Long non-coding RNA MIAT promotes cervical cancer proliferation and migration

2020 ◽  
Vol 168 (2) ◽  
pp. 183-190 ◽  
Author(s):  
Lei Zhang ◽  
Shuxia Ge ◽  
Bing Cao
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cell Model ◽  
Signalling Pathway ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna ◽  
Proliferation And Invasion

Abstract Cervical cancer is one of the most common cancers in the world while its pathological mechanisms are not well-elucidated. Long non-coding RNA (lncRNA) has been implicated in cancer development. The dysregulation of lncRNA myocardial infarction-associated transcript (MIAT) has been reported in several cancers while its role in cervical cancer is not described yet. In this study, the role of MIAT in cervical cancer was explored. We evaluated the expression of MIAT in cervical cancer tissues and cell lines. Furthermore, we explored the effects of MIAT on proliferation and invasion of cervical cancer using cell model and animal transplantation model. We also evaluated the effects of MIAT on activation of PI3K/Akt/mTOR signalling pathway. Our results show that MIAT was up-regulated in cervical cancer tissues and cell lines. Knocking down MIAT resulted in decreased cell proliferation, migration and invasion of cervical cancer cells and suppression of tumour growth in mice. Mechanically, knocking down MIAT suppressed the activation of PI3K/Akt signalling pathway. In conclusion, MIAT promotes cell proliferation and invasion in cervical cancer.

scholarly journals Long Non-Coding RNA PVT1/miR-150/ HIG2 Axis Regulates the Proliferation, Invasion and the Balance of Iron Metabolism of Hepatocellular Carcinoma

2018 ◽  
Vol 49 (4) ◽  
pp. 1403-1419 ◽  
Author(s):  
Yunxiuxiu Xu ◽  
Xinxi Luo ◽  
Wenguang He ◽  
Guangcheng Chen ◽  
Yanshan Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Iron Metabolism ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Background/Aims: To investigate the biological roles and underlying molecular mechanisms of long non-coding RNA (lncRNA) PVT1 in Hepatocellular carcinoma (HCC). Methods: qRT-PCR was performed to measure the expression of miRNA and mRNA. Western blot was performed to measure the protein expression. CCK-8 assay was performed to determine cell proliferation. Flow cytometry was performed to detect cell apoptosis. Wounding-healing assay and Transwell assay was performed to detect cell migration and invasion. Dual luciferase reporter assay was performed to verify the target relationship. Quantichrom iron assay was performed to check uptake level of cellular iron. Results: PVT1 expression was up-regulated in HCC tissues and cell lines. Function studies revealed that PVT1 knockdown significantly suppressed cell proliferation, migration and invasion, and induced cell apoptosis in vitro. Furthermore, PVT1 could directly bind to microRNA (miR)-150 and down-regulate miR-150 expression. Hypoxia-inducible protein 2 (HIG2) was found to be one target gene of miR-150, and PVT1 knockdown could inhibit the expression of HIG2 through up-regulating miR-150 expression. In addition, the expression of miR-150 was down-regulated, while the expression of HIG2 was up-regulated in HCC tissues and cell lines. Moreover, inhibition of miR-150 could partly reverse the biological effects of PVT1 knockdown on proliferation, motility, apoptosis and iron metabolism in vitro, which might be associated with dysregulation of HIG2. In vivo results showed that PVT1 knockdown suppressed tumorigenesis and iron metabolism disorder by regulating the expression of miR-150 and HIG2. Conclusion: Taken together, the present study demonstrates that PVT1/miR-150/HIG2 axis may lead to a better understanding of HCC pathogenesis and provide potential therapeutic targets for HCC.

scholarly journals Long non-coding RNA PVT1 indicates a poor prognosis of glioma and promotes cell proliferation and invasion via target EZH2

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Anqiang Yang ◽  
Handong Wang ◽  
Xiaobing Yang
Keyword(s):  
Cell Lines ◽  
Molecular Mechanisms ◽  
Malignant Tumors ◽  
Glioma Cells ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Expression Levels ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Proliferation And Invasion

Human glioma is one of the malignant tumors of the central nervous system (CNS). Its prognosis is poor, which is due to its genetic heterogeneity and our poor understanding of its underlying molecular mechanisms. The present study aimed to assess the relationship between plasmacytoma variant translocation 1 (PVT1) and enhancer of zeste homolog 2 (EZH2), and their effects on the proliferation and invasion of glioma cells. The expression levels of PVT1 and EZH2 in human glioma tissues and cell lines were measured using quantitative RT-PCR (qRT-PCR). Then, after siRNA-PVT1 and entire PVT1 sequence vector transfection, we determined the regulation roles of PVT1 in the proliferation, apoptosis, migration, and invasion of glioma cells. We found that the expression levels of both PVT1 and EZH2 were up-regulated in human glioma tissues and cell lines, and positively correlated with glioma malignancy. And, silencing of PVT1 expression resulted in decreased proliferation, increased apoptosis, and decreased migration and invasion. In addition, exogenous PVT1 led to increased EZH2 expression and increased proliferation and induced proliferation and invasion. These data inferred that long non-coding RNA PVT1 could be served as an indicator of glioma prognosis, and PVT1–EZH2 regulatory pathway may be a novel therapeutic target for treating glioma.

scholarly journals ZFAS1 functions as an oncogenic long non-coding RNA in bladder cancer

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Haifan Yang ◽  
Ge Li ◽  
Bo Cheng ◽  
Rui Jiang
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cell ◽  
Biological Function ◽  
Bladder Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna

