scholarly journals Downregulation of miR-181b-5p Inhibits the Viability, Migration, and Glycolysis of Gallbladder Cancer by Upregulating PDHX Under Hypoxia

2021 ◽  
Vol 11 ◽  
Author(s):  
Yiyu Qin ◽  
Yongliang Zheng ◽  
Cheng Huang ◽  
Yuanyuan Li ◽  
Min Gu ◽  
...  
Keyword(s):  
Cell Viability ◽  
Gallbladder Cancer ◽  
Microarray Analysis ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Luciferase Reporter ◽  
Glucose Assay ◽  
Normal Tissues ◽  
Tumor Tissues ◽  
Close Relationship

BackgroundGallbladder cancer (GBC) is a malignant cancer with poor prognosis. Evidences have shown that miRNAs are closely related to the occurrence of GBC; thus, we aimed to explore miRNAs, which plays an important role in the occurrence and development of GBC.MethodsMicroarray analysis was performed to investigate the differentially expressed miRNAs between five non-neoplastic gallbladder tissues (normal tissues) and five gallbladder tumor tissues (tumor tissues). RT-qPCR was performed to detect the level of miR-181b-5p in cells, and CCK-8 was performed to detect cell viability. Then, glucose assay kit or lactic acid assay kit was performed to detect the level of glucose consumption or lactate production. Next, transwell and wound healing assays were used to assess cell migration. In addition, dual-luciferase reporter assay was used to verify the relationship between miR-181b-5p and PDHX. At last, Western blotting was performed to determine the protein level of PDHX.ResultsMicroarray analysis suggested miR-181b-5p was significantly upregulated in GBC tumor tissue. KEGG analysis for the protein targets of miR-181b-5p indicates a close relationship existed between miR-181b-5p and glycolysis. In addition, the level of miR-181b-5p was notably increased in GBC-SD or G415 cells, compared with HIBEpiC cells. GBC cell viability was significantly decreased under hypoxia, and these decreases were exacerbated by miR-181b-5p antagomir. Moreover, glucose consumption or lactate production of GBC cells was significantly upregulated under hypoxia, whereas these increases were completely revered by miR-181b-5p antagomir. Further investigation revealed that PDHX was a direct target of miR-181b-5p.ConclusionIn this study, downregulation of miR-181b-5p inhibits the viability, migration, and glycolysis of GBC by upregulating PDHX under hypoxia. This finding suggested that miR-181b-5p might be considered as a novel therapeutic target for the treatment of GBC.

scholarly journals Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

2020 ◽  
Author(s):  
Liping Mu ◽  
Lili Wang ◽  
Shaoming Zhang ◽  
Qinghua Wang
Keyword(s):  
Colony Formation ◽  
Noncoding Rna ◽  
Neuroblastoma Cells ◽  
Lactate Production ◽  
Xenograft Model ◽  
Glucose Consumption ◽  
Luciferase Reporter ◽  
Glucose Assay

Abstract Background: Abnormal expression of long noncoding RNAs (lncRNAs) was usually involved in tumorigenesis and radiosensitivity of various cancers. The aim of this study was to explore the biological function and regulatory mechanism of lncRNA X-inactive specific transcript (XIST) in tumorigenesis and radiosensitivity of neuroblastoma (NB).Methods: The expression levels of XIST, microRNA-653-5p (miR-653-5p) and hexokinase 2 (HK2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Methylthiazolyldiphenyl tetrazolium bromide (MTT) assay, colony formation assay and transwell assay were utilized to detect cell viability, colony formation and cell invasion abilities. Glucose consumption or lactate production was measured by glucose assay kit or lactate assay kit, respectively. The mice xenograft model was established to investigate the role of XIST in vivo. The interaction between miR-653-5p and XIST or HK2 was predicted by starBase v2.0 and verified by dual-luciferase reporter assay. Western blot was used to measure the protein expression of HK2.Results: XIST and HK2 were highly expressed whilst miR-653-5p was lowly expressed in NB tissues and cells. XIST knockdown inhibited tumorigenesis by repressing NB cell proliferation and invasion. Meanwhile, XIST downregulation increased the radiosensitivity via inhibiting colony formation rates and glycolysis. Moreover, miR-653-5p could bind to XIST and its downregulation reversed the effects of XIST knockdown on tumorigenesis and radiosensitivity. Additionally, HK2 was a direct target of miR-653-5p and its overexpression attenuated the effects of miR-653-5p restoration on suppression of tumorigenesis and promotion of radiosensitivity. Besides, XIST functioned as a molecular sponge of miR-653-5p to regulate HK2 expression. Furthermore, XIST knockdown also suppressed tumor growth by upregulating miR-653-5p and downregulating HK2 in vivo.Conclusion: XIST interference inhibited tumorigenesis and increased radiosensitivity in NB by regulating miR-653-5p/HK2 axis, providing a novel therapeutic strategy for NB.

