scholarly journals Super-enhancer Associated Long Non-coding RNA AC005592.2 Promotes Tumor Progression by Regulating OLFM4 in Colorectal Cancer

2020 ◽  
Author(s):  
Linping Yan ◽  
Huanhuan Chen ◽  
Li Tang ◽  
Pan Jiang ◽  
Feng Yan
Keyword(s):  
Colorectal Cancer ◽  
Biological Effects ◽  
Differentially Expressed ◽  
Rna Seq ◽  
Invasion And Migration ◽  
Super Enhancer ◽  
Non Coding Rna ◽  
Attractive Therapeutic Target ◽  
And Migration ◽  
Long Non Coding Rna

Abstract Background: Super-enhancer-associated long non-coding RNAs (SE-lncRNAs) have been reported to play essential roles in tumorigenesis, but the fundamental mechanism of SE-lncRNAs in colorectal cancer (CRC) remains largely unknown. Methods: A microarray was performed to identify the differentially expressed SE-lncRNAs between CRC tissues and peritumoral tissues. A novel SE-lncRNA AC005592.2 was selected from these differentially expressed SE-lncRNAs to explore its effects in the CRC development. Fluorescence quantitative real-time PCR (qRT-PCR) was used to assay the expression of AC005592.2 in CRC tissues and cell lines. Functional assays were applied to identify the biological effects of AC005592.2 in CRC cells. Furthermore, RNA-seq was employed to predict potential targets of AC005592.2. Results: AC005592.2 was significantly increased in CRC tissues and cells. And the high expression of AC005592.2 was significantly associated with TNM stage and tumor differentiation of CRC patients. Knockdown of AC005592.2 suppressed CRC cell proliferation, invasion and migration, but promoted apoptosis, while AC005592.2 overexpression exerted precisely the opposite effects on CRC cells. Besides, AC005592.2 positively regulated the expression of olfactomedin 4 (OLFM4), which was also up-regulation in CRC tissues. Conclusion: The findings suggested that AC005592.2 is a crucial promoter of CRC progression, and may serve as an attractive therapeutic target for CRC.

scholarly journals Super-enhancer-associated long noncoding RNA AC005592.2 promotes tumor progression by regulating OLFM4 in colorectal cancer

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Linping Yan ◽  
Huanhuan Chen ◽  
Li Tang ◽  
Pan Jiang ◽  
Feng Yan
Keyword(s):  
Colorectal Cancer ◽  
Noncoding Rna ◽  
Biological Effects ◽  
Differentially Expressed ◽  
Rna Seq ◽  
Invasion And Migration ◽  
Super Enhancer ◽  
Attractive Therapeutic Target ◽  
And Migration ◽  
Fundamental Mechanism

Abstract Background Super-enhancer-associated long noncoding RNAs (SE-lncRNAs) have been reported to play essential roles in tumorigenesis, but the fundamental mechanism of SE-lncRNAs in colorectal cancer (CRC) remains largely unknown. Methods A microarray was performed to identify the differentially expressed SE-lncRNAs between CRC tissues and peritumoral tissues. A novel SE-lncRNA, AC005592.2, was selected from these differentially expressed SE-lncRNAs to explore its effects on CRC development. Fluorescence quantitative real-time PCR (qRT-PCR) was used to assay the expression of AC005592.2 in CRC tissues and cell lines. Functional assays were applied to identify the biological effects of AC005592.2 in CRC cells. Furthermore, RNA-seq was employed to predict potential targets of AC005592.2. Results AC005592.2 was significantly increased in CRC tissues and cells. High expression of AC005592.2 was significantly associated with TNM stage and tumor differentiation in CRC patients. Knockdown of AC005592.2 suppressed CRC cell proliferation, invasion and migration but promoted apoptosis, while AC005592.2 overexpression exerted the opposite effects on CRC cells. In addition, AC005592.2 positively regulated the expression of olfactomedin 4 (OLFM4), which was also upregulated in CRC tissues. Conclusion The findings suggested that AC005592.2 is a crucial promoter of CRC progression and may serve as an attractive therapeutic target for CRC.

Long Non-Coding RNA FLVCR1-AS1 Acts as miR-493-3p Sponge to Modulate Cancer Cell Proliferation, Invasion and Migration in Colorectal Cancer

2020 ◽  
Vol 10 (3) ◽  
pp. 306-314
Author(s):  
Tingyun Cui ◽  
Dechun Gui ◽  
Chao Gu ◽  
Shuai Yan ◽  
Yinzi Yue ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
Colorectal Cancer Cells ◽  
Colorectal Cancer Cell Lines ◽  
And Migration ◽  
Long Non Coding Rna