Long non-coding RNA (lncRNA) ZFAS1 (zinc finger antisense 1) has been suggested to have an oncogenic role in the tumorigenesis of human malignant tumors. However, the expression status and biological function of ZFAS1 in bladder cancer is still unknown. Thus, the purpose of the present study is to explore the clinical value of ZFAS1 in bladder cancer patients, and the biological function of ZFAS1 in bladder cancer cell. In the present study, we found ZFAS1 expression was increased in bladder cancer tissues compared with paired adjacent normal tissues through analyzing the Cancer Genome Atlas (TCGA) database. Furthermore, we confirmed that levels of ZFAS1 expression were elevated in bladder cancer tissues and cell lines compared with normal bladder tissues and normal uroepithelium cell line, respectively. Then, we observed that the expression level of ZFAS1 was positively associated with clinical stag, muscularis invasion, lymph node metastasis, and distant metastasis in bladder cancer patients. The experiments in vitro suggested that knockdown of ZFAS1 repressed bladder cancer cell proliferation via up-regulating KLF2 and NKD2 expression, and inhibited cell migration and invasion via down-regulating ZEB1 and ZEB2 expression. In conclusion, ZFAS1 is overexpressed in bladder cancer, and functions as an oncogenic lncRNA in regulating bladder cancer cell proliferation, migration, and invasion.

scholarly journals Knock Down of LINC00504 Represses Proliferation and Invasion via Regulation of miR-140-5p in Breast Cancer

2020 ◽  
Author(s):  
Tieying Hou ◽  
Long Ye ◽  
Qingsong Qin ◽  
Shulin Wu
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cancer Tissues ◽  
Proliferation And Invasion

Abstract Background: Breast cancer is one of the most common cancer in the world. Emerging evidence has demonstrated the critical role of long noncoding RNAs (lncRNAs) in the development of breast cancer. In this study, we aimed to investigate the role of LINC00504 in breast cancer progression. Methods: Quantification real-time PCR was used to analyzed the expression levels of LINC00504 and miR‐140-5p in breast cancer tissues and cell lines. Cell proliferation, migration and invasion were assessed by Cell Counting Kit‐8, transwell assay and Immunofluorescence. Dual-luciferase reporter assay and RNA Immunoprecipitation assay were performed to verify the interaction between LINC00504 and miR‐140-5p. The expression levels of VEGFA, CDH1 and VIM were demonstrated by western blot assays. Result: Here, we found that LINC00504 is up regulated in breast cancer tissues and cell lines. Down regulation of LINC00504 mediated by shRNA suppressed the proliferation, migration, and invasion of breast cancer cells in vitro and in vivo. Furthermore, LINC00504 was found to competitively regulate miR‐140-5p via targeting VEGFA. Inhibition of miR‐140-5p attenuated the knockdown-LINC00504 induced inhibition of breast cancer cell proliferation and invasion.Conclusion: Taken together, our results demonstrated the mechanism of the LINC00504–miR‐140-5p–VEGFA axis in breast cancer cell proliferation and invasion and may lead to new lncRNA-based diagnostics or therapeutics for breast cancer.

scholarly journals Long non-coding RNA H19 enhances cell proliferation and anchorage-independent growth of cervical cancer cell lines

2016 ◽  
Vol 242 (2) ◽  
pp. 184-193 ◽  
Author(s):  
Tawin Iempridee
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Transforming Growth Factor ◽  
Cancer Cell Lines ◽  
Cervical Cancer Cell ◽  
Multicellular Tumor Spheroid ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Long non-coding RNA H19 is aberrantly expressed in multiple malignancies and its expression levels correlate with recurrence, metastasis, and patient survival. Despite numerous reports documenting the role of H19 in carcinogenesis, its contribution to cervical cancer development is still largely unknown. In this study, I observed that H19 expression was elevated in cervical cancer cell lines and could be detected in extracellular vesicles in the culture medium. In addition, I demonstrated, by overexpression and knockdown experiments, that H19 promoted cell proliferation and multicellular tumor spheroid formation without significantly affecting apoptosis and cell migration. Finally, treatment with transforming growth factor beta and hypoxia-mimetic CoCl2 could modulate H19 levels in a cell line-specific manner. These findings indicate that H19 promotes both anchorage-specific and -independent growth of cervical cancer cell lines and may serve as a potential target for cancer diagnosis and therapy.

scholarly journals Long non-coding RNA FENDRR inhibits migration and invasion of cutaneous malignant melanoma cells

2020 ◽  
Vol 40 (3) ◽  
Author(s):  
Xu-e Chen ◽  
Pu Chen ◽  
Shanshan Chen ◽  
Jin Lu ◽  
Ting Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Malignant Melanoma ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Related Factors ◽  
Expression Levels ◽  
Non Coding Rna ◽  
Matrix Metallopeptidase ◽  
Long Non Coding Rna ◽  
A375 Cells

Abstract The present study aimed to investigate the effects of lncRNA FENDRR on the migration and invasion of malignant melanoma (MM) cells. The expression levels of FENDRR in MM tissues and MM cell lines were detected using qRT-PCR, followed by construction of FENDRR-knocked down and overexpressed stable cells. Then the effects of FENDRR on cell proliferation, migration and invasion were detected using MTT assay and Transwell assay. The protein expression levels of matrix metallopeptidase 2 (MMP2), MMP9, and related factors in JNK/c-Jun pathway were detected using Western blot. FENDRR was down-regulated in MM tissues and cell lines. Besides, its expression levels in different MM cells were diverse. Knockdown of FENDRR facilitated MM cells proliferation, migration and invasion in A375 cells, while overexpressing FENDRR had reverse results. In addition, MMPs and JNK/c-Jun pathway involved in the FENDRR-mediated regulation of MM cell proliferation, migration and invasion. Our results demonstrated that FENDRR mediated the metastasis phenotype of MM cells by inhibiting the expressions of MMP2 and MMP9 and antagonizing the JNK/c-Jun pathway.

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