Interplay between cancer cells and M2 macrophages is necessary for miR-550a-3-5p down-regulation-mediated HPV-positive OSCC progression

Abstract Background: Human papillomavirus (HPV)-positive oral squamous cell carcinoma (OSCC) is increasing worldwide with typically higher grade and stage, while better prognosis. microRNAs (miRNAs) has been shown to play a critical role in cancer, however, their role in HPV-positive OSCC progression remains unclear.Methods: miRNA microarray was performed to identify differentially expressed miRNAs. qRT-PCR and FISH were performed to determine the relative expression of miR-550a-3-5p. CCK-8, Flow cytometry, Wound healing, Cell invasion assays and xenograft experiments were conducted to analyze the biological roles of miR-550a-3-5p. Tumor-associated macrophages (TAMs) generation, co-culturing of cancer cells with TAMs, Western blot, Dual-luciferase reporter gene assay, Immunohistochemistry and animal studies were performed to explore the mechanisms underlying the functions of miR-550a-3-5p.Results: We identified 19 miRNAs differentially expressed in HPV-positive OSCC specimens and miR-550a-3-5p was down-regulated. The low expression of miR-550a-3-5p correlated with higher tumor size and nodal metastasis of HPV-positive OSCC patients. Then, we found that miR-550a-3-5p suppressed the migration, invasion and EMT of HPV-positive OSCC cells dependent on decreasing M2 macrophages polarization. Moreover, miR-550a-3-5p, down-regulated by E6 oncoprotein, inhibited M2 macrophages polarization by YAP/CCL2 signaling, which in turn abrogating EMT program in HPV-positive OSCC cells. In addition, in both xenografts and clinical HPV-positive OSCC samples, miR-550a-3-5p levels were inversely associated with YAP, CCL2 expressions and the number of M2 macrophages.Conclusions: E6/miR-550a-3-5p/YAP/CCL2 signaling induces M2 macrophages polarization to enhance EMT and progression, revealing a novel crosstalk between cancer cells and immune cells in HPV-positive OSCC microenvironment.

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Interplay between cancer cells and M2 macrophages is necessary for miR-550a-3-5p down-regulation-mediated HPV-positive OSCC progression

10.21203/rs.3.rs-23980/v1 ◽

2020 ◽

Author(s):

Mingxin Cao ◽

Weilong Zhang ◽

Xianghua Yu ◽

Jiashun Wu ◽

Xinwei Qiao ◽

...

Keyword(s):

Cancer Cells ◽

Critical Role ◽

Differentially Expressed ◽

Luciferase Reporter ◽

Vehicle Group ◽

M2 Macrophages ◽

Tumor Associated Macrophages ◽

Down Regulation ◽

Macrophages Polarization ◽

Gene Assay

Abstract Background: Human papillomavirus (HPV)-positive oral squamous cell carcinoma (OSCC) is increasing worldwide with typically higher grade and stage. Studies suggested that microRNAs (miRNAs) play a critical role in cancer; However, their role in HPV-positive OSCC progression remains unclear.Methods: miRNA microarray was performed to identify differentially expressed miRNAs. qRT-PCR and FISH were performed to determine the relative expression of miR-550a-3-5p. CCK-8, Flow cytometry, Wound healing, Cell invasion assays and xenograft experiments were conducted to analyze the biological roles of miR-550a-3-5p. Tumor-associated macrophages (TAMs) generation, co-culturing of cancer cells with TAMs, Western blot, Dual-luciferase reporter gene assay, Immunohistochemistry and animal studies were performed to explore the mechanisms underlying the functions of miR-550a-3-5p. Results: In this study, we identified 19 miRNAs differentially expressed in HPV-positive OSCC specimens. One of these, miR-550a-3-5p, was down-regulated in HPV-positive OSCC. This down-regulation correlated with higher tumor size and nodal metastasis. Biofunctional investigations revealed that miR-550a-3-5p inhibited tumor growth and progression in nude mice models without altering the in vitro migration, invasion and EMT of HPV-positive OSCC cells. After co-culturing cancer cells with tumor-associated macrophages (TAMs), we found that the effects of miR-550a-3-5p on suppressing migration, invasion and EMT of HPV-positive OSCC cells were dependent on decreasing M2 macrophages polarization. Moreover, we identified that miR-550a-3-5p, down-regulated by E6 oncoprotein, inhibited M2 macrophages polarization by YAP/CCL2 signaling, which in turn abrogating EMT program in HPV-positive OSCC cells. Using YAP inhibitor, verteporfin (VP) in a HPV-positive OSCC model of transgenic mice also showed that tumors were less progressive when compared to those in Vehicle group. In both xenografts and clinical HPV-positive OSCC samples, miR-550a-3-5p levels were inversely associated with YAP, CCL2 expressions and the number of M2 macrophages.Conclusions: E6/miR-550a-3-5p/YAP/CCL2 signaling induces M2 macrophages polarization to enhance EMT and progression, revealing a novel crosstalk between cancer cells and immune cells in HPV-positive OSCC microenvironment.

