scholarly journals The role of microRNA-572 in the proliferation and chemotherapeutic treatment of prostate cancer

2021 ◽  
Vol 49 (5) ◽  
pp. 030006052110143
Author(s):  
Mingcui Zang ◽  
Xun Guo ◽  
Manqiu Chen
Keyword(s):  
Prostate Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Prostate Tumorigenesis ◽  
Expression Levels ◽  
Matrigel Invasion ◽  
Tensin Homolog ◽  
Docetaxel Treatment ◽  
Induced Apoptosis

Objective MicroRNAs (miRNAs) regulate prostate tumorigenesis and progression by involving different molecular pathways. In this study, we examined the role of miR-572 in prostate cancer (PCa). Methods The proliferation rates of LNCaP and PC-3 PCa cells were studied using MTT assays. Transwell migration and Matrigel invasion assays were performed to evaluate cell migration and invasion, respectively. Protein expression levels were examined using western blotting. Docetaxel-induced apoptosis was evaluated by Caspase-Glo3/7 assays. The putative miR-572 binding site in the phosphatase and tensin homolog (PTEN) 3ʹ untranslated region (3ʹ UTR) was assessed with dual-luciferase reporter assays. Additionally, miR-572 expression levels in human PCa tissues were examined by qRT-PCR assays. Results Upregulation of miR-572 promoted proliferation, migration, and invasion of PCa cells. Overexpression of miR-572 decreased sensitivity of PCa cells to docetaxel treatment by reducing docetaxel-induced apoptosis. MiR-572 can regulate migration and invasion in PCa cells. Furthermore, miR-572 could regulate expression of PTEN and p-AKT in PCa cells by directly binding to the PTEN 3ʹ UTR. MiR-572 expression levels were increased in human PCa tissues and associated with PCa stage. Conclusions miR-572 displayed essential roles in PCa tumor growth and its expression level may be used to predict docetaxel treatment in these tumors.

scholarly journals LINC01006 facilitates cell proliferation, migration and invasion in prostate cancer through targeting miR-34a-5p to up-regulate DAAM1

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Enhui Ma ◽  
Qianqian Wang ◽  
Jinhua Li ◽  
Xinqi Zhang ◽  
Zhenjia Guo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Prostate Gland ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Protein Coding ◽  
Novel Target

Abstract Background Prostate cancer (PCa) is a kind of malignancy occurring in the prostate gland. Substantial researches have proved the major role of long noncoding RNAs (lncRNAs) in PCa. However, the role of long intergenic non-protein coding RNA 1006 (LINC01006) in PCa has not been investigated yet. Methods RT-qPCR was used to examine the expression levels of LINC01006 and its downstream targets. The function of LINC01006 in PCa was tested by in vitro and in vivo assays. With application of RNA pull down, RNA immunoprecipitation (RIP) and luciferase reporter assays, the interaction among LINC01006, miR-34a-5p and disheveled associated activator of morphogenesis 1 (DAAM1) were verified. Results LINC01006 expression presented high in PCa cell lines. LINC01006 silencing suppressed cell proliferative, migratory, invasive capacities while accelerated apoptotic rate. Besides, LINC01006 knockdown also suppressed tumor growth and metastasis in vivo. Furthermore, miR-34a-5p, a tumor suppressor in PCa, was sponged by LINC01006. Moreover, DAAM1 was targeted by miR-34a-5p and promoted PCa progression. More intriguingly, rescue assays suggested that the inhibitory effect of LINC01006 knockdown on PCa development was offset by DAAM1 overexpression. Conclusions LINC01006 promoted PCa progression by sponging miR-34a-5p to up-regulate DAAM1, providing a novel target for PCa therapy.

scholarly journals MiR-145-5p Inhibits the Invasion of Prostate Cancer and Induces Apoptosis by Inhibiting WIP1

