Long Noncoding RNA LINC00634 Functions as an Oncogene in Esophageal Squamous Cell Carcinoma Through the miR-342-3p/Bcl2L1 Axis

Many long noncoding RNAs reportedly have tumor suppressive roles or are oncogenic in esophageal cancer. We have previously performed a chip-based expression analysis of primary esophageal cancer tissues and found that the expression of LINC00634 in these tissues was higher than that in nontumor tissues. Quantitative real-time–polymerase chain reaction, cell counting kit-8, flow cytometry, caspase3/7 assay, dual-luciferase reporter assay, and restore assay were used to detect the proliferative and apoptotic effects of LINC00634 in esophageal cancer cells. The results showed that the expression of LINC00634 in these tissues was higher than that in nontumor tissues and associated with tumor–node–metastasis (TNM) stage of patients. Knockdown of LINC00634 decreased cell viability and increased cell apoptosis levels in EC9706 and EC1 cells. LINC00634 could target Bcl2L1 through miR-342-3p. In this study, we show that LINC00634 is upregulated in esophageal cancer. We also show that the knockdown of LINC00634 decreased cell viability and increased cell apoptosis levels in EC9706 and EC1 cells through the miR-342-3p/Bcl2L1 axis.

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Long noncoding RNA FTX ameliorates hydrogen peroxide-induced cardiomyocyte injury by regulating the miR-150/KLF13 axis

Open Life Sciences ◽

10.1515/biol-2020-0100 ◽

2020 ◽

Vol 15 (1) ◽

pp. 1000-1012

Author(s):

Yamin Zhang ◽

Xiaoying Fan ◽

Hua Yang

Keyword(s):

Hydrogen Peroxide ◽

Cell Viability ◽

Cell Apoptosis ◽

Noncoding Rna ◽

Ischemia Reperfusion ◽

Myocardial Reperfusion ◽

Cell Counting ◽

Luciferase Reporter ◽

H9c2 Cells

AbstractBackgroundMyocardial reperfusion is an effective therapy for acute myocardial infarction (AMI). However, ischemia/reperfusion (I/R) injury following myocardial reperfusion is a significant limitation for AMI treatment. Five prime to Xist (FTX) was recognized as a biomarker of multiple diseases, including heart disease. However, the molecular mechanism of FTX in I/R injury is unclear.MethodsCell viability was evaluated by using cell counting kit-8 (CCK-8) assay. Apoptosis was analyzed by using a caspase-3 activity detection kit and flow cytometry. The expression of FTX, microRNA (miR)-150, and Kruppel-like factor 13 (KLF13) was measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The interaction of miR-150 and FTX or KLF13 was confirmed by a dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Protein expression of KLF13 was examined by Western blot. The role of FTX was detected in I/R-injured heart tissues in vivo.ResultsHydrogen peroxide (H2O2) induced cardiomyocyte injury by decreasing cell viability and expediting cell apoptosis. However, FTX alleviated cardiomyocyte injury by promoting cell proliferation and restricting cell apoptosis of H9C2 cells that were treated with H2O2. In addition, we discovered that FTX directly interacted with miR-150, while KLF13 was a target of miR-150. Rescue experiments showed that miR-150 neutralized the FTX-mediated promotion of cell progression and restriction of cell apoptosis in H9C2 cells treated with H2O2. KLF13 knockdown restored the effect of miR-150 on increased proliferation and decrease in apoptosis in H2O2-treated cardiomyocytes. Furthermore, FTX enhanced the expression of KLF13 protein through interaction with miR-150. Upregulation of FTX repressed apoptosis in I/R-injured heart tissues in vivo.ConclusionFTX relieves H2O2-induced cardiomyocyte injury by increasing KLF13 expression via depletion of miR-150, thus providing a novel therapeutic target for the alleviation of I/R injury.

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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 non-coding RNA LINC00467 regulates hepatocellular carcinoma progression by modulating miR-9-5p/PPARA expression

Open Biology ◽

10.1098/rsob.190074 ◽

2019 ◽

Vol 9 (9) ◽

pp. 190074 ◽

Cited By ~ 6

Author(s):

Kerui Cai ◽

Tieling Li ◽

Ling Guo ◽

Haifeng Guo ◽

Wei Zhu ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Viability ◽

Ectopic Expression ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Peroxisome Proliferator ◽

