scholarly journals Unregulated long non-coding RNA-AK058003 promotes the proliferation, invasion and metastasis of breast cancer by regulating the expression levels of the γ-synuclein gene

2015 ◽  
Vol 9 (5) ◽  
pp. 1727-1732 ◽  
Author(s):  
KAI HE ◽  
PEILIN WANG
Keyword(s):  
Breast Cancer ◽  
Invasion And Metastasis ◽  
Expression Levels ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA Lnc-408 promotes invasion and metastasis of breast cancer cell by regulating LIMK1

Oncogene ◽  
2021 ◽  
Author(s):  
Yina Qiao ◽  
Ting Jin ◽  
Shengdong Guan ◽  
Shaojie Cheng ◽  
Siyang Wen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Noncoding Rna ◽  
Causes Of Death ◽  
Invasion And Metastasis ◽  
Lymphatic Metastases ◽  
Non Coding Rna ◽  
Promising Target ◽  
Mesenchymal Transformation ◽  
Long Non Coding Rna ◽  
Mcf 7

AbstractInvasion and metastasis are the leading causes of death in patients with breast cancer (BC), and epithelial-mesenchymal transformation (EMT) plays an essential role in this process. Here, we found that Lnc-408, a novel long noncoding RNA (lncRNA), is significantly upregulated in BC cells undergoing EMT and in BC tumor with lymphatic metastases compared with those without lymphatic metastases. Lnc-408 can enhance BC invasion and metastasis by regulating the expression of LIMK1. Mechanistically, Lnc-408 serves as a sponge for miR-654-5p to relieve the suppression of miR-654-5p on its target LIMK1. Knockdown or knockout of Lnc-408 in invasive BC cells clearly decreased LIMK1 levels, and ectopic Lnc-408 in MCF-7 cells increased LIMK1 expression to promote cell invasion. Lnc-408-mediated enhancement of LIMK1 plays a key role in cytoskeletal stability and promotes invadopodium formation in BC cells via p-cofilin/F-actin. In addition, the increased LIMK1 also facilitates the expression of MMP2, ITGB1, and COL1A1 by phosphorylating CREB. In conclusion, our findings reveal that Lnc-408 promotes BC invasion and metastasis via the Lnc-408/miR-654-5p/LIMK1 axis, highlighting a novel promising target for the diagnosis and treatment of BC.

scholarly journals Long non-coding RNA MAFG-AS1 promotes proliferation and metastasis of breast cancer by modulating STC2 pathway

2020 ◽  
Author(s):  
Shihao Di ◽  
Die Lu ◽  
Chunni Chen ◽  
Tianshi Ma ◽  
Zigui Zou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Target Gene ◽  
Invasion And Metastasis ◽  
Cancer Proliferation ◽  
Downstream Target ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
Downstream Target Gene ◽  
Proliferation And Metastasis ◽  
Long Non Coding Rna

Abstract Objective Breast cancer is the most common cancer in Chinese women. A number of studies proposed that long non-coding RNA plays an essential role in the regulation of invasion and metastasis of various forms of malignancy, including lung cancer, gastric cancer and bladder cancer. In this study, a long non-coding RNA MAFG-AS1 was explored in detail to understand the significance in the etiology of breast cancer.Methods Quantitative reverse transcription PCR (qRT-PCR) was used to examine the expression level of LncRNA MAFG-AS1 in tissues and cell lines. The association of LncRNA MAFG-AS1 expression and the postoperative prognosis was analyzed by the Kaplan-Meier method and log-rank test. Cell proliferation was evaluated in vitro and in vivo . Transwell assays were performed to examine the cell migration. Cell cycle and apoptosis was evaluated by flowcytometry analysis. The downstream target gene STC2 of LncRNA MAFG-AS1 was screened using the microarray analysis, which was validated by qRT-PCR, functional analysis, and rescue experiment.Results Expression of LncRNA MAFG-AS1 in the breast cancer tissues was significantly higher than the precancerous lesions. Elevated expression level of LncRNA MAFG-AS1 was correlated to the larger GTV (gross tumor volume), negative expression of ER, PR, Her2, lymph node metastasis, and poor prognosis. The potency of breast cancer proliferation, invasion and metastasis was inhibited in the absence of LncRNA MAFG-AS1.Tumorigenic capacity of breast cancer cells was inhibited in the absence of LncRNA MAFG-AS1. The downstream target gene regulated by LncRNA MAFG-AS1 was screened out by gene chip technology, GO analysis and QRT-PCR ultimately. Disrupted STC2 suppressed the cell proliferation and metastasis when the level of LncRNA MAFG-AS1 elevated.Conclusion The LncRNA MAFG-AS1 triggers tumorigenesis in the breast cancer and regulates breast cancer proliferation and metastasis by modulating the downstream target gene STC2. Results from our study indicates that LncRNA MAFG-AS1 can be used.

scholarly journals Long non-coding RNA BRE-AS1 inhibits the proliferation, migration, and invasion of cancer cells in triple-negative breast cancer and predicts patients’ survival by downregulating miR-21