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Sevoflurane inhibits proliferation, invasion, but enhances apoptosis of lung cancer cells by Wnt/β-catenin signaling via regulating lncRNA PCAT6/ miR-326 axis

Open Life Sciences ◽

10.1515/biol-2020-0017 ◽

2020 ◽

Vol 15 (1) ◽

pp. 159-172

Author(s):

Guoning Su ◽

Zhibing Yan ◽

Min Deng

Keyword(s):

Lung Cancer ◽

Cancer Cells ◽

Volatile Anesthetic ◽

Lung Cancer Cells ◽

Luciferase Reporter ◽

Dependent Manner ◽

Luciferase Reporter Gene ◽

Western Blot Assay ◽

Gene Assay ◽

Cancer Tissues

AbstractSevoflurane was frequently used as a volatile anesthetic in cancer surgery. However, the potential mechanism of sevoflurane on lung cancer remains largely unclear. In this study, lung cancer cell lines (H446 and H1975) were treated by various concentrations of sevoflurane. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assessment and colony formation assay were performed to detect the cell viability and proliferation, separately. Also, transwell assay or flow cytometry assay was applied as well to evaluate the invasive ability or apoptosis in lung cancer cells, respectively. Western blot assay was employed to detect the protein levels of β-catenin and Wnt5a. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the expression level of prostate cancer-associated transcript 6 (PCAT6) and miR-326 in lung cancer tissues and cells. The target interaction between miR-326 and PCAT6 or Wnt5a was predicted by bioinformatics analysis and verified by the dual-luciferase reporter gene assay. Sevoflurane inhibited the abilities on viability, proliferation, invasion, and activation of Wnt/β-catenin signaling, but promoted apoptosis of H446 and H1975 cells in a dose-dependent manner. The expression of PCAT6 was increased in lung cancer tissues and cells, except for that of miR-326. Besides, sevoflurane could lead to expressed limitation of PCAT6 or improvement of miR-326. This process presented a stepwise manner. Up-regulation of PCAT6 restored the suppression of sevoflurane on abilities of proliferation, invasion, rather than apoptosis, and re-activated the Wnt5a/β-catenin signaling in cells. Moreover, the putative binding sites between miR-326 and PCTA6 or Wnt5a were predicted by starBase v2.0 software online. PCAT6 suppressing effects on cells could be reversed by pre-treatment with miR-326 vector. The promotion of Wnt5a inverted effects led from miR-326 or sevoflurane. Our study indicated that sevoflurane inhibited the proliferation, and invasion, but enhanced the apoptosis in lung cancer cells by regulating the lncRNA PCAT6/miR-326/Wnt5a/β-catenin axis.

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Blockade of LINC01605-enriched exosome generation in M2 macrophages impairs M2 macrophage-induced proliferation, migration, and invasion of human dermal fibroblasts

International Journal of Immunopathology and Pharmacology ◽

10.1177/20587384211016724 ◽

2021 ◽

Vol 35 ◽

pp. 205873842110167

Author(s):

Zhensen Zhu ◽

Bo Chen ◽

Liang Peng ◽

Songying Gao ◽

Jingdong Guo ◽

...