scholarly journals LINC00665 Targets miR-214-3p/MAPK1 Axis to Accelerate Hepatocellular Carcinoma Growth and Warburg Effect

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Hongyu Wan ◽  
Yi Tian ◽  
Juan Zhao ◽  
Xiao Su
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Viability ◽  
Colony Formation ◽  
Warburg Effect ◽  
Aerobic Glycolysis ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Tumor Formation ◽  
Luciferase Reporter

Inhibition of aerobic glycolysis is a hopeful method for cancer treatment. In this study, we aimed to explore LINC00665/miR-214-3p/MAPK1 role in regulating cell viability and aerobic glycolysis in hepatocellular carcinoma (HCC). The expressions of LINC00665 in 50 paired HCC tissues and normal tissues were determined by qRT-PCR. Pearson analysis was applied to evaluate the association between the expression levels of miR-214-3p, LINC00665, and MAPK1 in HCC tissues. The interactions between miR-214-3p and LINC00665 or MAPK1 were determined by luciferase reporter assay and RNA immunoprecipitation. CCK-8 and colony formation assays were used for cell viability evaluation. Lactate production, glucose consumption, and ATP levels were measured to assess Warburg effect. The results showed that LINC00665 was overexpressed in HCC, which positively associated with MAPK1 level and negatively associated with miR-214-3p level in HCC tissues. Overexpression of LINC00665 led to significant enhancements in cell viability and colony formation, whereas this effect was weakened when miR-214-3p was overexpressed or MAPK1 was downregulated. In addition, deletion of LINC00665 expression repressed tumor formation in vivo. Mechanically, LINC00665 increased MAPK1 expression through binding to miR-214-3p. Collectively, this study revealed that LINC00665 accelerated cell growth and Warburg effect through sponging miR-214-3p to increase MAPK1 expression in HCC.

scholarly journals Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

2020 ◽  
Author(s):  
Liping Mou ◽  
Lili Wang ◽  
Shaoming Zhang ◽  
Qinghua Wang
Keyword(s):  
Colony Formation ◽  
Noncoding Rna ◽  
Neuroblastoma Cells ◽  
Lactate Production ◽  
Xenograft Model ◽  
Glucose Consumption ◽  
Luciferase Reporter ◽  
Glucose Assay ◽  
Rna Immunoprecipitation

