1 was lowly expressed in SOC, which was correlated with the poor prognosis of SOC patients. Low expression of LIFR‐AS1 in SOC was associated with the tumor size, clinical stage, lymph node metastasis, and distant metastasis. LIFR‐AS1 overexpression promoted the expressions of cleaved caspase‐3 and E‐cadherin while suppressing the malignant behaviors (proliferation, migration, and invasion) of SOC cells, the expressions of PCNA, N‐cadherin, and Snail. Besides, silencing LIFR‐AS1 exerted the effects opposite to overexpressed LIFR‐AS1.ConclusionLIFR‐AS1 overexpression inhibits biological behaviors of SOC cells, which may be a new therapeutic method.     

LncRNA LINC00534 regulates cell proliferation and migration via the miR‐494‐3p/PTEN axis in HTR‐8/SVneo cells

BackgroundLncRNA LINC00534 has been found to be differentially expressed in placental tissue samples of preeclampsia (PE), but the exact mechanism is still unclear.MethodsIn vitro assays were carried out in HTR‐8/SVneo cells using various methods, including cell counting kit‐8 (CCK‐8), transwells, flow cytometry, and Western blotting (WB) and quantitative polymerase chain reaction. RNA pull‐down and bioinformatics analysis were applied to examine other potential underlying mechanisms involved.ResultsWe found that there was a high expression of LINC00534 in the placental tissues of patients with PE. LINC00534 overexpression (OE) significantly inhibited cell proliferation and migration as well as accelerated cell apoptosis in HTR8/SVneo cells. The knockdown of LINC00534 produced an opposite trend. Mechanistically, LINC00534 promoted the expressions of PTEN (Phosphatase and tensin homolog) through decreasing miR‐494‐3p. Further rescue studies showed that LINC00534 played a role by targeting mir‐494‐3p, which controlled the growth and migration of HTR‐8/SVneo trophoblast cells via regulating PTEN/PI3K/AKT (Phosphatidylinositol3‐kinase/protein kinase B). Moreover, lncRNA pull‐down assay identified 198 potential bound proteins for LINC00534. Those proteins were mostly involved in RNA processing and modification, posttranslational modification, protein turnover, and chaperones.ConclusionOverall, by suppressing HTR8/SVneo cell growth and migration via the miR‐494‐3p/PTEN axis and other mechanisms, LINC00534 offers new insight into PE pathogenesis.     

Hsa_circ_0050102 regulates the pancreatic cancer development via miR‐218‐5p/PPME1 axis

BackgroundPancreatic cancer (PC) is a malignancy worldwide. Circular RNAs (circRNAs) affects the growth of PC, nonetheless the mechanism is blurry. Here, we reconnoitered the parts of hsa_circ_0050102 in PC.MethodsHsa_circ_0050102, microRNA‐218‐5p (miR‐218‐5p) and protein phosphatase methylesterase 1 (PPME1) abundances were indicated by quantitative RT‐PCR or Western blot. Moreover, the cell functions were uncovered. Additionally, the relation of miR‐218‐5p and hsa_circ_0050102 or PPME1 was identified by dual‐luciferase reporter assay. Ultimately, the mice teats were utilized to quantity the part of hsa_circ_0050102.ResultsHsa_circ_0050102 and PPME1 contents were increased, and the miR‐218‐5p was dwindled in PC. Hsa_circ_0050102 lack subdued cell vitality, colony formation, cell migration and invasion, and angiogenesis, but endorsed cell apoptosis in PC cells. Furthermore, miR‐218‐5p was established to block the development of PC cells via PPME1. Hsa_circ_0050102 bound to miR‐218‐5p to adjust the content of PPME1.ConclusionHsa_circ_0050102 expedited the expansion of PC through growing PPME1 abundance by adjusting miR‐218‐5p.     