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jianming Sun ◽  
Linggang Deng ◽  
Ye Gong
Keyword(s):  
Prostate Cancer ◽  
Molecular Mechanisms ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Anticancer Effects ◽  
Polymerase Chain

Prostate cancer (PCa) is a common malignant tumor of the male genitourinary system that seriously affects the quality of life of patients. Studying the pathogenesis and therapeutic targets of PCa is important. In this study, we investigated the role of miR-145-5p in PCa and its potential molecular mechanisms. The expression levels of miR-145-5p in PCa tissues and adjacent control tissues were detected by real-time quantitative polymerase chain reaction. The effects of miR-145-5p overexpression on PCa were studied using cell proliferation, migration, and invasion experiments. Furthermore, WIP1 was the target gene of miR-145-5p through the bioinformatics website and dual-luciferase reporter gene experiment. Further studies found that WIP1 downregulation could inhibit the proliferation, invasion, and cloning of PCa cells. Overexpression of WIP1 reversed the anticancer effects of miR-145. The anticancer effect of miR-145 was achieved by inhibiting the PI3K/AKT signaling pathway and upregulating ChK2 and p-p38MAPK. Taken together, these results confirmed that miR-145-5p inhibited the growth and metastasis of PCa cells by inhibiting the expression of proto-oncogene WIP1, thereby playing a role in tumor suppression in PCa and may become a potential therapeutic target for the treatment of PCa.

scholarly journals Suppression of ANT2 by miR-137 Inhibits Prostate Tumorigenesis

2021 ◽  
Vol 12 ◽  
Author(s):  
Heyuan Zhang ◽  
Nanhui Chen ◽  
Zhihai Deng ◽  
Yang Mai ◽  
Limin Deng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Target Gene ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Prostate Tumorigenesis ◽  
Direct Target Gene ◽  
Reporter Assays ◽  
Serious Disease ◽  
Cancer Tissues

Prostate cancer (PCa) is a serious disease that affects men’s health. To date, no effective and long-lasting treatment option for this condition is available in clinical practice. ANT2 is highly expressed in a variety of hormone-related cancers, but its relationship and regulatory mechanism with PCa are unclear. In this study, we found that ANT2 expression was significantly upregulated in PCa tissues relative to control samples. Genetic knockdown of ANT2 effectively inhibited, while overexpression promoted, proliferation, migration, and invasion of PCa cells. In addition, miR-137 expression was reduced in prostate cancer tissues relative to control tissues. We identified a regulatory site for miR-137 in the 3′-UTR of ANT2 mRNA; luciferase reporter assays indicated that ANT2 is a direct target gene for miR-137. Transfecting cells with miR-137 mimics and/or an ANT2-encoding plasmid revealed that ANT2 promotes proliferation, migration, and invasion of PCa, whereas co-expression of miR-137 mimics inhibited these behaviors. These observations suggest that miR-137 mimics inhibit development of PCa by antagonizing expression of ANT2. Furthermore, tumorigenic assays in nude mice showed that miR-137 inhibitors abolished the inhibitory effect of ANT2 knockdown on PCa tumor growth. Collectively, our findings suggest that ANT2, a target gene of miR-137, is intimately involved in development of PCa, providing new evidence for the mechanism underlying pathogenesis of PCa as well as new options for targeted therapy.

scholarly journals Effect of microRNA-29b on proliferation, migration, and invasion of endometrial cancer cells

2019 ◽  
Vol 47 (8) ◽  
pp. 3803-3817
Author(s):  
Jian Kong ◽  
Xiuting He ◽  
Yan Wang ◽  
Jie Li
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Water Soluble ◽  
Migration And Invasion ◽  
Chemotherapy Response ◽  
Aberrant Expression ◽  
Altered Expression ◽  
Matrigel Invasion ◽  
Tensin Homolog ◽  
Induced Apoptosis