Reaction Cell ◽

Non Coding Rna ◽

Long Non Coding Rna

The aim of this study was to analyse the expression pattern and elucidate the mechanistic involvement of long non-coding RNA LINC00467 in hepatocellular carcinoma (HCC). The relative expression of LINC00467 and microRNA (miR)-9-5p was determined by real-time polymerase chain reaction. Cell viability was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The cell proliferation was analysed by cell counting. Cell migration and invasion were monitored by Transwell assay. The luciferase reporter assay was employed to investigate the regulatory effect of miR-9-5p on LINC00467 and peroxisome proliferator-activated receptor alpha (PPARA). The endogenous PPARA protein was quantified by western blotting. It was found that LINC00467 was aberrantly decreased in HCC. The ectopic expression of LINC00467 significantly suppressed cell viability, proliferation, migration and invasion. LINC00467 functioned as a sponge for miR-9-5a and negatively regulated miR-9-5p expression. We also identified PPARA as the direct target of miR-9-5p. siRNA-mediated knockdown of PPARA in LINC00467-proficient cells promoted cell viability, migration and invasion. Our data indicate the critical involvement of LINC00467/miR-9-5p/PPARA signalling in the incidence and progression of HCC.

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Long noncoding RNA LINC00958 suppresses apoptosis and radiosensitivity of colorectal cancer through targeting miR-422a

Cancer Cell International ◽

10.1186/s12935-021-02188-0 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Hong Liang ◽

Qiuyan Zhao ◽

Zhonglin Zhu ◽

Chao Zhang ◽

Hui Zhang

Keyword(s):

Colorectal Cancer ◽

Cell Proliferation ◽

Cell Apoptosis ◽

Noncoding Rna ◽

Luciferase Reporter ◽

Potential Biomarker ◽

Reporter Assays ◽

Cancer Tissues

Abstract Background Long noncoding RNAs (lncRNAs) have been elucidated to participate in the development and progression of various cancers. In this study, we aimed to explore the underlying functions and mechanisms of LINC00958 in colorectal cancer. Methods LINC00958 expression in colorectal cancer tissues was examined by qRT-PCR. The correlations between LINC00958 expression and clinical characteristics and prognosis were evaluated. The biological functions of LINC00958 were detected by CCK-8, MTT, colony formation and flow cytometric analyses. RNA pulldown, RIP and luciferase reporter assays were used to confirm the regulatory effects of LINC00958 on miR-422a. Rescue experiments were performed to detect the effects of miR-422a on the roles of LINC00958. Results LINC00958 was upregulated in colorectal cancer tissues and cell lines. High LINC00958 levels were positively associated with T stage and predicted poor prognosis. Cell experiments showed that LINC00958 promoted cell proliferation and suppressed apoptosis and sensitivity to radiotherapy in vitro and promoted tumor growth in vivo. Bioinformatics analysis predicted the binding site of miR-422a on LINC00958. Mechanistically, RNA pulldown, RIP and luciferase reporter assays demonstrated that LINC00958 specifically targeted miR-422a. In addition, we found that miR-422a suppressed MAPK1 expression by directly binding to the 3’-UTR of MAPK1, thereby inhibiting cell proliferation and enhancing cell apoptosis and radiosensitivity. Furthermore, miR-422a rescued the roles of LINC00958 in promoting MAPK1 expression and cell proliferation and decreasing cell apoptosis and radiosensitivity. Conclusions LINC00958 promoted MAPK1 expression and cell proliferation and suppressed cell apoptosis and radiosensitivity by targeting miR-422a, which suggests that it is a potential biomarker for the prognosis and treatment of colorectal cancer.

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Mechanism and Role of the Neuropeptide LGI1 Receptor ADAM23 in Regulating Biomarkers of Ferroptosis and Progression of Esophageal Cancer

Disease Markers ◽

10.1155/2021/9227897 ◽

2021 ◽

Vol 2021 ◽

pp. 1-15

Author(s):

Chen Chen ◽

Jun Zhao ◽

Jing-ni Liu ◽

Chenyu Sun

Keyword(s):

