scholarly journals LncRNA TMPO-AS1 facilitates the proliferation and metastasis of NSCLC cells by up-regulating ERBB2 via sponging miR-204-3p

2020 ◽  
Vol 34 ◽  
pp. 205873842095894
Author(s):  
Xiaobo Yu ◽  
Qiang Lin ◽  
Fabing Liu ◽  
Fu Yang ◽  
Jingyu Mao ◽  
...  
Keyword(s):  
Colony Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Regulatory Relationship ◽  
Qrt Pcr ◽  
Tyrosine Kinase 2 ◽  
Non Coding Rna ◽  
Gene Assay ◽  
Rna Immunoprecipitation

Introduction: This study aims at probing into the expression and biological function of long non-coding RNA (lncRNA) TMPO-AS1 in non-small cell lung cancer (NSCLC), and exploring its regulatory role for miR-204-3p and erb-b2 receptor tyrosine kinase 2 (ERBB2). Methods: In this study, paired NSCLC samples were collected, and the expression levels of TMPO-AS1, miR-204-3p and ERBB2 were examined by quantitative real-time polymerase chain reaction (qRT-PCR); proliferative ability and colony formation ability were detected by CCK-8 assay and plate colony formation assay, respectively; flow cytometry was performed to detect the effect of TMPO-AS1 on apoptosis; Transwell assay was used to detect the changes of migration and invasion; qRT-PCR and Western blot were utilised to analyse the changes of miR-204-3p and ERBB2 regulated by TMPO-AS1; luciferase reporter gene assay and RNA immunoprecipitation assay were employed to determine the regulatory relationship between TMPO-AS1 and miR-204-3p. Results: We demonstrated that TMPO-AS1 was significantly up-regulated in cancerous tissues of NSCLC samples, and positively correlated with the expression of ERBB2, while negatively correlated with miR-204-3p. After transfection of TMPO-AS1 shRNAs into NSCLC cells, the malignant phenotypes of NSCLC cells were significantly inhibited, while overexpression of TMPO-AS1 had opposite effects; TMPO-AS1 was also demonstrated to regulate the expression of miR-204-3p by sponging it, and indirectly modulate the expression of ERBB2. Conclusion: Collectively, we conclude that TMPO-AS1 has the potential to be the ‘ceRNA’ to regulate the expression of ERBB2 by sponging miR-204-3p in NSCLC.

lncRNA KCNQ1OT1 promotes the proliferation, migration and invasion of retinoblastoma cells by upregulating HIF-1α via sponging miR-153-3p

2020 ◽  
Vol 68 (8) ◽  
pp. 1349-1356
Author(s):  
Yujin Wang ◽  
Jixiang Wang ◽  
Hongyan Hao ◽  
Xiangxia Luo
Keyword(s):  
Colony Formation ◽  
Rna Binding ◽  
Hypoxia Inducible Factor ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Tissue Samples ◽  
Qrt Pcr ◽  
Gene Assay

It is reported that lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) is oncogenic in many cancers. This work aimed at probing into its expression and biological functions in retinoblastoma (RB) as well as its regulatory effects on miR-153-3p and hypoxia-inducible factor-1α (HIF-1α). In our study, RB samples in pair were collected, and quantitative real-time PCR (qRT-PCR) was employed for examining the expression levels of KCNQ1OT1, miR-153-3p and HIF-1α. KCNQ1OT1 short hairpin RNAs were transfected into SO-Rb50 and HXO-RB44 cell to inhibit the expression of KCNQ1OT1. The proliferative activity, colony formation ability and apoptosis were examined through cell counting kit-8 assay, colony formation assays, Transwell assay and flow cytometry, respectively. qRT-PCR and western blot analysis were used for analyzing the changes of miR-153-3p and HIF-1α induced by KCNQ1OT1. The regulatory relationships between miR-153-3p and KCNQ1OT1, miR-153-3p and HIF-1α were examined by dual luciferase reporter gene assay and RNA-binding protein immunoprecipitation assay. The results of our study showed that KCNQ1OT1 expression was markedly enhanced in RB tissue samples, and KCNQ1OT1 knockdown had an inhibitory effect on the proliferation, migration, invasion and viability of RB cells. There were two validated binding sties between KCNQ1OT1 and miR-153-3p, and KCNQ1OT1 negatively regulated the expression of miR-153-3p in RB cells. HIF-1α was a target gene of miR-153-3p, and could be positively regulated by KCNQ1OT1. In conclusion, our study indicates that KCNQ1OT1 can increase the malignancy of RB cells via regulating miR-153-3p/HIF-1α axis.

