Long noncoding RNA LINC01615 promotes keloid development via sponging miR-590-3p to regulate FGF2 expression

Abstract Background A keloid is a benign human skin tumor that resulted by fibrous overgrowths during wound healing. Long noncoding RNAs (lncRNAs) are indicated to involve in the development of keloid. However, the role of lncRNA LINC01615 in regulating keloid development and the underlying mechanism are still unknown. Methods The expression levels of LINC01615, miR-590-3p and fibroblast growth factor 2 (FGF2) mRNA were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of apoptosis-related proteins, α-smooth muscle actin (α-SMA), collagens and FGF2 were measured by western blot. The effect of LINC01615 on keloid development was assessed by cell proliferation, apoptosis and collagen deposition of keloid fibroblasts which were determined by Cell Counting Kit-8 (CCK-8), flow cytometry assay and the protein levels of collagens, respectively. The relationships between LINC01615 and miR-590-3p, miR-590-3p and FGF2 were predicated by online software and confirmed by dual-luciferase reporter assay and RNA pull-down assay. Results We first found that LINC01615 was upregulated in keloid tissues and fibroblasts, and LINC01615 promoted cell proliferation and collagen deposition and suppressed apoptosis in keloid fibroblasts. LINC01615 targeted miR-590-3p and downregulated miR-590-3p expression, and overexpression of miR-590-3p inhibited the development of keloid. Then, FGF2 was identified as a target of miR-590-3p. LINC01615 facilitated keloid development via regulating FGF2 expression through miR-590-3p. Conclusion Our study demonstrated that LINC01615 contributed to keloid development via the miR-590-3p/FGF2 axis.

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Knockdown of long noncoding RNA HOTAIR inhibits osteoarthritis chondrocyte injury by miR-107/CXCL12 axis

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-021-02547-7 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Jipeng Lu ◽

Zhongxiong Wu ◽

Ying Xiong

Keyword(s):

Cell Proliferation ◽

Western Blot ◽

Cell Apoptosis ◽

Noncoding Rna ◽

Underlying Mechanism ◽

Joint Disease ◽

Cell Counting ◽

Luciferase Reporter ◽

Cxcl12 Expression ◽

Ecm Degradation

Abstract Background Osteoarthritis (OA) is a joint disease characterized via destruction of cartilage. Chondrocyte damage is associated with cartilage destruction during OA. Long noncoding RNAs (lncRNAs) are implicated in the regulation of chondrocyte damage in OA progression. This study aims to investigate the role and underlying mechanism of lncRNA homeobox antisense intergenic RNA (HOTAIR) in OA chondrocyte injury. Methods Twenty-three OA patients and healthy controls without OA were recruited. Chondrocytes were isolated from OA cartilage tissues. HOTAIR, microRNA-107 (miR-107) and C-X-C motif chemokine ligand 12 (CXCL12) levels were measured by quantitative real-time polymerase chain reaction and western blot. Cell proliferation, apoptosis and extracellular matrix (ECM) degradation were measured using cell counting kit-8, flow cytometry and western blot. The target interaction was explored by bioinformatics, luciferase reporter and RNA immunoprecipitation assays. Results HOTAIR expression was enhanced, and miR-107 level was reduced in OA cartilage samples. HOTAIR overexpression inhibited cell proliferation, but induced cell apoptosis and ECM degradation in chondrocytes. HOTAIR knockdown caused an opposite effect. MiR-107 was sponged and inhibited via HOTAIR, and knockdown of miR-107 mitigated the effect of HOTAIR silence on chondrocyte injury. CXCL12 was targeted by miR-107. CXCL12 overexpression attenuated the roles of miR-107 overexpression or HOTAIR knockdown in the proliferation, apoptosis and ECM degradation. CXCL12 expression was decreased by HOTAIR silence, and restored by knockdown of miR-107. Conclusion HOTAIR knockdown promoted chondrocyte proliferation, but inhibited cell apoptosis and ECM degradation in OA chondrocytes by regulating the miR-107/CXCL12 axis.