Abstract Background: Abnormal expression of long noncoding RNAs (lncRNAs) was usually involved in tumorigenesis and radiosensitivity of various cancers. The aim of this study was to explore the biological function and regulatory mechanism of lncRNA X-inactive specific transcript (XIST) in tumorigenesis and radiosensitivity of neuroblastoma (NB).Methods: The expression levels of XIST, microRNA-653-5p (miR-653-5p) and hexokinase 2 (HK2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Methylthiazolyldiphenyl tetrazolium bromide (MTT) assay, colony formation assay and transwell assay were utilized to detect cell viability, colony formation and cell invasion abilities. Glucose consumption or lactate production was measured by glucose assay kit or lactate assay kit, respectively. The mice xenograft model was established to investigate the role of XIST in vivo. The interaction between miR-653-5p and XIST or HK2 was predicted by starBase v2.0 and verified by dual-luciferase reporter, RNA Immunoprecipitation (RIP) and RNA pull-down assays. Western blot was used to measure the protein expression of HK2.Results: XIST and HK2 were highly expressed whilst miR-653-5p was lowly expressed in NB tissues and cells. XIST knockdown inhibited tumorigenesis by repressing NB cell proliferation and invasion. Meanwhile, XIST downregulation increased the radiosensitivity via inhibiting colony formation rates and glycolysis. Moreover, miR-653-5p could bind to XIST and its downregulation reversed the effects of XIST knockdown on tumorigenesis and radiosensitivity. Additionally, HK2 was a direct target of miR-653-5p and its overexpression attenuated the effects of miR-653-5p restoration on suppression of tumorigenesis and promotion of radiosensitivity. Besides, XIST functioned as a molecular sponge of miR-653-5p to regulate HK2 expression. Furthermore, XIST knockdown also suppressed tumor growth by upregulating miR-653-5p and downregulating HK2 in vivo.Conclusion: XIST interference inhibited tumorigenesis and increased radiosensitivity in NB by regulating miR-653-5p/HK2 axis, providing a novel therapeutic strategy for NB.

scholarly journals Silencing circSLAMF6 represses cell glycolysis, migration, and invasion by regulating the miR-204-5p/MYH9 axis in gastric cancer under hypoxia

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Xinhui Fang ◽  
Yangqiu Bai ◽  
Lida Zhang ◽  
Songze Ding
Keyword(s):  
Gastric Cancer ◽  
Lactate Production ◽  
Xenograft Model ◽  
Glucose Consumption ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Glucose Assay

Abstract Background: Gastric cancer (GC) is a malignant tumor of the digestive tract. Hypoxia plays an important role in the development of cancer, including GC. The present study aimed to investigate the role of circular RNA SLAMF6 (circSLAMF6) in the progression of GC under hypoxia. Methods: The expression of circSLAMF6, microRNA-204-5p (miR-204-5p) and myosin heavy chain 9 (MYH9) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). GC cells were maintained under hypoxia (1% O2) for experiments in vitro. Glucose consumption and lactate production were determined by a Glucose Assay Kit and a Lactate Assay Kit, respectively. Levels of all protein were detected by Western blot. Cell migration and invasion were examined by Transwell assay. The interaction between miR-204-5p and circSLAMF6 or MYH9 was analyzed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Murine xenograft model was established to explore the role of circSLAMF6 in vivo. Results: CircSLAMF6 expression was increased in GC cells under hypoxia. Hypoxia promoted glycolysis, migration, and invasion in GC cells, which were reversed by circSLAMF6 knockdown. CircSLAMF6 was validated as a miR-204-5p sponge, and MYH9 was a target of miR-204-5p. Functionally, miR-204-5p inhibitor weakened the inhibition of circSLAMF6 knockdown on GC cell progression under hypoxia. Besides, MYH9 depletion suppressed glycolysis, migration, and invasion in GC cells under hypoxia. Importantly, circSLAMF6 deficiency inhibited tumor growth in vivo by regulating the miR-204-5p/MYH9 axis. Conclusion: CircSLAMF6 was involved in glycolysis, migration, and invasion by regulating the miR-204-5p/MYH9 axis in GC cells under hypoxia.

scholarly journals Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

2020 ◽  
Author(s):  
Liping Mou ◽  
Lili Wang ◽  
Shaoming Zhang ◽  
Qinghua Wang
Keyword(s):  
Colony Formation ◽  
Noncoding Rna ◽  
Neuroblastoma Cells ◽  
Lactate Production ◽  
Xenograft Model ◽  
Glucose Consumption ◽  
Luciferase Reporter ◽  
Glucose Assay