Esophageal Cancer ◽

Cell Lines ◽

Noncoding Rna ◽

The Cancer Genome Atlas ◽

Cell Counting ◽

Luciferase Reporter ◽

Cerna Network ◽

And Migration ◽

Proliferation And Migration

Background. According to recent studies, ferroptosis is closely related to the efficacy and prognosis of tumour treatment. However, the role of ferroptosis in esophageal squamous cell carcinoma (ESCC) has not been explored comprehensively. Materials and Methods. The esophageal cancer (EC) transcriptome data was downloaded from The Cancer Genome Atlas (TCGA), then analyzed, to obtain the differentially expressed messenger RNA (mRNA), microRNA (miRNA), and long noncoding RNA (lncRNA) between groups with the low and high Ferroptosis Potential Index (FPI) and construct a ferroptosis-associated ceRNA network. In addition, the expression of ARHGEF26-AS1 and miR-372-3p in ESCC cell lines was assessed, and the appropriate cell lines were selected. The interaction between ARHGEF26-AS1, miR-372-3p, and ADAM23 was also determined through a dual-luciferase reporter assay. Moreover, the Western blot, Cell Counting Kit-8 (CCK-8), wound healing, cell viability, and cell death assays were conducted to establish the biological functions of the ARHGEF26-AS1/miR-372-3p/ADAM23 pathway in ESCCs. Results. An FPI scoring model reflecting the activity of the ferroptosis pathway was constructed, and a ferroptosis-associated ceRNA network was established. The findings revealed that low expression of ADAM23 and ARHGEF26-AS1 as well as high expression of miR-372-3p was associated with poor prognosis and a lower FPI score in EC patients. Functionally, overexpression of ADAM23 and ARHGEF26-AS1 and the miR-372-3p inhibitor not only promoted ferroptosis in ESCC cells in vitro but also inhibited the proliferation and migration of cells. Mechanistically, ARHGEF26-AS1 upregulated the expression of ADAM23 by competitively binding to miR-372-3p. Conclusions. The study showed that the lncRNA, ARHGEF26-AS1 acts as a miR-372-3p sponge that regulates the neuropeptide LGI1 receptor ADAM23 expression. This in turn not only inhibits the proliferation and migration of ESCC cells but also upregulates the ferroptosis pathway. A neuropeptide-related ferroptosis regulatory pathway was identified in this study.

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MiR-103a-3p antagonism attenuates pneumonia via inactivating the PI3K/AKT/NF-κB signaling pathway by targeting PTEN

10.21203/rs.2.20468/v1 ◽

2020 ◽

Author(s):

Lin Xu ◽

Qingying Song ◽

Zhanghong Ouyang ◽

Xiangyan Zhang ◽

Cheng Zhang

Keyword(s):

Cell Viability ◽

Signaling Pathway ◽

Cell Apoptosis ◽

Cell Counting ◽

Luciferase Reporter ◽

Enzyme Linked Immunosorbent Assay ◽

Expression Levels ◽

Tensin Homolog ◽

Factor Α

Abstract Pneumonia accounts for approximately 15% mortalities in adolescents worldwide. MicroRNAs (miRNAs) regulate numerous diseases including pneumonia. miRNA and mRNA expression levels were detected by real time polymerase chain reaction (RT-qPCR). Protein expression levels were determined by enzyme-linked immunosorbent assay (ELISA) and western blot. The interaction between phosphatase and tensin homolog on chromosome ten (PTEN) and miR-103a-3p was explored by dual luciferase reporter assay. Cell viability and cell apoptosis were detected by cell Counting Kit-8 (CCK-8) and flow cytometry. Herein, we discovered that PTEN was decreased and miR-103a-3p was overexpressed in Ana-1 cells of in vitro pneumonia model. miR-103a-3p downregulated the expression levels of PTEN. AntagomiR-103a-3p reversed the increased cell apoptosis and decreased cell viability and inflammatory cytokine expression levels (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6) induced by LPS in Ana-1 cells by PTEN. AntagomiR-103a-3p inhibited the activation of PTEN/PI3K/AKT/NF-κB signaling pathway induced by LPS in Ana-1 cells. Taken together, our findings exhibited that miR-103a-3p attenuated LPS induced pneumonia by blocking the activation of PTEN/PI3K/AKT/NF-κB signaling pathway and the following cell apoptosis as well as release of proinflammatory cytokines, suggesting that miR-103a-3p might serve as a novel therapeutic target for the treatment of pneumonia.

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Knockdown of NCK1-AS1 inhibits the development of atherosclerosis by targeting miR-1197/COX10 axis

Journal of Biological Engineering ◽

10.1186/s13036-021-00281-6 ◽

2022 ◽

Vol 16 (1) ◽

Author(s):

Bin Zhang ◽

Juncheng Wang ◽

Lei Du ◽

Lufei Shao ◽

Yourui Zou ◽

...