Keyword(s):

Noncoding Rna ◽

Dermal Fibroblast ◽

Dermal Fibroblasts ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

M2 Macrophage ◽

M2 Macrophages ◽

Luciferase Reporter Gene ◽

Gene Assay

Activated M2 macrophages are involved in hypertrophic scar (HS) formation via manipulating the differentiation of fibroblasts to myofibroblasts having the proliferative capacity and biological function. However, the function of exosomes derived from M2 macrophages in HS formation is unclear. Thus, this study aims to investigate the role of exosomes derived by M2 in the formation of HS. To understand the effect of exosomes derived from M2 macrophages on formation of HS, M2 macrophages were co-cultured with human dermal fibroblast (HDF) cells. Cell Counting Kit-8 assay was performed to evaluate HDF proliferation. To evaluate the migration and invasion of HDFs, wound-healing and transwell invasion assays were performed, respectively. To investigate the interaction between LINC01605 and miR-493-3p, a dual-luciferase reporter gene assay was adopted; consequently, an interaction between miR-493-3p and AKT1 was detected. Our results demonstrated that exosomes derived from M2 macrophages promoted the proliferation, migration, and invasion of HDFs. Additionally, we found that long noncoding RNA LINC01605, enriched in exosomes derived from M2 macrophages, promoted fibrosis of HDFs and that GW4869, an inhibitor of exosomes, could revert this effect. Mechanistically, LINC01605 promoted fibrosis of HDFs by directly inhibiting the secretion of miR-493-3p, and miR-493-3p down-regulated the expression of AKT1. Exosomes derived from M2 macrophages promote the proliferation and migration of HDFs by transmitting LINC01605, which may activate the AKT signaling pathway by sponging miR-493-3p. Our results provide a novel approach and basis for further investigation of the function of M2 macrophages in HS formation.

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A Potential miRNA-mRNA Network for Dementia and Hernia Crosstalk

BioMed Research International ◽

10.1155/2021/4324068 ◽

2021 ◽

Vol 2021 ◽

pp. 1-14

Author(s):

De-jian Chen ◽

Da-peng Li

Keyword(s):

Reporter Gene ◽

Expression Profiles ◽

Differentially Expressed ◽

Luciferase Reporter ◽

Clinical Samples ◽

Luciferase Reporter Gene ◽

Tissue Samples ◽

Regulatory Pathways ◽

Gene Assay ◽

Potential Link

Background. It has been reported that there may be a potential link between hernia and dementia. However, the exact mechanisms of their association have not been established. This study is aimed at constructing miRNA-mRNA networks to elucidate on the potential link between dementia and hernia. Methods. Gene expression profiles for dementia, herniation, and skeletal muscle were downloaded from the GEO database after which differentially expressed mRNAs and miRNAs were obtained. In addition, fascia tissue samples were obtained during surgery. A total of 41 patients were recruited in this study, and expression levels of candidate genes were examined using quantitative RT-PCR. Luciferase reporter gene assays were used to identify potential miRNA-mRNA regulatory pathways. Results. Differentially expressed mRNAs and miRNAs were screened. A potential miRNA-mRNA network revealing the crosstalk mechanism between herniation and dementia was identified. Single cell analysis revealed that PI16 was highly enriched in adipose tissues, skeletal muscles, and in the skin. GSEA enrichment analysis showed that PI16 is involved in adipose metabolism, muscle functions, and energy metabolism. In clinical samples, PI16 was found to be upregulated in hernia, while miR-4451 was found to be downregulated. The luciferase reporter gene assay revealed that downregulation of circulating miR-4451 may be responsible for the upregulated PI16 expression in hernia sacs. Conclusions. We constructed an miRNA-mRNA network that shows the potential association between dementia and hernia. We also found that miR-4451 regulates the PI16 expression, which may be a key target and biomarker for hernia pathogenesis and dementia crosstalk.

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MiR-125b Inhibits Cell Proliferation and Induces Apoptosis in Human Colon Cancer SW480 Cells via Targeting STAT3

Recent Patents on Anti-Cancer Drug Discovery ◽

10.2174/1574892816666210708165037 ◽

2021 ◽

Vol 16 ◽

Author(s):

Junhe Zhang ◽

Wenwen Yang ◽

Yunxi Xiao ◽

Linlin Shan

Keyword(s):