Abstract Background: Abnormal expression of long noncoding RNAs (lncRNAs) was usually involved in tumorigenesis and radiosensitivity of various cancers. The aim of this study was to explore the biological function and regulatory mechanism of lncRNA X-inactive specific transcript (XIST) in tumorigenesis and radiosensitivity of neuroblastoma (NB). Methods: The expression levels of XIST, microRNA-653-5p (miR-653-5p) and hexokinase 2 (HK2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Methylthiazolyldiphenyl tetrazolium bromide (MTT) assay, colony formation assay and transwell assay were utilized to detect cell viability, colony formation and cell invasion abilities. Glucose consumption or lactate production was measured by glucose assay kit or lactate assay kit, respectively. The mice xenograft model was established to investigate the role of XIST in vivo . The interaction between miR-653-5p and XIST or HK2 was predicted by starBase v2.0 and verified by dual-luciferase reporter assay. Western blot was used to measure the protein expression of HK2. Results: XIST and HK2 were highly expressed whilst miR-653-5p was lowly expressed in NB tissues and cells. XIST knockdown inhibited tumorigenesis by repressing NB cell proliferation and invasion. Meanwhile, XIST downregulation increased the radiosensitivity via inhibiting colony formation rates and glycolysis. Moreover, miR-653-5p could bind to XIST and its downregulation reversed the effects of XIST knockdown on tumorigenesis and radiosensitivity. Additionally, HK2 was a direct target of miR-653-5p and its overexpression attenuated the effects of miR-653-5p restoration on suppression of tumorigenesis and promotion of radiosensitivity. Besides, XIST functioned as a molecular sponge of miR-653-5p to regulate HK2 expression. Furthermore, XIST knockdown also suppressed tumor growth by upregulating miR-653-5p and downregulating HK2 in vivo . Conclusion: XIST interference inhibited tumorigenesis and increased radiosensitivity in NB by regulating miR-653-5p/HK2 axis, providing a novel therapeutic strategy for NB.

scholarly journals LncRNA SNHG5 promotes the glycolysis and proliferation of breast cancer cell through regulating BACH1 via targeting miR-299

Breast Cancer ◽  
2021 ◽  
Author(s):  
Shu-Lin Huang ◽  
Zhong-Cheng Huang ◽  
Chao-Jie Zhang ◽  
Jing Xie ◽  
Shan-Shan Lei ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Malignant Tumors ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Luciferase Reporter ◽  
Inhibitory Effects ◽  
Glucose Assay ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background Breast cancer (BC) is one of the most common malignant tumors in women. Accumulating studies have been reported that long non-coding RNA (lncRNA) SNHG5 is highly expressed in BC. However, the specific molecular mechanism of SNHG5 in BC is unclear. Methods Gene and protein expressions in BC cell were detected by qRT-PCR and western blotting. The proliferation and cell cycle were measured using colony formation assay and flow cytometry analysis, separately. The glucose consumption and lactate production were determined by using the glucose assay kit and lactate assay kit. A dual-luciferase reporter assay was performed to measure the interaction between miR-299 and SNHG5 or BACH1. Results SNHG5 and BACH1 expressions were increased in BC cell while miR-299 level was decreased. SNHG5 increased BACH1 expression by directly targeting miR-299. SNHG5 silencing or miR-299 overexpression suppressed the proliferation of BC cell, arrested the cell cycle in the G1 cell phase, and decreased the glucose consumption and lactate production of BC cell. However, inhibition of miR-299 or overexpression of BACH1 could reverse the inhibitory effects of sh-SNHG5 on cell proliferation and glycolysis in BC. Conclusion SNHG5 promoted the BC cell growth and glycolysis through up-regulating BACH1 expression via targeting miR-299. These findings may improve the diagnostic and therapeutic approaches to BC.

scholarly journals Long noncoding RNA XIST suppresses tumorigenesis and enhances radiosensitivity in neuroblastoma cells through regulating miR-653-5p/HK2 axis

2020 ◽  
Author(s):  
Liping Mou ◽  
Lili Wang ◽  
Shaoming Zhang ◽  
Qinghua Wang
Keyword(s):  
Colony Formation ◽  
Noncoding Rna ◽  
Neuroblastoma Cells ◽  
Lactate Production ◽  
Xenograft Model ◽  
Glucose Consumption ◽  
Luciferase Reporter ◽  
Glucose Assay