Objective Aberrant expression of microRNAs is a key regulator of tumorigenesis and progression in endometrial cancer. We assessed the effect of microRNA-29b (miR-29b) on proliferation, chemosensitivity, migration, and invasion of endometrial cancer cells. Methods The proliferation of endometrial cancer cells was examined by water-soluble tetrazolium (WST)-1 assay. The effects of miR-29b on migration and invasion were evaluated by transwell migration and Matrigel invasion assays. Western blotting was used to assess protein expression levels after altered expression of miR-29b. The effect of miR-29b on cisplatin-induced apoptosis was examined by Caspase-Glo 3/7 assay. Results miR-29b inhibited proliferation and decreased migration and invasion of endometrial cancer cells. It also enhanced the sensitivity of endometrial cancer cells to cisplatin and increased cisplatin-induced apoptosis by regulating expression of BAX and Bcl-2. Moreover, miR-29b changed the expression level of phosphatase and tensin homolog (PTEN) and p-AKT by directly binding to the 3′ untranslated region of PTEN. Conclusion miR-29b played important roles in proliferation and progression in endometrial cancer cells by direct regulation of PTEN. It might be used as a biomarker to predict chemotherapy response and prognosis in endometrial cancer.

scholarly journals MicroRNA-625 inhibits cell invasion and epithelial–mesenchymal transition by targeting SOX4 in laryngeal squamous cell carcinoma

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Yuan Li ◽  
Chenjuan Tao ◽  
Lili Dai ◽  
Caixia Cui ◽  
Chaohui Chen ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Expression Levels

AbstractIntroduction: Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer, but the molecular mechanisms underlying its development and progression remain largely elusive. The purpose of the present study is to investigate the expression profile and functional role of microRNA-625 (miR-625) in LSCC.Materials and methods: LSCC tissues and adjacent normal tissues were collected from 86 LSCC patients. The expression levels of miR-625 and SOX4 mRNA in tissues and cells were detected by RT-qPCR analysis. The expression levels of SOX4 and EMT-related proteins were detected by western blot analysis. In vitro cell proliferation, migration, and invasion were detected by MTT assay, colony formation assay, wound healing assay, and transwell invasion assay, respectively. Dual-luciferase reporter assay was performed to verify the binding relationship between miR-625 and the 3′-UTR of SOX4.Results: The results demonstrated that miR-625 is significantly down-regulated in clinical LSCC tissues, and its low expression may be closely associated with unfavorable clinicopathological characteristics of LSCC patients. Overexpression of miR-625 significantly suppressed the proliferation, migration, invasion, and EMT of LSCC cells. Furthermore, SOX4 was validated as a direct target of miR-625 in LSCC cells, and rescue experiments suggested that restoration of SOX4 blocked the tumor suppressive role of miR-625 in LSCC cells.Conclusions: Taken together, these findings highlighted a critical role of miR-625 in the pathogenesis of LSCC, and restoration of miR-625 could be considered as a potential therapeutic strategy against this fatal disease.

MicroRNA-483-3p Promotes Proliferation, Migration, and Invasion and Induces Chemoresistance of Wilms’ Tumor Cells

2019 ◽  
Vol 23 (2) ◽  
pp. 144-151 ◽  
Author(s):  
Guanghua Che ◽  
Hang Gao ◽  
Jing Tian ◽  
Qibo Hu ◽  
Hongchang Xie ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Epithelial Mesenchymal Transition ◽  
Wilms Tumor ◽  
Migration And Invasion ◽  
Chemotherapy Response ◽  
Aberrant Expression ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Matrigel Invasion ◽  
Induced Apoptosis