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

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.

scholarly journals LncRNA Testis-specific transcript, Y-linked 15 (TTTY15) promotes proliferation, migration and invasion of colorectal cancer cells via regulating miR-29a-3p/DVL3 axis

2020 ◽  
Author(s):  
Ming-zheng Cao ◽  
Ying Ba ◽  
Yue-feng Li
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Colony Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Qrt Pcr ◽  
Gene Assay ◽  
Colorectal Cancer Cells ◽  
Proliferation And Metastasis

Abstract Background: Long non-coding RNA TTTY15 is oncogenic in prostate cancer, however its expression and function in colorectal cancer remain largely unknown.Methods: Paired colorectal cancer samples/adjacent tissues were collected, and the expression levels of TTTY15, miR-29a-3p and disheveled segment polarity protein 3 (DVL3) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). TTTY15 shRNAs were transfected into HT-29 and HCT-116 cell lines using lipofectamine reagent; the proliferation and colony formation were detected by CCK-8 assay and plate colony formation assay. qRT-PCR and western blot were used to analyze the changes of miR-29a-3p and DVL3; luciferase reporter gene assay was used to determine the regulatory relationship between miR-29a-3p and TTTY15, miR-29a-3p and DVL3.Results: TTTY15 was significantly up-regulated in cancerous tissues of colorectal cancer samples, positively correlated with the expression of DVL3, while negatively correlated with miR-29a-3p. After TTTY15 shRNAs were transfected into colorectal cancer cells, the proliferation and metastasis of cancer cells were significantly inhibited. TTTY15 shRNAs could reduce the expression of DVL3 on both mRNA and protein levels, and the luciferase activity of TTTY15 sequence was also inhibited by miR-29a-3p. DVL3 was also validated as a target gene of miR-29a-3p.Conclusion: TTTY15 is abnormally upregulated in colorectal cancer tissues, and it can modulate the proliferation and metastasis of colorectal cancer cells. It function as the ceRNA to regulate the expression of DVL3 by sponging miR-29a-3p.

The long non-coding RNA cytoskeleton regulator (CYTOR) sponges microRNA-206 (miR-206) to promote proliferation and invasion of HP75 cells

2021 ◽  
Vol 21 ◽  
Author(s):  
Hu Keqi ◽  
Liu Handong
Keyword(s):  
Cell Lines ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Chi Square ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
Hp75 Cells ◽  
Long Non Coding Rna

Background: The role and mechanism of long non-coding RNA cytoskeleton regulator (CYTOR) in invasive pituitary adenomas (IPA) has not been elucidated previously. Objective: This study aimed to investigate the interaction between CYTOR and miR-206 and their roles in IPA using HP75 cells as the model. Methods: The expression levels of CYTOR and miR-206 were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in IPA tissues and cell lines. The Chi-square test was used to analyze the correlation between CYTOR expression and clinical-pathological parameters. HP75 cell proliferation was detected by Cell Counting Kit-8 assay and colony formation assay. Scratch healing experiments and Transwell assay were used to detect migration and invasion of HP75 cells. The relationship between CYTOR and miR-206 was predicted by bioinformatics and verified by qRT-PCR and dual-luciferase reporter gene method. Result: CYTOR is up-regulated in IPA tissues and cell lines. The high expression of CYTOR is associated with adenoma invasiveness and adenoma size of the patients. Down-regulation of CYTOR decreases the proliferation, migration and invasion of HP75 cells, while up-regulation of miR-206 can inhibit proliferation, migration and invasion of HP75 cells. MiR-206 is identified as a target of CYTOR and could be negatively regulated by it in IPA. Discussion: CYTOR, as a tumor-promoting factor, facilitates the proliferation, migration and invasion of HP75 cells through sponging miR-206. Conclusion: The CYTOR-miR-206 axis provides new insights into the diagnosis and treatment of IPA.