This study aimed to investigate the effect and mechanism of long non-coding RNA FLVCR1-AS1 on proliferation, invasion and migration of colorectal cancer. QRT-PCR was used to detect the expression of FLVCR1-AS1 in colorectal cancer. The target genes of FLVCR1-AS1 were predicted using the StarBase and Luciferase assay. The biological function of miR-493-3p through a series of in vitro experiments. We examined the expression of FLVCR1-AS1 in colorectal cancer cell lines was remarkably increased. Interference with FLVCR1-AS1 inhibits proliferation, invasion and migration of colorectal cancer cell lines. MiR-493-3p is a targeted miRNA of lncRNA FLVCR1-AS1, and overexpression of miR-493-3p inhibits proliferation of colorectal cancer cells, invasion and migration of colorectal cancer cells, and it can be reversed by lncRNA FLVCR1-AS1. LncRNA FLVCR1-AS1 acts as miR-493-3p sponge to modulate cancer cell proliferation, invasion and migration in colorectal cancer.

scholarly journals Long non-coding RNA XIST regulates ovarian cancer progression via modulating miR-335/BCL2L2 axis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qingjuan Meng ◽  
Ningning Wang ◽  
Guanglan Duan
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna

Abstract Background X inactivation-specific transcript (XIST) is the long non-coding RNA (lncRNA) related to cancer, which is involved in the development and progression of various types of tumor. However, up to now, the exact role and molecular mechanism of XIST in the progression of ovarian cancer are not clear. We studied the function of XIST in ovarian cancer cells and clinical tumor specimens. Methods RT-qPCR was performed to detect the expression levels of miR-335 and BCL2L2 in ovarian cancer cells and tissues. MTT and transwell assays were carried out to detect cell proliferation, migration, and invasion abilities. Western blot was performed to analyze the expression level of BCL2L2. The interaction between miR-335 and XIST/BCL2L2 was confirmed using a luciferase reporter assay. Results The inhibition of XIST can inhibit the proliferation invasion and migration of human ovarian cancer cells. In addition, the miR-335/BCL2L2 axis was involved in the functions of XIST in ovarian cancer cells. These results suggested that XIST could regulate tumor proliferation and invasion and migration via modulating miR-335/BCL2L2. Conclusion XIST might be a carcinogenic lncRNA in ovarian cancer by regulating miR-335, and it can serve as a therapeutic target in human ovarian cancer.

scholarly journals The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR)

2017 ◽  
Vol 43 (1) ◽  
pp. 405-418 ◽  
Author(s):  
Yaoyao Xiong ◽  
Long Wang ◽  
Yuan Li ◽  
Minfeng Chen ◽  
Wei He ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Cancer Growth ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
Bladder Cancer Cells ◽  
And Migration ◽  
Cancer Tissues ◽  
Long Non Coding Rna

Backgrounds/Aims: Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is involved in the progression of several tumors. The interaction between lncRNA and miRNA or miRNA’s target genes is reported to play crucial roles in malignancy. In addition, Androgen receptor (AR) is considered to be involved in bladder cancer progression. In this study, we investigated the role of XIST in human bladder cancer and its interaction with miR-124 and AR. Methods: XIST and AR expression was detected in bladder tumor samples and cell lines. Effects of XIST and AR on bladder cancer cells growth, invasion and migration were analyzed. Bioinformatic analysis and luciferase assays were used to identify the interaction among XIST, AR and miR-124. The correlations of miR-124 with XIST and AR in bladder cancer samples were statistically analyzed. Results: XIST and AR were upregulated in bladder cancer tissues and positively correlated. Higher XIST and AR expression were related to poorer TNM stage of bladder cancer. XIST knockdown reduced bladder cancer cells’ proliferation, invasion and migration. While this inhibitory effect could be partially restored by AR overexpression. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3’UTR of AR to regulate its expression. MiR-124 inhibition partially restored the XIST knockdown-induced reduction of AR, c-myc, p27, MMP13 and MMP9 expression. In bladder cancer tissues, miR-124 level was inversely correlated with the expression of XIST and AR, respectively. Conclusion: These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.

scholarly journals LncRNA-MALAT1-mediated Axl promotes cell invasion and migration in human neuroblastoma

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769979 ◽  
Author(s):  
Shaojie Bi ◽  
Chunyan Wang ◽  
Yixin Li ◽  
Wei Zhang ◽  
Juan Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Invasion ◽  
Neuroblastoma Cells ◽  
Great Influence ◽  
Regulatory Mechanisms ◽  
Human Neuroblastoma ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna

Overexpression of Axl has been noted to correlate with several human cancers. However, the regulatory mechanisms and effects of Axl in human neuroblastoma development remain unclear. Here, we explore the expression of Axl in neurobalstoma and related upstream regulatory mechanisms of invasion and migration. We found that Axl was overexpressed in metastatic neuroblastoma tissues and positively associated with long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1. Meanwhile, our data suggested that metastasis-associated lung adenocarcinoma transcript 1 upregulated Axl expression in neuroblastoma cells, resulting in cell invasion and migration. Furthermore, we found that targeting Axl by inhibitor R428 significantly suppressed the abilities of tumor cell invasion and migration. In summary, these results suggested that Axl, which is regulated by long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1, may exert great influence on invasion and migration of neuroblastoma.

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