Keyword(s):

Cell Viability ◽

Inflammatory Cytokines ◽

Cell Apoptosis ◽

Cell Model ◽

Human Cancer ◽

Density Lipoprotein ◽

Cell Counting ◽

Luciferase Reporter ◽

Blood Samples ◽

Qrt Pcr

Abstract Background Although long non-coding RNA (lncRNA) NCK1-AS1 plays important roles in human cancer, its function in atherosclerosis (AS) remains unclear. Method The expression of NCK1-AS1 in AS blood samples was detected by qRT-PCR. Oxidized low-density lipoprotein (ox-LDL) was used to construct the AS cell model, and quantitative real-time polymerase chain reaction (qRT-PCR) assay was used to evaluate NCK1-AS1 level. Cell phenotypes including proliferation and apoptosis were assessed by Cell Counting Kit-8 (CCK-8) assay and flow cytometer, respectively. The malondialdehyde level was measured to evaluate oxidative stress. The expression of apoptosis-related proteins was evaluated by western blot. The expression of inflammatory cytokines (IL-1β, IL-6 and TNK-α) was measured by qRT-PCR and ELISA assays. The relationship among NCK1-AS1, miR-1197 and COX10 was determined by bioinformatic analysis and luciferase reporter assay. Results NCK1-AS1 was significantly upregulated in AS blood samples and ox-LDL stimulated vascular smooth muscle cells (VSMCs). Knockdown of NCK1-AS1 increased cell viability, reduced cell apoptosis and MDA level, and also inhibited the expression of inflammatory cytokines (IL-1β, IL-6 and TNK-α) in ox-LDL stimulated VSMCs. NCK1-AS1 could positively regulate COX10 expression by directly sponging miR-1197. Moreover, co-transfection of sh-NCK1-AS1 and miR-1197 inhibitor, or co-transfection of sh-NCK1-AS1 and pc-COX10 (COX10 overexpressing plasmid) obviously reduced cell viability, promoted cell apoptosis, and increased MDA level in VSMCs followed by ox-LDL treatment for 24 h compared to that in sh-NCK1-AS1 transfected VSMCs. Conclusion Our study revealed that knockdown of NCK1-AS1 attenuated the development of AS by regulating miR-1197/COX10 axis, suggesting that this lncRNA might be a potential therapeutic target for AS.

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Circ_0003998 enhances doxorubicin resistance in hepatocellular carcinoma by regulating miR-218-5p/EIF5A2 pathway

Diagnostic Pathology ◽

10.1186/s13000-020-01056-1 ◽

2020 ◽

Vol 15 (1) ◽

Author(s):

Xiaomin Li ◽

Jiefeng He ◽

Xiaojing Ren ◽

Haichao Zhao ◽

Haoliang Zhao

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Viability ◽

Translation Initiation Factor ◽

Cell Counting ◽

Initiation Factor ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Circular Rnas ◽

Reaction Cell

Abstract Background The involvement of circular RNAs (circRNAs) in chemoresistance of tumors has been identified. Herein, this study aims to investigate the role and the underlying mechanism of circ_0003998 in doxorubicin (DOX) resistance in hepatocellular carcinoma (HCC). Methods The expression of circ_0003998 and microRNA (miR)-218-5p and eukaryotic translation initiation factor 5A-2 (EIF5A2) mRNA was detected using quantitative real-time polymerase chain reaction. Cell viability, migration and invasion were analyzed using cell counting kit-8, colony formation and transwell assay, respectively. The levels of matrix metallopeptidase 9 (MMP-9), E-cadherin, Vimentin, N-cadherin and EIF5A2 protein were detected using western blot. The interaction between miR-218-5p and circ_0003998 or EIF5A2 was confirmed by dual-luciferase reporter assay. In vivo experiments were performed using murine xenograft models. Results Circ_0003998 was elevated in HCC tissues, DOX-resistant tissues and cells, and circ_0003998 knockdown promoted DOX-sensitivity in HCC by inhibiting resistant cell viability, migration, invasion and EMT in vitro and enhanced DOX cytotoxicity in vivo. Bioinformatics analysis revealed circ_0003998 inhibited miR-218-5p expression, which was clarified to be a target of circ_0003998, and circ_0003998 knockdown sensitized HCC cell to DOX by sponging miR-218-5p. EIF5A2 was a target of miR-218-5p, and miR-218-5p mitigated DOX resistance in HCC cells through modulating EIF5A2 expression. Additionally, circ_0003998 served as a competing endogenous RNA for miR-218-5p to regulate EIF5A2 expression. Conclusion Circ_0003998 knockdown sensitized HCC cell to DOX by regulating miR-218-5p/EIF5A2 axis, indicating new markers of poor response to DOX and potential therapeutic strategies for the chemotherapy of HCC.

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LncRNA SNHG1 protects the cardiac muscle cells from hypoxia/ re-oxygenation injury in vitro by targeting microRNA-21-5p and miR-30a-5p

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v20i1.14 ◽

2021 ◽

Vol 20 (1) ◽

pp. 89-94

Author(s):

Youbin Liu ◽

Tingting Zang ◽

Ying Fan ◽

Jinglong Li ◽

Meng Chen ◽

...