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Long noncoding RNA LBX2-AS1-modulated miR-4766-5p regulates gastric cancer development through targeting CXCL5

Cancer Cell International ◽

10.1186/s12935-020-01579-z ◽

2020 ◽

Vol 20 (1) ◽

Author(s):

LiPan Peng ◽

ZeZhong Chen ◽

GuangChuan Wang ◽

ShuBo Tian ◽

Shuai Kong ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Noncoding Rna ◽

Mrna Level ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Polymerase Chain ◽

Dual Luciferase Reporter Assay

Abstract Background Long noncoding RNAs (LncRNAs) have been reported to critically regulate gastric cancer (GC). Recently, it was reported that LBX2 antisense RNA 1 (LBX2-AS1) is abnormally expressed in GC. However, the role of LBX2-AS1 in the malignancy of GC is worth further discussion. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the LBX2-AS1, miR-4766-5p and C-X-C motif chemokine (CXCL5) expression in GC tissues and cells. Dual-luciferase reporter assay was applied to examine the target relationship between LBX2-AS1 and miR-4766-5p or miR-4766-5p and CXCL5. Cell counting kit-8 (CCK-8) and Transwell assays were used to detect cell proliferation, migration and invasion rates. The protein expression of CXCL5 was confirmed using western blot. The RNA pull down experiment was used to verify the specificity of LBX2-AS1 and miR-4766-5p on BGC-823 and SGC-7901 cells. Results LBX2-AS1 was up-regulated in GC tissues and cells, and its knockdown suppressed proliferation, migration and invasion of GC cells. While, overexpression of LBX2-AS1 increased proliferation and increased CXCL5 mRNA level. CXCL5 improved cell proliferation, migration and invasion of GC cells. LBX2-AS1 could bind to miR-4766-5p to regulate CXCL5 expression. Overexpression of CXCL5 overturned those effects of miR-4766-5p in GC cells. RNA Pull down shown that BGC-823 and SGC-7901 cells, miR-4766-5p specifically binds to LBX2-AS1. Conclusions In short, this study demonstrated that LBX2-AS1 promoted proliferation, migration and invasion through up-regulation CXCL5 mediated by miR-4766-5p in GC. The LBX2-AS1/miR-4766-5p/CXCL5 regulatory axis provides a theoretical basis for the research on lncRNA-directed therapeutics in GC.

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LncRNA KCNQ1OT1 promotes the development of diabetic nephropathy by regulating miR-93-5p/ROCK2 axis

Diabetology & Metabolic Syndrome ◽

10.1186/s13098-021-00726-4 ◽

2021 ◽

Vol 13 (1) ◽

Author(s):

Li Zhao ◽

Huaqian Chen ◽

Lin Wu ◽

Zhengdong Li ◽

Ren Zhang ◽

...

Keyword(s):

Cell Proliferation ◽

Diabetic Nephropathy ◽

Mesangial Cells ◽

Coiled Coil ◽

Cell Counting ◽

Luciferase Reporter ◽

Glomerular Mesangial Cells ◽

Cell Models ◽

Protein Levels ◽

Induced Apoptosis

Abstract Background Long non-coding RNAs (lncRNAs) have been reported to play vital roles in diabetic nephropathy (DN). The aim of this study was to explore the function of mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in DN. Methods DN cell models were established using high glucose (HG) treatment in human glomerular mesangial cells (HGMC) and human renal glomerular endothelial cells (HRGEC). The expression levels of KCNQ1OT1, microRNA-93-5p (miR-93-5p), and Rho associated coiled-coil containing protein kinase 2 (ROCK2) mRNA was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. ROCK2 and apoptosis/fibrosis-related protein levels were examined by western blot. The predicted interaction between miR-93-5p and KCNQ1OT1 or ROCK2 was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results KCNQ1OT1 was upregulated in DN patients and DN cell models. KCNQ1OT1 knockdown inhibited cell proliferation and fibrosis and induced apoptosis in DN cell models. MiR-93-5p was a direct target of KCNQ1OT1, and miR-93-5p inhibition restored the KCNQ1OT1 knockdown-mediated effects on cell proliferation, fibrosis and apoptosis in DN cell models. In addition, ROCK2 was identified as a target of miR-93-5p, and miR-93-5p overexpression suppressed cell proliferation and fibrosis and accelerated apoptosis by targeting ROCK2 in DN cell models. Moreover, KCNQ1OT1 regulated ROCK2 expression by binding to miR-93-5p. Conclusion KCNQ1OT1 knockdown inhibited cell proliferation and fibrosis and induced apoptosis in DN by regulating miR-93-5p/ROCK2 axis, providing potential value for the treatment of DN.