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jianchao Gao ◽  
Sisi Wang ◽  
Zhisheng Zhang ◽  
Jun Li
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Direct Interaction ◽  
Migration And Invasion ◽  
Control Group ◽  
Expression Levels ◽  
Cell Behaviors ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background BRE-AS1 is a recently identified tumor suppressor in non-small cell lung cancer. It role in other human diseases remains elusive. Methods Differential expression of BRE-AS1 in with triple-negative breast cancer (TNBC) patients (n = 74, patient group) and healthy volunteers (n = 58, control group) was studied with RT-qPCR. The direct interaction between BRE-AS1 and premature microRNA-21 (miR-21) was assessed by RNA pull-down assay. The interactions among BRE-AS1, miR-21 and PTEN were evaluated by overexpression assays. CCK-8 assay and Transwell assay were used to evaluate cell behaviors. Results BRE-AS1 was downregulated in TNBC, while miR-21 was highly expressed in TNBC. Low expression levels of lncRNA BRE-AS1 and high expression levels of miR-21 were significantly correlated with unfavorable survival outcomes. BRE-AS1 and miRNA-21 were inversely correlated across TNBC samples, not control samples. BRE-AS1 decreased miR-21 expression and increased PTEN expression while miR-21showed no role in BRE-AS1 expression. RNA pull-down assay illustrated that BRE-AS1 may sponge premature miR-21 to suppress it maturation. Overexpression of BRE-AS1 decreased cell behaviors, while overexpression of miR-21 promoted cell behaviors. MiR-21 suppressed the role of BRE-AS1 in cancer cell behaviors. Conclusion Therefore, BRE-AS1 may inhibit TNBC by downregulating miR-21.

CASC15：A tumor-associated long non-coding RNA

2020 ◽  
Vol 26 ◽  
Author(s):  
Bei Wang ◽  
Wen Xu ◽  
Yuxuan Cai ◽  
Chong Guo ◽  
Gang Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Therapeutic Target ◽  
Cancer Colorectal ◽  
Tumor Development ◽  
Pathophysiological Mechanism ◽  
Biological Processes ◽  
Non Coding Rna ◽  
Cancer Côlon ◽  
The Relationship ◽  
Long Non Coding Rna

Background: CASC15, one of long non-coding RNA, is involved in the regulation of many tumor biological processes, and is expected to become a new biological therapeutic target. This paper aims to elucidate the pathophysiological function of CASC15 in various tumors. Methods: The relationship between CASC15 and tumors was analyzed by searching references, and summarizes the specific pathophysiological mechanism of CASC15. Results: LncRNA CASC15 is closely related to tumor development, and has been shown to be abnormally high expressed in all kinds of tumors, including breast cancer, cervical cancer, lung cancer, hepatocellular carcinoma, gastric cancer, bladder cancer, colon cancer, colorectal cancer, cardiac hypertrophy, intrahepatic cholangiocarcinoma, leukemia, melanoma, tongue squamous cell carcinoma, nasopharyngeal carcinoma. However, CASC15 has been found to be downexpressed abnormally in ovarian cancer, glioma and neuroblastoma. Besides, it is identified that CASC15 can affect the proliferation, invasion and apoptosis of tumors. Conclusion: LncRNA CASC15 has the potential to become a new therapeutic target or marker for a variety of tumors.

scholarly journals Long Non-coding RNA GAS5 Worsens Coronary Atherosclerosis Through MicroRNA-194-3p/TXNIP Axis

2021 ◽  
Author(s):  
Yanbing Li ◽  
Yu Geng ◽  
Boda Zhou ◽  
Xuejiao Wu ◽  
Ou Zhang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Atherosclerosis ◽  
Growth Arrest ◽  
Interacting Protein ◽  
Expression Levels ◽  
Thioredoxin Interacting Protein ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Regulatory Effects ◽  
Long Non Coding Rna

AbstractIt is formerly conducted that long non-coding RNA growth arrest-specific 5 (GAS5) is involved in the process of coronary atherosclerosis (AS). The regulatory effects of GAS5 on the microRNA (miR)-194-3p/thioredoxin-interacting protein (TXNIP) axis in AS have been insufficiently explored yet. Thereafter, this work is started from GAS5/miR-194-3p/TXNIP axis in AS. AS rats were modeled to obtain their coronary vascular tissues and endothelial cells (ECs), in which GAS5, miR-194-3p, and TXNIP expression were tested. ECs were identified by immunohistochemistry. The mechanism among GAS5, miR-194-3p, and TXNIP was determined. ECs were transfected with inhibited GAS5 or overexpressed miR-194-3p to decipher their functions in proliferation and apoptosis of ECs in AS. Raised GAS5 and TXNIP and degraded miR-194-3p expression levels exhibited in AS. GAS5 bound to miR-194-3p while miR-194-3p targeted TXNIP. Depleting GAS5 or restoring miR-194-3p enhanced proliferation and depressed apoptosis of ECs in AS. This work clearly manifests that inhibited GAS5 facilitates the growth of ECs through miR-194-3p-targeted TXNIP in AS, consolidating the basal reference to the curing for AS.

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