scholarly journals LncRNA testis-specific transcript, Y-linked 15 (TTTY15) promotes proliferation, migration and invasion of colorectal cancer cells via regulating miR-29a-3p/DVL3 axis

2020 ◽  
pp. 1-11
Author(s):  
Xiao-Ying Zheng ◽  
Ming-Zheng Cao ◽  
Ying Ba ◽  
Yue-Feng Li ◽  
Jun-Ling Ye
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Colony Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Qrt Pcr ◽  
Specific Transcript ◽  
Gene Assay ◽  
Colorectal Cancer Cells ◽  
Proliferation And Metastasis

BACKGROUND: Long non-coding RNA testis-specific transcript, Y-linked 15 (TTTY15) is oncogenic in prostate cancer, however its expression and function in colorectal cancer remain largely unknown. METHODS: Paired colorectal cancer samples/adjacent tissues were collected, and the expression levels of TTTY15, miR-29a-3p and disheveled segment polarity protein 3 (DVL3) were examined by quantitative real-time polymerase chain reaction (qRT-PCR); TTTY15 shRNA and overexpression plasmids were transfected into HT29 and HCT-116 cell lines using lipofectamine reagent, respectively; the proliferation and colony formation were detected by CCK-8 assay and plate colony formation 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 TTTY15, miR-29a-3p and DVL3. RESULTS: TTTY15 was significantly up-regulated in cancerous tissues of colorectal cancer samples, positively correlated with the expression of DVL3, while negatively correlated with the expression of miR-29a-3p. After TTTY15 shRNAs were transfected into colorectal cancer cells, the proliferation and metastasis of cancer cells were significantly inhibited, while TTTY15 overexpression had opposite biological effects. TTTY15 shRNA could reduce the expression of DVL3 on both mRNA and protein levels, and the luciferase activity of TTTY15 sequence was also inhibited by miR-29a-3p. DVL3 was also validated as a target gene of miR-29a-3p, and it could be repressed by miR-29a-3p mimics or TTTY15 shRNA. CONCLUSION: TTTY15 is abnormally upregulated in colorectal cancer tissues, and it can modulate the proliferation and metastasis of colorectal cancer cells. It functions as the ceRNA to regulate the expression of DVL3 by sponging miR-29a-3p.

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

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.

scholarly journals The Long Intergenic Noncoding RNA 00707 Sponges MicroRNA-613 (miR-613) to Promote Proliferation and Invasion of Gliomas

2020 ◽  
Vol 19 ◽  
pp. 153303382096209
Author(s):  
Handong Liu ◽  
Keqi Hu
Keyword(s):  
Glioma Cell ◽  
Glioma Cells ◽  
Expression Level ◽  
Luciferase Reporter ◽  
Clinicopathological Parameters ◽  
Migration And Invasion ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
Gene Assay ◽  
Proliferation And Invasion

Background: Glioma is one of the most deadly malignant tumors in humans. Long non-coding RNA (lncRNA) plays a key role in the occurrence, development and invasion of tumors by regulating oncogenic and tumor suppressor pathways. However, the role and action mechanism of long intergenic non-coding RNA 00707 (LINC00707) in gliomas have not been elucidated. This study aimed to investigate the interaction between LINC00707 and miR-613 as well as its role in gliomas. Materials and Methods: The expression levels of LINC00707 and miR-613 were detected by qRT-PCR. The chi-square test was used to analyze the correlation between LINC00707 expression and clinicopathological parameters. CCK-8 and colony formation assays were used to detect glioma cell proliferation; and wound healing and transwell assays were used to detect glioma cell migration and invasion. The relationship between LINC00707 and miR-613 was predicted by Starbase, and verified by qRT-PCR and dual luciferase reporter gene assay. Results: LINC00707 was up-regulated in gliomas. Up-regulated LINC00707 increased the proliferation, migration and invasion of glioma cells, and silenced LINC00707 reduced these abilities. The increase of the expression level of LINC00707 down-regulated miR-613 in glioma cells, while the inhibition of the expression level of LINC00707 up-regulated miR-613 in glioma cells. The high expression of LINC00707 was related to the Karnofsky performance status (KPS) score and WHO staging. LINC00707 could offset the ability of miR-613 to inhibit glioma proliferation and invasion. Conclusion: LINC00707 promotes proliferation and invasion of glioma cells by sponging miR-613. The regulatory axis of LINC00707/miR-613 provides new insights into the mechanism and treatment of gliomas.