LncRNA SNHG1 promotes renal cell carcinoma progression through regulation of HMGA2 via sponging miR‐103a

BackgroundLong noncoding RNAs (LncRNAs) plays a vital role in tumorigenesis and development. The molecular mechanism of SNHG1 in renal cell carcinoma (RCC) has not been illustrated. The aim of this research was to explore the expression and function of LncRNA SNHG1 in RCC.Material and MethodsThe expression of SNHG1 in clinical tissues and RCC cell lines was detected. Luciferase reporter assay was performed to verify the correlation between SNHG1, miR‐103a, and HMGA2. CCK‐8 assay was performed to examine cell viability. Cell apoptosis was analyzed using flow cytometry. Cell invasion capacity was determined by Transwell assays. The protein level of HMGA2 was analyzed by Western blotting.ResultsThe expression of SNHG1 markedly increased in RCC tissues and cell lines. Subsequent studies identified SNHG1 as a miRNA sponge for miR‐103a. In addition, SNHG1 knockdown and miR‐103a overexpression significantly inhibited progression of RCC. miR‐103a also regulated HMGA2 levels.ConclusionOur findings showed that SNHG1 was upregulated in RCC cells and tissues. SNHG1 promoted the malignant characteristics of RCC cells. Its regulatory effect may be regulation of HMGA2 by sponging miR‐103a. Therefore, Our study facilitates the understanding of SNHG1 function in RCC.     

LncRNA TUG1 functions as a ceRNA for miR‐1‐3p to promote cell proliferation in hepatic carcinogenesis

BackgroundHepatocellular carcinoma (HCC) is characterised by high malignancy, metastasis and recurrence, but the specific mechanism that drives these outcomes is unclear. Recent studies have shown that long noncoding RNAs (lncRNAs) can regulate the proliferation and apoptosis of hepatic cells.MethodsWe searched for lncRNAs and microRNAs (miRNAs), which can regulate IGF1 expression, through a bioinformatics website, and predicted that lncRNA taurine‐upregulated gene 1 (TUG1) would have multiple targets for miR‐1‐3p binding, meaning that lncRNA TUG1 played an adsorption role. A double luciferase assay was used to verify the targeting relationship between lncRNA TUG1 and miR‐1‐3p. Western blotting and qPCR were used to verify the targeting relationship between miR‐1‐3p and IGF1, and qPCR was used to verify the regulatory relationship between the lncRNA TUG1‐miR‐1‐3p‐IGF1 axis. CCK‐8 was used to detect the growth activity of miRNA‐transfected L‐O2 cells, and flow cytometry was used to detect cell cycle changes and apoptosis.ResultThe proliferation cycle of L‐O2 cells transfected with miR‐1‐3p mimics was significantly slowed. Flow cytometry showed that the proliferation of L‐O2 cells was slowed, and the apoptosis rate was increased. In contrast, when L‐O2 cells were transfected with miR‐1‐3p inhibitor, the expression of IGF1 was significantly upregulated, and the cell proliferation cycle was significantly accelerated. Flow cytometry showed that the cell proliferation rate was accelerated, and the apoptosis rate was reduced.ConclusionLncRNA TUG1 can adsorb miR‐1‐3p as a competitive endogenous RNA (ceRNA) to promote the expression of IGF1 and promote cell proliferation in hepatic carcinogenesis.     

Hsa_circ_0002082 up‐regulates Centromere Protein F via abolishing miR‐508‐3p to promote breast cancer progression

BackgroundCircular RNAs (circRNAs) dysregulation has been revealed to function in the pathological processes of cancers. Herein, the role and mechanisms of hsa_circ_0002082 in breast cancer (BC) progression were elucidated.MethodsIn vivo and in vitro functional experiments were conducted, and the interaction between miR‐508‐3p and hsa_circ_0002082 or Centromere Protein F (CENPF) was elucidated.ResultsHsa_circ_0002082 expression was higher in BC tissues and cell lines. Functionally, knockdown of hsa_circ_0002082 induced apoptosis and suppressed proliferation and metastasis in BC cells in vitro. Mechanistically, hsa_circ_0002082 targeted miR‐508‐3p, which was confirmed to be decreased in BC. MiR‐508‐3p overexpression suppressed BC cell malignant phenotypes, moreover, inhibition of miR‐508‐3p attenuated the anticancer action of hsa_circ_0002082 silencing on BC cells. Besides that, miR‐508‐3p targeted CENPF, CENPF was highly expressed in BC, CENPF up‐regulation reversed the suppressive impacts of miR‐508‐3p on BC cell growth and metastasis. Besides, hsa_circ_0002082 silencing impeded BC growth in nude mice.ConclusionKnockdown of hsa_circ_0002082 suppresses breast cancer growth and metastasis by miR‐508‐3p/CENPF axis, suggesting that hsa_circ_0002082 may be a promising target for breast cancer treatment.