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CircCDC45 promotes the malignant progression of glioblastoma by modulating the miR-485-5p/CSF-1 axis

BMC Cancer ◽

10.1186/s12885-021-08803-7 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Rongcai Liu ◽

Weimin Dai ◽

An Wu ◽

Yunping Li

Keyword(s):

Cell Proliferation ◽

Cancer Progression ◽

Biological Effects ◽

Cell Counting ◽

Luciferase Reporter ◽

Circular Rnas ◽

Invasion And Migration ◽

Protein Levels

Abstract Background Glioblastoma (GBM) is characterized by progressive growth and metastasis. Numerous studies claim that the deregulation of circular RNAs (circRNAs) is associated with cancer progression. However, the role of circRNAs in GBM is largely limited. The purpose of this study was to investigate the functions of circCDC45 in GBM and provide a feasible functional mechanism to support its role. Methods The expression of circCDC45, miR-485-5p and colony-stimulating factor 1 (CSF-1) mRNA was examined using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed using cell counting kit − 8 (CCK-8) assay and colony formation assay. Cell migration and cell invasion were monitored using transwell assay. The protein levels of proliferation-related markers and CSF-1 were determined using western blot. The target relationship was predicted using bioinformatics tools and validated using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Animal models were constructed to verify the role of circCDC45 in vivo. Results The expression of circCDC45 and CSF-1 was elevated in GBM tissues and cells, while the expression of miR-485-5p was declined. Downregulation of circCDC45 or CSF-1 blocked GBM cell proliferation, invasion and migration as well as tumor growth in vivo. In mechanism, circCDC45 positively regulated the expression of CSF-1 by targeting miR-485-5p. Inhibition of miR-485-5p reversed the biological effects caused by circCDC45 downregulation in GBM cells. Conclusion CircCDC45 promoted the progression of GBM by mediating the miR-485-5p/CSF-1 axis, and circCDC45 might be a promising plasmatic biomarker for GBM diagnosis and treatment.

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Long noncoding RNA SNHG14 regulates ox-LDL-induced atherosclerosis cell proliferation and apoptosis by targeting miR-186-5p/WIPF2 axis

Human & Experimental Toxicology ◽

10.1177/0960327120940363 ◽

2020 ◽

Vol 40 (1) ◽

pp. 47-59

Author(s):

Z Tao ◽

Z Cao ◽

X Wang ◽

D Pan ◽

Q Jia

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Noncoding Rna ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Cell Counting ◽

Luciferase Reporter ◽

Interacting Protein ◽

Downstream Target ◽

Proliferation And Apoptosis

To investigate the role of small nucleolus RNA host gene 14 (SNHG14) in the progression of atherosclerosis (AS), bioinformatics analysis, and other relevant experiments (cell counting kit-8, flow cytometry, quantitative real-time polymerase chain reaction, luciferase reporter, RNA immunoprecipitation, RNA pull-down, and western blot assays) were done. The current study revealed that SNHG14 level was high in the serum of AS patients and oxidized low-density lipoprotein (ox-LDL)-induced AS cell lines. Besides, we found that SNHG14 accelerated cell proliferation while inhibited cell apoptosis in ox-LDL-induced AS cell lines. Next, SNHG14 was confirmed to be a sponge for miR-186-5p in AS cells, and it was validated that SNHG14 regulated AS cell proliferation and apoptosis by sponging miR-186-5p. Moreover, we uncovered that WAS-interacting protein family member 2 (WIPF2) was a downstream target of miR-186-5p in AS cells. Finally, it was demonstrated that miR-186-5p modulated AS cell proliferation and apoptosis via targeting WIPF2. To conclude, our research disclosed that SNHG14 affected ox-LDL-induced AS cell proliferation and apoptosis through miR-186-5p/WIPF2 axis, which may provide a theoretical basis for the treatment and diagnosis of AS.

