Overexpression of long non-coding RNA MCM3AP-AS1 in breast cancer tissues compared to adjacent non-tumour tissues

2020 ◽  
pp. 1-5
Author(s):  
A Riahi ◽  
M Hosseinpour-Feizi ◽  
A Rajabi ◽  
M Akbarzadeh ◽  
V Montazeri ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA ROR recruits histone transmethylase MLL1 to up-regulate TIMP3 expression and promote breast cancer progression

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Aixia Hu ◽  
Fan Hong ◽  
Daohong Li ◽  
Yuwei Jin ◽  
Lingfei Kon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Cancer Prognosis ◽  
Non Coding Rna ◽  
Novel Target ◽  
Cancer Tissues ◽  
Long Non Coding Rna

Abstract Background As a significant cause of cancer deaths worldwide, breast cancer continues to be a troublesome malignancy. Long non-coding RNAs (lncRNAs) have been implicated in the development of breast cancer. Abnormal methylation has been associated with unfavorable breast cancer prognosis. Herein, the current study aimed to elucidate the role of lncRNA ROR in breast cancer. Methods RT-qPCR was performed to determine whether lncRNA ROR was highly expressed in breast cancer tissues, while lncRNA ROR expression was detected in both the nuclear and cytoplasm of breast cancer cells. MCF-7 cells were subsequently introduced with oe-lncRNA ROR, sh-lncRNA ROR to explore the effects of lncRNA ROR on cell proliferation, invasion and apoptosis. Results RIP, RNA pull-down and ChIP assays provided evidence suggesting that lncRNA ROR recruited transmethylase MLL1 to promote H3K4 trimethylation that enhanced TIMP3 transcription. The rescue experiments demonstrated that lncRNA ROR knockdown could inhibit the progression of breast cancer via the downregulation of TIMP3. Finally, the in vivo experiment findings consistently highlighted the suppressive effects of lncRNA ROR silencing on tumor growth. Conclusion Taken together, our study demonstrates that silencing of lncRNA ROR inhibits breast cancer progression via repression of transmethylase MLL1 and TIMP3, emphasizing the potential of lncRNA ROR as a novel target against breast cancer.

scholarly journals Long non-coding RNA PVT1 facilitates cell proliferation by epigenetically regulating FOXF1 in breast cancer

RSC Advances ◽  
2018 ◽  
Vol 8 (5) ◽  
pp. 2740-2750
Author(s):  
Guangcheng Guo ◽  
Fang Wang ◽  
Mingli Han ◽  
Yuanting Gu ◽  
Xin Duan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Non Coding Rna ◽  
Cancer Tissues ◽  
Long Non Coding Rna ◽  
Variant Translocation

Plasmacytoma variant translocation 1 (PVT1) expression was elevated in breast cancer tissues and correlated to breast cancer progression and prognosis.

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 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.

Targeting long non-coding RNA ASBEL with oligonucleotide antagonist for breast cancer therapy

2017 ◽  
Vol 489 (4) ◽  
pp. 386-392 ◽  
Author(s):  
Yang Xia ◽  
Xiangqian Xiao ◽  
Xiongwei Deng ◽  
Fang Zhang ◽  
Xiaofei Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Therapy ◽  
Breast Cancer Therapy ◽  
Non Coding Rna ◽  
Long Non Coding Rna

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 Long non-coding RNA CRALA is associated with poor response to chemotherapy in primary breast cancer

2017 ◽  
Vol 8 (6) ◽  
pp. 582-591 ◽  
Author(s):  
Yudong Li ◽  
Baoxiao Wang ◽  
Hongna Lai ◽  
Shunying Li ◽  
Qiuting You ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Primary Breast Cancer ◽  
Poor Response ◽  
Non Coding Rna ◽  
Response To Chemotherapy ◽  
Long Non Coding Rna
Sign in / Sign up

Export Citation Format

Share Document