Keyword(s):

Cardiovascular Diseases ◽

Cell Viability ◽

Cardiac Muscle ◽

Cell Apoptosis ◽

Noncoding Rna ◽

Molecular Mechanisms ◽

Muscle Cells ◽

Protective Role ◽

Luciferase Reporter ◽

Cardiac Muscle Cells

Purpose: Cardiovascular diseases are responsible for numerous deaths globally. Long noncoding RNA SNHG1 has presented its protective role in cardiomyocytes previously. Herein, we examined the underlying molecular mechanisms of SNHG1 in cardiac muscle cells from hypoxia and re-oxygenation (H/R) in vitro.Methods: RT-qPCR measured expression of SNHG1, miR-21-5p and miR-30a-5p in rat cardiac muscle cell line HL-1 before and after H/R treatment and cell transfection, which was applied to regulate expression of SNHG1, miR-21-5p and miR-30a-5p for further use. The flow cytometry method was used to compare changes in cellular apoptosis, and cell viability was measured by CCK-8 method.Bioinformatics predicted the bindings ofSNHG1 and miR-21-5p / miR-30a-5p while the luciferase reporter assays further verified this.Results: The outcomes revealedthat SNHG1 was downregulated and meanwhile miR-21-5p / miR-30a5p was elevated that enhanced apoptosis and reduced cell viability in HL-1 cells. However, overexpressed SNHG1 inhibited cell apoptosis and increased cell viability brought by H/R. In addition, SNHG1 targeted at miR-21-5p/ miR-30a-5p, which contributed to the inter-regulation in between. Furthermore, interactive experiments revealed that upregulation of miR-21-5p/ miR-30a-5p added to the cell apoptosis which was induced by H/R and partially counteracted by the upregulation of SNHG1.Conclusion: In this study we have demonstrated the protective role of SNHG1 in the moderation of H/R-induced HL-1 apoptosis and viability through suppression of miR-21-5p/miR-30a-5p. This offers new perspective into the molecular interpretation of cardiovascular diseases such as ischemic reperfusion injury. Keywords: SNHG1; apoptosis; Hypoxia/Re-oxygenation injury;miR-21-5p; miR-30a-5p; Cardiovascular diseases

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Exosomes Mediated Transfer of Circ_0000337 Contributes to Cisplatin (CDDP) Resistance of Esophageal Cancer by Regulating JAK2 via miR-377-3p

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.673237 ◽

2021 ◽

Vol 9 ◽

Author(s):

Rukun Zang ◽

Xiaowen Qiu ◽

Yipeng Song ◽

Yang Wang

Keyword(s):

Drug Resistance ◽

Esophageal Cancer ◽

Cell Growth ◽

Cancer Cells ◽

Janus Kinase ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Esophageal Cancer Cells

Background: Chemoresistance remains a major obstacle to the treatment of esophageal cancer patients. Exosome-mediated transfer of circular RNAs (circRNAs) has been reported to be related to drug resistance in esophageal cancer. This study is designed to explore the role and mechanism of exosomal circ_0000337 on CDDP resistance in esophageal cancer.Methods: Cell viability, proliferation, colony number, apoptosis, migration, and invasion were assessed by Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, and transwell assays. Circ_0000337, microRNA-377 (miR-377-3p), and Janus kinase 2 (JAK2) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Exosomes were isolated and detected by differential centrifugation and a transmission electron microscope. Protein levels of CD9, CD63, and JAK2 were tested by Western blot assay. The binding relationship between miR-377-3p and circ_0000337 or JAK2 was predicted by circinteractome or Starbase and then verified by dual-luciferase reporter assay and RNA pull-down assay. The biological role of exosomal circ_0000337 and CDDP on esophageal cancer cell growth was examined by the xenograft tumor model in vivo.Results: Circ_0000337 and JAK2 were highly expressed, and miR-377-3p was decreased in CDDP-resistant esophageal cancer tissues and cells. Moreover, circ_0000337-containing exosomes secreted by CDDP-resistant esophageal cancer cells could promote CDDP resistance, cell growth, and metastasis in CDDP-sensitive esophageal cancer cells in vitro. The mechanical analysis discovered that circ_0000337 functioned as a sponge of miR-377-3p to regulate JAK2 expression. Exosomal circ_0000337 increased the drug resistance of esophageal cancer in vivo.Conclusion: Exosomal circ_0000337 accelerated CDDP resistance of esophageal cancer cells partly by regulating the miR-377-3p/JAK2 axis, hinting a promising therapeutic target for the esophageal cancer treatment.

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