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PCGEM1 Promotes Proliferation, Migration And Invasion In Prostate Cancer By Sponging miR-506 To Upregulate TRIAP1

10.21203/rs.3.rs-878010/v1 ◽

2021 ◽

Author(s):

He Liu ◽

Xin He ◽

Tianjiao Li ◽

Yi Qu ◽

Lina Xu ◽

...

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Noncoding Rna ◽

Suppressive Effect ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Invasion And Migration ◽

Gene Level ◽

And Migration

Abstract Background: The important role of long noncoding RNAs (lncRNAs) in cancer has been demonstrated in many studies. Prostate cancer gene expression marker 1 (PCGEM1) is a lncRNA specifically expressed within the prostate and overexpressed in many cancer cells. Numerous studies have shown that PCGEM1 promotes cell proliferation, invasion and migration. However, the specific mechanism of PCGEM1 within prostate cancer (PCa) has not been elucidated. MicroRNA-506-3p (miR-506-3p) is a noncoding RNA, and studies have indicated that miR-506-3p is downregulated in prostate cancer cell lines and functions as a tumor suppressor.Methods: The TCGA (GEPIA) database (http://gepia.cancer-pku.cn/) was employed to measure PCGEM1 levels in PCa. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the PCGEM1 gene level. CCK-8 (Cell Counting Kit-8) and colony formation assays were used to detect cell proliferation, and Transwell assays were applied to assess cell invasion and migration. The interacting ability of miR-506-3p with PCGEM1 or TRIAP1 was validated through a dual-luciferase reporter assay. TRIAP1 protein expression was detected by Western blotting.Results: PCGEM1 expression was increased in PCa tissues and cells. In PCa tissues, High PCGEM1 expression was associated with high Gleason score, distant metastasis and extracapsular extension. In addition, PCGEM1 knockdown inhibited PCa cell (C4-2B and PC-3) proliferation, invasion and migration. miR-506-3p may interact with PCGEM1 or TRIAP1, and the suppressive effect of PCGEM1 knockdown was reversed when TRIAP1 or a miR-506-3p inhibitor was cotransfected.Conclusion: PCGEM1 expression increased in PCa cells and tissues, enhancing PCa cell proliferation, migration and invasion by sponging miR-506 to upregulate TRIAP1.

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LINC00202 promotes retinoblastoma progression by regulating cell proliferation, apoptosis, and aerobic glycolysis through miR-204-5p/HMGCR axis

Open Life Sciences ◽

10.1515/biol-2020-0047 ◽

2020 ◽

Vol 15 (1) ◽

pp. 437-448

Author(s):

Aimin Wu ◽

Xuewei Zhou ◽

Linglong Mi ◽

Jiang Shen

Keyword(s):