Wilms’ tumor is the most common pediatric renal malignancy. MiRNAs are important regulators in multiple cancers including Wilms’ tumor. In this study, we examined the role of miR-483-3p on proliferation, chemosensitivity, migration, and invasion of Wilms’ tumor cells. The proliferation of Wilms’ tumor cells was examined using WST-1 assay. The migration and invasion of Wilms’ tumor cells were evaluated by transwell migration assay and matrigel invasion assay. The protein expression levels were detected by Western blot. The effect of miR-483-3p on doxorubicin-induced apoptosis in Wilms’ tumor cells was evaluated by caspase-Glo3/7 assay. Forced expression of miR-483-3p promoted the proliferation, migration, and invasion in Wilms’ tumor cells. Meanwhile, miR-483-3p decreased the sensitivity of Wilms’ tumor cells after doxorubicin treatment. MiR-483-3p inhibited the doxorubicin-induced apoptosis in Wilms’ tumor cells by the regulation of BAX and Bcl-2 expression. Furthermore, miR-483-3p regulated epithelial–mesenchymal transition by affecting the expression of E-cadherin, N-cadherin, snail, and vimentin in Wilms’ tumor cells. Further studies showed that the expression levels of PTEN and p-AKT in Wilms’ tumor cells were changed after aberrant expression of miR-483-3p by binding to 3′-UTR of PTEN. Our study suggests that miR-483-3p played important roles in proliferation and progression in Wilms’ tumor cells and might serve as a potential prognostic biomarker and predict chemotherapy response in Wilms’ tumor.

scholarly journals Inhibition of cancer cell-derived exosomal microRNA-183 suppresses cell growth and metastasis in prostate cancer by upregulating TPM1

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yanping Dai ◽  
Xiaoqin Gao
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Expression Patterns ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Emerging evidence continues to highlight the significant role of microRNAs (miRNAs) in the regulation of cancer growth and metastasis. Herein, the current study aimed to elucidate the role of exosomal miR-183 in prostate cancer development. Methods Initially, public microarray-based gene expression profiling of prostate cancer was employed to identify differentially expressed miRNAs. The putative target gene TPM1 of miR-183 was subsequently predicted, followed by the application of a luciferase reporter assay and examination of the expression patterns in prostate cancer patients and cell lines. The effects of miR-183 and TPM1 on processes such as cell proliferation, invasion and migration were evaluated using in vitro gain- and loss-of-function experiments. The effect of PC3 cells-derived exosomal miR-183 was validated in LNCaP cells. In vivo experiments were also performed to examine the effect of miR-183 on prostate tumor growth. Results High expression of miR-183 accompanied with low expression of TPM1 was detected in prostate cancer. Our data indicated that miR-183 could target and downregulate TPM1, with the overexpression of miR-183 and exosomal miR-183 found to promote cell proliferation, migration, and invasion in prostate cancer. Furthermore, the tumor-promoting effect of exosome-mediated delivery of miR-183 was subsequently confirmed in a tumor xenograft model. Conclusions Taken together, the key findings of our study demonstrate that prostate cancer cell-derived exosomal miR-183 enhance prostate cancer cell proliferation, invasion and migration via the downregulation of TPM1, highlighting a promising therapeutic target against prostate cancer.

scholarly journals Long noncoding RNA LINC00261 suppresses prostate cancer tumorigenesis through upregulation of GATA6-mediated DKK3

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Yang Li ◽  
Hai Li ◽  
Xin Wei
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Prostate Cancer Progression ◽  
Aberrant Expression

Abstract Background Prostate cancer is one of the leading causes of cancer death in males. Recent studies have reported aberrant expression of lncRNAs in prostate cancer. This study explores the role of LINC00261 in prostate cancer progression. Methods The differentially expressed genes, transcription factors, and lncRNAs related to prostate cancer were predicted by bioinformatics analysis. Prostate cancer tissue samples and cell lines were collected for the determination of the expression of LINC00261 by reverse transcription quantitative polymerase chain reaction. The binding capacity of LINC00261 to the transcription factor GATA6 was detected by RIP, and GATA6 binding to the DKK3 promoter region was assessed by ChIP. In addition, luciferase reporter system was used to verify whether LINC00261 was present at the DKK3 promoter. After gain- and loss-of function approaches, the effect of LINC00261 on prostate cancer in vitro and in vivo was assessed by the determination of cell proliferation, invasion and migration as well as angiogenesis. Results LINC00261, GATA6, and DKK3 were poorly expressed in prostate cancer. LINC00261 could inhibit transcriptional expression of DKK3 by recruiting GATA6. Overexpression of LINC00261 inhibited prostate cancer cells proliferation, migration, and invasion as well as angiogenesis, which could be reversed by silencing DKK3. Furthermore, LINC00261 could also suppress the tumorigenicity of cancer cells in vivo. Conclusions Our study demonstrates the inhibitory role of LINC00261 in prostate cancer progression, providing a novel biomarker for early detection of prostate cancer.