Colon Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Luciferase Reporter ◽

Colon Cancer Cells ◽

Luciferase Reporter Gene ◽

Luciferase Reporter Gene Assay ◽

Gene Assay ◽

Proliferation And Apoptosis ◽

Sw480 Cells

Background: Colon cancer is one of the most common types of cancer worldwide. Multiple studies have unveiled the key role of microRNAs (miRNAs) in the development of various types of cancer. However, the mechanism of action of miR-125b in the development and progression of colon cancer remains unknown. Objective: In this study, we explored the association of miR-125b and signal transducer and activator of transcription 3 (STAT3) and its role in the proliferation and apoptosis of SW480 colon cancer cells. Methods: The miR-125b expression in NCM460, SW480, HT29, and HCT8 cells was detected using quantitative real-time polymerase chain reaction (qRT-PCR). SW480 cells were transfected with lentiviruses of GFP–miR–125b and GFP–NC to establish a stable miR-125b overexpression colon cancer cell model and a control model. The targeting relationship between miR-125b and STAT3 was analyzed using bioinformatics and verified by the dual-luciferase reporter gene assay. Cell proliferation and apoptosis were assessed using the Cell Counting Kit-8 assay and TUNEL staining. The expression levels of STAT3, Bcl-2, and Bax were analyzed using Western blot analysis. Results: It was found that the relative mRNA expression of miR-125b was decreased in SW480, HT29, and HCT8 cells compared with that in NCM460 cells (P<0.05). The luciferase reporter gene assay confirmed that miR-125b downregulated the STAT3 gene expression (P<0.05). Overexpression of miR-125b inhibited proliferation and promoted apoptosis in SW480 colon cancer cells and was accompanied by upregulated Bax expression and downregulated Bcl-2 expression (P<0.05). Re-expression of STAT3 promoted cell proliferation and inhibited cell apoptosis, whereas Bcl-2 expression increased, and Bax expression decreased (P<0.05). Conclusion: The miR-125b regulates the expression of Bax and Bcl-2 by downregulating the expression of STAT3, thereby inhibiting proliferation and inducing apoptosis of SW480 colon cancer cells.

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LncRNA DSCAM-AS1 Promotes Proliferation, Migration and Invasion of Colorectal Cancer Cells via Modulating miR-144-5p/CDKL1

10.21203/rs.3.rs-51209/v1 ◽

2020 ◽

Author(s):

Jiaping Pei ◽

Xiaozhao Deng

Keyword(s):

Colorectal Cancer ◽

Cancer Cells ◽

Sw480 Cell ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Luciferase Reporter Gene ◽

Regulatory Relationship ◽

Qrt Pcr ◽

Gene Assay ◽

And Function

Abstract Background LncRNA DSCAM-AS1 is oncogenic in several cancers. However, DSCAM-AS1 expression and function in colorectal cancer (CRC) remain far from being fully elucidated. Methods Paired CRC tissues/adjacent tissues were collected, and the expression levels of DSCAM-AS1, miR-144-5p and CDKL1 were examined by qRT-PCR; DSCAM-AS1 shRNA was transfected into HCT-116 and SW480 cell lines to establish cell models. The proliferation was detected through CCK-8 assay and plate colony formation assay. Transwell assay was used to evaluate the migration and invasion. QRT-PCR and western blot were adopted to analyze changes in miR-144-5p and CDKL1; luciferase reporter gene assay was performed to determine the regulatory relationship between miR-144-5p and DSCAM-AS1, miR-144-5p and CDKL1. Results DSCAM-AS1 was notably up-regulated in CRC samples, positively correlated with CDKL1 expression, while negatively correlated with miR-144-5p. After the transfection of DSCAM-AS1 shRNAs into cancer cells, the proliferative and metastatic ability of cancer cells were impeded. DSCAM-AS1 could reduce the expression level of miR-144-5p by binding with it. Additionally, CDKL1 was also validated as a target gene of miR-144-5p, and DSCAM-AS1 was proved to indirectly regulate CDKL1 expression. Conclusion DSCAM-AS1 was aberrantly up-regulated in CRC, and it can modulate the cells proliferative and metastatic ability. It has the ability to be the “ceRNA” to regulate CDKL1 expression via sponging miR-144-5p.

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Screening and validation of differentially expressed microRNAs and target genes in hypertensive mice induced by cytomegalovirus infection

Bioscience Reports ◽

10.1042/bsr20202387 ◽

2020 ◽

Vol 40 (12) ◽

Cited By ~ 1

Author(s):

YunZhong Shi ◽

DongMei Xi ◽

XiaoNi Zhang ◽

Zhen Huang ◽

Na Tang ◽

...