Cell Proliferation ◽

Noncoding Rna ◽

Caspase 3 ◽

Aerobic Glycolysis ◽

Xenograft Model ◽

Cell Counting ◽

Luciferase Reporter ◽

Reaction Cell

AbstractLINC00202 is a newly identified long noncoding RNA (lncRNA) and has been demonstrated to involve in the progression of retinoblastoma (RB). Here, we further explored the role and the underlying molecular mechanism of LINC00202 on RB malignant properties and glycolysis. LINC00202, microRNA (miR)-204-5p, and 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR) mRNA were detected by a quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were analyzed using cell counting kit-8 assay and colony formation assay and flow cytometry, respectively. Glucose metabolism was calculated by measuring the extracellular acidification rate (ECRA). Western blot was used to detect the levels of HMGCR, ki67, pro-caspase-3, cleaved-caspase-3, and lactate dehydrogenase A chain (LDHA). The interaction between miR-204-5p and LINC00202 or HMGCR was analyzed by the dual-luciferase reporter assay. Murine xenograft model was established to conduct in vivo experiments. LINC00202 expression was upregulated in RB tumor tissues and LINC00202 knockdown inhibited RB cell proliferation, glycolysis, and stimulated apoptosis in vitro as well as impeded tumor growth in vivo. MiR-204-5p directly bound to LINC00202 and HMGCR in RB cells, and LINC00202 functioned as a competing endogenous RNA in regulating HMGCR through competitively binding to miR-204-5p. More importantly, the regulation of malignant properties and glycolysis of RB cells mediated by LINC00202 could be reversed by abnormal miR-204-5p or HMGCR expression in RB cells. In all, LINC00202 promoted RB cell proliferation, glycolysis, and suppressed apoptosis by regulating the miR-204-5p/HMGCR axis, suggesting a novel therapeutic target for patients with RB.

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Long Noncoding RNA LIPE-AS1 Drives Prostate Cancer Progression by Functioning as a Competing Endogenous RNA for microRNA-654-3p and Thereby Upregulating Hepatoma-Derived Growth Factor

Urologia Internationalis ◽

10.1159/000516676 ◽

2021 ◽

pp. 1-16

Author(s):

Boyu Tian ◽

E. Chunxiang ◽

Yang Xiang ◽

Peng Teng

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Growth Factor ◽

Noncoding Rna ◽

Molecular Mechanisms ◽

The Cancer Genome Atlas ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Competing Endogenous Rna

Introduction: Information regarding the expression and roles of LIPE antisense RNA 1 (LIPE-AS1) in prostate cancer (PCa) progression is currently limited. We experimentally determined LIPE-AS1 expression in PCa tissues and cell lines. The specific functions of LIPE-AS1 in the oncogenicity of PCa were explored by evaluating a series of cellular functions. Moreover, the molecular mechanisms underlying the oncogenic roles of LIPE-AS1 in PCa were investigated. Methods: The expression level of LIPE-AS1 was determined via quantitative reverse transcription polymerase chain reaction. Functional experiments, including the Cell Counting Kit-8 assay, Transwell migration and invasion assays, and tumor xenograft experiments, were used to determine the effects of LIPE-AS1 on PCa cells. The putative miRNA-binding LIPE-AS1 was predicted via bioinformatics analysis and further verified using the luciferase reporter and RNA immunoprecipitation assays. Results: LIPE-AS1 was expressed at high levels in PCa cells; this result is consistent with that of The Cancer Genome Atlas database. Patients with PCa manifesting high LIPE-AS1 expression had shorter overall survival than those manifesting low LIPE-AS1 expression. Downregulated LIPE-AS1 inhibited PCa cell proliferation, migration, and invasion in vitro and impaired tumor growth in vivo. With respect to its mechanism, LIPE-AS1 functioned as a competing endogenous RNA for microRNA-654-3p (miR-654-3p) in PCa cells, and hepatoma-derived growth factor (HDGF) was the direct target of miR-654-3p. HDGF was positively regulated by LIPE-AS1 in PCa cells via the absorption of miR-654-3p. Rescue experiments confirmed that miR-654-3p downregulation or HDGF overexpression counteracts the inhibitory effects of LIPE-AS1 depletion on PCa cell proliferation, migration, and invasion. Conclusion: LIPE-AS1 promotes PCa malignancy by targeting the miR-654-3p/HDGF axis. Determining the LIPE-AS1/miR-654-3p/HDGF pathway may increase our understanding of PCa pathogenesis and contribute toward a wider applied scope.