MicroRNA-1-3p inhibits the proliferation and migration of oral squamous cell carcinoma cells by targeting DKK1

2018 ◽  
Vol 96 (3) ◽  
pp. 355-364 ◽  
Author(s):  
Zhenshi Wang ◽  
Jiaolong Wang ◽  
Zhihua Chen ◽  
Kun Wang ◽  
Lianshui Shi
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Colony Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Dkk1 Expression ◽  
Gene Assay

We investigated the functional role and mechanism of miR-1-3p and DKK1 in oral squamous cell carcinoma (OSCC) cells. The level of miR-1-3p and DKK1 expression were detected in OSCC tissues and cells using reverse-transcription – quantitative PCR and Western blot. A dual luciferase reporter gene assay was applied to confirm the targeting relationship between miR-1-3p and DKK1. Functional assays, including MTT, Transwell, colony formation, and flow cytometry analysis were conducted to verify their effect on cell progressions. MTT, colony formation, and Transwell assays indicated that the proliferation, migration, and invasion of SCC-4 cells was impaired with high miR-1-3p expression but promoted with high DKK1 expression. The results from cell cycle analysis and annexin-V–PI assays for apoptosis suggested that miR-1-3p suppressed the transit of SCC-4 cells from G0/G1 to S and induced apoptosis. In summary, miR-1-3p suppressed the progression of OSCC by inhibiting DKK1 expression.

Long Non-Coding RNA ARAP1-AS1 Facilitates the Progression of Cervical Cancer by Regulating miR-149-3p and POU2F2

Pathobiology ◽  
2021 ◽  
pp. 1-12
Author(s):  
Ling Zhou ◽  
Xiao-li Xu
Keyword(s):  
Cervical Cancer ◽  
Tumor Model ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Injection Model ◽  
Rna Immunoprecipitation ◽  
Long Non Coding Rna

<b><i>Background:</i></b> Emerging research has demonstrated that long non-coding RNAs (lncRNAs) attach great importance to the progression of cervical cancer (CC). LncRNA ARAP1-AS1 was involved in the development of several cancers; however, its role in CC is far from being elucidated. <b><i>Methods:</i></b> Real-time PCR (RT-PCR) was employed to detect ARAP1-AS1 and miR-149-3p expression in CC samples. CC cell lines (HeLa and C33A cells) were regarded as the cell models. The biological effect of ARAP1-AS1 on cancer cells was measured using CCK-8 assay, colony formation assay, flow cytometry, Transwell assay and wound healing assay in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Furthermore, interactions between ARAP1-AS1 and miR-149-3p, miR-149-3p and POU class 2 homeobox 2 (POU2F2) were determined by bioinformatics analysis, qRT-PCR, Western blot, luciferase reporter and RNA immunoprecipitation assay, respectively. <b><i>Results:</i></b> The expression of ARAP1-AS1 was enhanced in CC samples, while miR-149-3p was markedly suppressed. Additionally, ARAP1-AS1 overexpression enhanced the viability, migration, and invasion of CC cells. ARAP1-AS1 downregulated miR-149-3p via sponging it. ARAP1-AS1 and miR-149-3p exhibited a negative correlation in CC samples. On the other hand, ARAP1-AS1 enhanced the expression of POU2F2, which was validated as a target gene of miR-149-3p. <b><i>Conclusion:</i></b> ARAP1-AS1 was abnormally upregulated in CC tissues and indirectly modulated the POU2F2 expression via reducing miR-149-3p expression. Our study identified a novel axis, ARAP1-AS1/miR-149-3p/POU2F2, in CC tumorigenesis.

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

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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