Abstract Background Abnormal expression of long noncoding RNAs (lncRNAs) was often involved in tumorigenesis and radiosensitivity of various cancers. The aim of this study was to explore the biological function and regulatory mechanism of lncRNA X-inactive specific transcript (XIST) in tumorigenesis and radiosensitivity of neuroblastoma. Methods The expression of XIST, microRNA-329-3p (miR-653-5p) and hexokinase 2 (HK2) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Methylthiazolyldiphenyl tetrazolium bromide (MTT) assay, colony formation assay and transwell assay were utilized to detect cell viability, colony formation and cell invasion abilities. Glucose consumption or lactate production was measured by glucose assay kit or lactate assay kit, respectively. The mice xenograft model was established to investigate the role of XIST in vivo. The interaction between miR-653-5p and XIST or HK2 was predicted by starBase v2.0 and verified by dual-luciferase reporter assay. Western blot was used to measure the protein expression of HK2. Results XIST and HK2 were highly expressed while miR-653-5p was lowly expressed in neuroblastoma tissues and cells. XIST knockdown inhibited tumorigenesis by repressing cell proliferation and invasion, and increased the radiosensitivity via inhibiting colony formation rates and glycolysis. XIST knockdown also suppressed tumor growth in vivo. Moreover, miR-653-5p could bind to XIST and its downregulation reversed the effects of XIST knockdown on tumorigenesis and radiosensitivity. Additionally, HK2 was a direct target of miR-653-5p and its overexpression attenuated the effects of miR-653-5p restoration on suppression of tumorigenesis and promotion of radiosensitivity. Besides, XIST functioned as a molecular sponge of miR-653-5p to regulate HK2 expression. Conclusion XIST interference inhibited tumorigenesis and increased radiosensitivity via regulating miR-653-5p/HK2 axis, providing a novel therapeutic strategy for neuroblastoma.

scholarly journals Blocking circ-CNST suppresses malignant behaviors of osteosarcoma cells and inhibits glycolysis through circ-CNST-miR-578-LDHA/PDK1 ceRNA networks

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Rui Hu ◽  
Shan Chen ◽  
Jianxin Yan
Keyword(s):  
Colony Formation ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Pyruvate Dehydrogenase Kinase ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Physical Interaction ◽  
U2os Cells

Abstract Background CircRNA CNST (circ-CNST) is a newly identified biomarker for prognosis of osteosarcoma (OS). However, its role in OS progression remains to be well documented. Methods Expression of circ-CNST, microRNA (miR)-578, lactate dehydrogenase A (LDHA), and pyruvate dehydrogenase kinase 1 (PDK1) was detected by quantitative real-time polymerase chain reaction and Western blotting. The physical interaction was confirmed by dual-luciferase reporter assay. Cell behaviors and glycolysis were measured by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide assay, colony formation assay, flow cytometry, transwell assays, xenograft experiment, and commercial kits. Results Circ-CNST was upregulated in human OS tissues and cells, accompanied with downregulation of miR-578 and upregulation of LDHA and PDK1. There were negative correlations between miR-578 expression and circ-CNST or LDHA/PDK1 in OS tissues. Moreover, high circ-CNST/LDHA/PDK1 or low miR-578 might predict shorter overall survival, advanced TNM stages, and lymph node metastasis. Physically, miR-578 was targeted by circ-CNST, and miR-578 could target LDHA/PDK1. Functionally, blocking circ-CNST and restoring miR-578 enhanced apoptosis rate and suppressed cell proliferation, colony formation, migration, and invasion in 143B and U2OS cells, accompanied with decreased glucose consumption, lactate production, and adenosine triphosphate (ATP)/adenosine diphosphate (ADP) ratio. Furthermore, in vivo growth of U2OS cells was retarded by silencing circ-CNST. Depletion of miR-578 could counteract the suppressive role of circ-CNST deficiency in 143B and U2OS cells, and restoring LDHA or PDK1 partially reversed the role of miR-578 inhibition as well. Conclusion Circ-CNST knockdown could antagonize malignant behaviors and glycolysis of OS cells by regulating miR-578-LDHA/PDK1 axes.