Keyword(s):

Target Genes ◽

Reporter Gene Assay ◽

Differentially Expressed ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Mcmv Infection ◽

Luciferase Reporter Gene Assay ◽

Qrt Pcr ◽

Gene Assay ◽

Differentially Expressed Mirnas

Abstract Introduction: Multiple studies have suggested an association between cytomegalovirus (CMV) infection and essential hypertension (EH). MicroRNAs (miRNAs) play a critical role in the development of EH by regulating the expression of specific target genes. However, little is known about the role of miRNAs in CMV-induced EH. In the present study, we compared the miRNA expression profiles of samples from normal and murine cytomegalovirus (MCMV)-infected C57BL/6 mice using high-throughput sequencing analysis. Methods: We collected the thoracic aorta, heart tissues, and peripheral blood from 20 normal mice and 20 MCMV-infected mice. We identified differentially expressed miRNAs in the peripheral blood samples and predicted their target genes using bioinformatics tools. We then experimentally validated them using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and the target genes with double luciferase reporter gene assay. Results: We found 118 differentially expressed miRNAs, among which 9 miRNAs were identified as potential MCMV infection-induced hypertension regulators. We then validated the expression of two candidate miRNAs, mmu-miR-1929-3p and mcmv-miR-m01-4-5p, using qRT-PCR. Furthermore, the dual-luciferase reporter gene assay revealed that the 3′-untranslated region (UTR) of endothelin A receptor (Ednra) messenger RNA (mRNA) contained a binding site for mmu-miR-1929-3p. Collectively, our data suggest that MCMV infection can raise the blood pressure and reduce mmu-miR-1929-3p expression in C57BL/6 mice. Moreover, we found that mmu-miR-1929-3p targets the 3′-UTR of the Ednra mRNA. Conclusion: This novel regulatory axis could aid the development of new approaches for the clinical prevention and control of EH.

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PGM5-AS1 Inhibits the Malignant Phenotype of Colon Cancer Cells by Regulating PAEP and NME1

10.21203/rs.3.rs-72192/v1 ◽

2020 ◽

Author(s):

Bingqing Hui ◽

Chen Lu ◽

Jing Wang ◽

Yetao Xu ◽

Yuchen Yang ◽

...

Keyword(s):

Colon Cancer ◽

Alternative Splicing ◽

Cancer Cells ◽

Target Genes ◽

Luciferase Reporter ◽

Colon Cancer Cells ◽

Luciferase Reporter Gene ◽

Malignant Phenotype ◽

Data Set ◽

Gene Assay

Abstract Background: An increasing number of long non-coding RNAs (lncRNAs) is recognized to be associated with drug resistance in CRC.Methods: For identifying differentially expressed target genes regarding PGM5-AS1, RNA transcriptome sequencing was performed. The mechanism by which PGM5-AS1 regulates its target genes was explored by performing experiments such as fluorescent in situ hybridization assay, dual luciferase reporter gene assay and RNA immunoprecipitation. Results: The lncRNA PGM5-AS1 was identified by analyzing data from the original microarray data set of colon cancer (GSE75970). PGM5-AS1 additionally suppressed acquired oxaliplatin resistance in CRC cells. Malignant phenotype of PGM5-AS1 was inhibited by recruiting SRSF3 to activate alternative splicing and being a sponge specific to hsa-miR-423-5p.Conclusions: Downregulation of PGM5-AS1 in oxaliplatin-resistant colon cancer tissues and cell lines is induced by transcriptional inhibition of GFI1B. PGM5-AS1 recruited SRSF3 to activate alternative splicing to downregulate the expression of PAEP. In addition, PGM5-AS1 could competitively bind with hsa-miR-423-5p to upregulate the expression of NME1. PGM5-AS1 inhibits the proliferation, invasion, migration and acquired oxaliplatin resistance of colon cancer cells through these two pathways.