scholarly journals Expression and role of microRNA-663b in childhood acute lymphocytic leukemia and its mechanism

Open Medicine ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. 863-871
Author(s):  
Xuehua Liu ◽  
Haixia Zhang ◽  
Baorong Zhang ◽  
Xiaohong Zhang
Keyword(s):  
Jurkat Cell ◽  
Acute Lymphocytic Leukemia ◽  
Malignant Tumors ◽  
Lymphocytic Leukemia ◽  
Jurkat Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Before And After ◽  
Induced Apoptosis

AbstractRecent studies have shown that microRNAs (miRNAs) play a key role in various malignant tumors. MiR-663b has been found to have important roles in several cancers, however, the role of miR-663b in T cell acute lymphocytic leukemia (T-ALL) remains unclear. Therefore, we speculated that miR-663b might also play a crucial role in the development and process of T-ALL. In the present study, we found that miR-663b was up-regulated in the blood of children with T-ALL and T-ALL cell lines. TargetScan and dual luciferase reporter assay results showed that CD99 was a direct target of miR-663b. In order to further study the biological function of miR-663b in the development of T-ALL and to clarify its potential molecular mechanism, we detected the changes in proliferation, apoptosis, migration, and invasion of T-ALL cell line Jurkat before and after miR-663b inhibitor transfection. We found that miR-663b inhibitor inhibited Jurkat cell proliferation and induced apoptosis. In addition, miR-663b inhibitor repressed Jurkat cell migration and invasion. All these effects of miR-663b inhibitor on Jurkat cells were eliminated by CD99-silencing. These results have provided a new theoretical basis and strategy for the diagnosis and treatment of T-ALL.

Functional characterization of HIC, a P2Y1 agonist, as a p53 stabilizer for prostate cancer cell death induction

2021 ◽  
Author(s):  
Hien Thi Thu Le ◽  
Akshaya Murugesan ◽  
Nuno R Candeias ◽  
Olli Yli-Harja ◽  
Meenakshisundaram Kandhavelu
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Functional Characterization ◽  
Migration And Invasion ◽  
Prostate Cancer Cells ◽  
Cancer Cell Death ◽  
Induced Apoptosis

Background: (1-(2-hydroxy-5-nitrophenyl)(4-hydroxyphenyl)methyl)indoline-4-carbonitrile (HIC), an agonist of the P2Y1 receptor (P2Y1R), induces cell death in prostate cancer cells. However, the molecular mechanism behind the inhibition of HIC in prostate cancer remains elusive. Methods and results: Here, to outline the inhibitory role of HIC on prostate cancer cells, PC-3 and DU145 cell lines were treated with the respective IC50 concentrations, which reduced cell proliferation, adherence properties and spheroid formation. HIC was able to arrest the cell cycle at G1/S phase and also induced apoptosis and DNA damage, validated by gene expression profiling. HIC inhibited the prostate cancer cells’ migration and invasion, revealing its antimetastatic ability. P2Y1R-targeted HIC affects p53, MAPK and NF-κB protein expression, thereby improving the p53 stabilization essential for G1/S arrest and cell death. Conclusion: These findings provide an insight on the potential use of HIC, which remains the mainstay treatment for prostate cancer.

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