scholarly journals Circ_0001421 facilitates glycolysis and lung cancer development by regulating miR-4677-3p/CDCA3

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Koudong Zhang ◽  
Hang Hu ◽  
Juan Xu ◽  
Limin Qiu ◽  
Haitao Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Tumor Progression ◽  
Lactate Production ◽  
Tumor Formation ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Glucose Assay

Abstract Background Lung cancer (LC) is a malignant tumor originating in the bronchial mucosa or gland of the lung. Circular RNAs (circRNAs) are proved to be key regulators of tumor progression. However, the regulatory effect of circ_0001421 on lung cancer tumorigenesis remains unclear. Methods The expression levels of circ_0001421, microRNA-4677-3p (miR-4677-3p) and cell division cycle associated 3 (CDCA3) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Methyl thiazolyl tetrazolium (MTT), Transwell and Tumor formation assays were performed to explore the role of circ_0001421 in LC. Glucose consumption and lactate production were examined by a Glucose assay kit and a Lactic Acid assay kit. Western blot was utilized to examine the protein levels of Hexokinase 2 (HK2) and CDCA3. The interaction between miR-4677-3p and circ_0001421 or CDCA3 was confirmed by dual-luciferase reporter assay. Results Circ_0001421 was increased in LC tissues and cells, and knockdown of circ_0001421 repressed cell proliferation, migration, invasion and glycolysis in vitro. Meanwhile, circ_0001421 knockdown inhibited LC tumor growth in vivo. Mechanistically, circ_0001421 could bind to miR-4677-3p, and CDCA3 was a target of miR-4677-3p. Rescue assays manifested that silencing miR-4677-3p or CDCA3 overexpression reversed circ_0001421 knockdown-mediated suppression on cell proliferation, migration, invasion and glycolysis in LC cells. Conclusion Circ_0001421 promoted cell proliferation, migration, invasion and glycolysis in LC by regulating the miR-4677-3p/CDCA3 axis, which providing a new mechanism for LC tumor progression.

scholarly journals MicroRNA-518-3p suppresses cell proliferation, invasiveness, and migration in colorectal cancer via targeting TRIP4

2020 ◽  
Vol 98 (5) ◽  
pp. 575-582
Author(s):  
Heng Yang ◽  
Jia Ren ◽  
Yu Bai ◽  
Jielin Jiang ◽  
Shiyao Xiao
Keyword(s):  
Colorectal Cancer ◽  
Cell Viability ◽  
Colony Formation ◽  
Thyroid Hormone Receptor ◽  
Formation Rate ◽  
Negative Control ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Closure Rate ◽  
Normal Tissues

MicroRNA (miR)-518-3p has been shown to function as a tumor suppressor. This study was conducted to investigate the effects of miR-518-3p in colorectal cancer (CRC). The miR-518-3p mimic, mimic negative control (NC), miR-518-3p inhibitor, inhibitor-NC, ShRNA-TRIP4, and ShRNA-NC vectors were transfected into SW480 cells using Lipofectamine 2000. Cell viability was detected using CCK-8. Colony formation, cell invasiveness, and cell migration were assessed by plate colony formation, Transwell assays, and wound healing assays, respectively. Relative mRNA and protein levels were detected using RT–qPCR and Western blot, respectively. The target gene thyroid hormone receptor interactor 4 (TRIP4) of miR-518-3p was identified and further verified using dual-luciferase reporter assay. Compared with normal tissues, levels of miR-518-3p were decreased and TRIP4 was significantly increased in the tissues from patients with CRC. Following transfection with a miR-518-3p mimic or ShRNA-TRIP4, cell viability decreased in a time-dependent manner, and colony formation rate, wound closure rate, and the number of invasive cells were much lower for the transfected cells than in the corresponding NC and control groups. miR-518-3p overexpression or silencing of TRIP4 significantly down-regulated the expression of MMP-2 and MMP-9. Knockdown of miR-518-3p had the opposite effects, and TRIP4 was identified as a target of miR-518-3p. The inhibitory effects of miR-518-3p on the progressions of CRC are associated with TRIP4.

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