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HOTAIR Competitively Binds MiRNA330 as a Molecular Sponge to Increase the Resistance of Gastric Cancer to Trastuzumab

Current Cancer Drug Targets ◽

10.2174/1568009620666200504114000 ◽

2020 ◽

Vol 20 (9) ◽

pp. 700-709 ◽

Cited By ~ 3

Author(s):

Liangyu Bie ◽

Suxia Luo ◽

Dan Li ◽

Yan Wei ◽

Yu Mu ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Lentiviral Vector ◽

Luciferase Reporter ◽

Tumor Proliferation ◽

Trastuzumab Resistance ◽

Luciferase Reporter Gene ◽

Gastric Cancer Cells ◽

Strong Expression ◽

Gene Assay

Background: HOTAIR, one of the most widely studied long non-coding RNAs in tumors, is closely related to tumor proliferation, migration, invasion and chemoresistance. Objective: Here, we studied the mechanism behind proliferation and chemoresistance processes. Methods: A total of 75 samples were collected from patients who underwent surgical resection of their gastric cancer and received trastuzumab treatment. Primary cells were isolated and cultured. We also developed a cell line overexpressing HOTAIR by constructing a lentiviral vector. These cell lines were studied using an array of established biomolecular methods. Results: We found that HOTAIR levels were inversely associated with sensitivity to trastuzumab in gastric cancer and that overexpression of HOTAIR can promote the proliferation and invasion of gastric cancer cells. The sensitivity of cells overexpressing HOTAIR to two different types of human epidermal growth factor receptor 2 (HER2) inhibitors (trastuzumab and afatinib) showed that overexpression of HOTAIR is specific for trastuzumab resistance. Furthermore, luciferase reporter gene assay and western blot assay showed that there is a HOTAIR-miRNA330-ERBB4 competitive endogenous RNA regulatory network with miRNA330 as the core. Conclusion: HOTAIR can not only promote tumor proliferation but also enhance the resistance of tumor cells to drugs. Our experimental data not only showed strong expression of HOTAIR in gastric cancer, but also that strong expression of HOTAIR caused the sensitivity of gastric cancer cells to trastuzumab, which is a useful reference for postoperative medication.

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LncRNA BLACAT1 Promotes Proliferation, Migration and Invasion of Prostate Cancer Cells via Regulating miR-29a-3p/DVL3 Axis

Technology in Cancer Research & Treatment ◽

10.1177/1533033820972342 ◽

2021 ◽

Vol 20 ◽

pp. 153303382097234

Author(s):

Bo Liao ◽

Shuangquan Chen ◽

Yugen Li ◽

Zhaohui Yang ◽

Ying Yang ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Prostate Cancer Cells ◽

Luciferase Reporter Gene ◽

Qrt Pcr ◽

Gene Assay ◽

Proliferative Ability

Background: Long non-coding RNA bladder cancer associated transcript 1 (BLACAT1) is oncogenic in several types of cancers. However, little is known concerning its expression and function in prostate cancer. Methods: Paired prostate cancer samples were collected, and the expression levels of BLACAT1, miR-29a-3p and disheveled segment polarity protein 3 (DVL3) were examined by quantitative real-time polymerase chain reaction (qRT-PCR); BLACAT1 shRNAs were transfected into PC-3 and LNCaP cell lines, and proliferative ability was detected by cell counting kit-8 (CCK-8) assay; qRT-PCR and Western blot were used to analyze the changes of miR-29a-3p and DVL3; dual-luciferase reporter gene assay was used to determine the regulatory relationships between miR-29a-3p and BLACAT1, and miR-29a-3p and DVL3. Results: BLACAT1 expression was significantly up-regulated in cancerous tissues of prostate cancer samples and positively correlated with the expression of DVL3, while negatively associated with miR-29a-3p. After the transfection of BLACAT1 shRNAs into prostate cancer cells, the proliferative ability and metastatic ability of cancer cells were significantly inhibited; BLACAT1 shRNAs could reduce the expression of DVL3 on both mRNA and protein expressions levels, the luciferase activity of BLACAT1 reporter was inhibited by miR-29a-3p, and DVL3 was validated as a target gene of miR-29a-3p. Conclusion: BLACAT1 expression is abnormally up-regulated in prostate cancer tissues. BLACAT1 can modulate the proliferative and metastatic ability of prostate cancer cells and have the potential to be the “ceRNA” to regulate the expression of DVL3 by sponging miR-29a-3p.

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