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Long noncoding RNA SNHG14 promotes hepatocellular carcinoma progression by regulating miR-876-5p/SSR2 axis

Journal of Experimental & Clinical Cancer Research ◽

10.1186/s13046-021-01838-5 ◽

2021 ◽

Vol 40 (1) ◽

Author(s):

Zhibin Liao ◽

Hongwei Zhang ◽

Chen Su ◽

Furong Liu ◽

Yachong Liu ◽

...

Keyword(s):

Noncoding Rna ◽

Animal Experiments ◽

Luciferase Reporter ◽

Western Blot Assay ◽

Downstream Target ◽

Protein Levels ◽

Elevated Expression ◽

Rna Immunoprecipitation

Abstract Background Aberrant expressions of long noncoding RNAs (lncRNAs) have been demonstrated to be related to the progress of HCC. The mechanisms that SNHG14 has participated in the development of HCC are obscure. Methods Quantitative real-time PCR (qRT-PCR) was used to measure the lncRNA, microRNA and mRNA expression level. Cell migration, invasion and proliferation ability were evaluated by transwell and CCK8 assays. The ceRNA regulatory mechanism of SNHG14 was evaluated by RNA immunoprecipitation (RIP) and dual luciferase reporter assay. Tumorigenesis mouse model was used to explore the roles of miR-876-5p in vivo. The protein levels of SSR2 were measured by western blot assay. Results In this study, we demonstrated that SNHG14 was highly expressed in HCC tissues, meanwhile, the elevated expression of SNHG14 predicted poor prognosis in patients with HCC. SNHG14 promoted proliferation and metastasis of HCC cells. We further revealed that SNHG14 functioned as a competing endogenous RNA (ceRNA) for miR-876-5p and that SSR2 was a downstream target of miR-876-5p in HCC. Transwell, CCK8 and animal experiments exhibited miR-876-5p inhibited HCC progression in vitro and in vivo. By conducting rescue experiments, we found the overexpression of SSR2 or knocking down the level of miR-876-5p could reverse the suppressive roles of SNHG14 depletion in HCC. Conclusion SNHG14 promotes HCC progress by acting as a sponge of miR-876-5p to regulate the expression of SSR2 in HCC.

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Circ_0003266 sponges miR-503-5p to suppress colorectal cancer progression via regulating PDCD4 expression

BMC Cancer ◽

10.1186/s12885-021-07997-0 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Caihong Wen ◽

Xiaoqing Feng ◽

Honggang Yuan ◽

Yong Gong ◽

Guangsheng Wang

Keyword(s):

Colorectal Cancer ◽

Cell Proliferation ◽

Cell Lines ◽

Cancer Progression ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Circular Rnas ◽

Pdcd4 Expression ◽

Novel Target

Abstract Background Circular RNAs (circRNAs) feature prominently in tumor progression. However, the biological function and molecular mechanism of circ_0003266 in colorectal cancer (CRC) require further investigation. Methods Circ_0003266 expression in 46 pairs CRC tissues / adjacent tissues, and CRC cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR); after circ_0003266 was overexpressed or knocked down in CRC cells, cell proliferation, apoptosis, migration, and invasion were evaluated by the cell counting kit-8 (CCK-8), flow cytometry, and Transwell assays, respectively; the interaction among circ_0003266, miR-503-5p, and programmed cell death 4 (PDCD4) was confirmed using bioinformatics analysis and dual-luciferase reporter assay; PDCD4 protein expression in CRC cells was quantified using Western blot. Results Circ_0003266 was significantly lowly expressed in CRC tissues and cell lines. Circ_0003266 overexpression markedly repressed CRC cell proliferation, migration, and invasion, and accelerated the cell apoptosis, but its overexpression promoted the malignant phenotypes of CRC cells. PDCD4 was a direct target of miR-503-5p and circ_0003266 promoted PDCD4 expression by competitively sponging miR-503-5p. Conclusion Circ_0003266 suppresses the CRC progression via sponging miR-503-5p and regulating PDCD4 expressions, which suggests that circ_0003266 may serve as a novel target for the treatment of CRC.

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