LncRNA NEAT1 Regulates Cell Viability and Invasion in Esophageal Squamous Cell Carcinoma through the miR-129/CTBP2 Axis

Li, Yong; Chen, Dong; Gao, Xiang; Li, Xiaohui; Shi, Gongning

doi:10.1155/2017/5314649

Cited by 75 publications

(53 citation statements)

References 40 publications

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“…The striking enrichment of NRAD1 in basal-like breast cancer and TNBC suggests that NRAD1 may serve as an attractive diagnostic or prognostic target. In agreement with previous reports [122,123], our analysis also showed that NEAT1 and MALAT1 were enriched in ER+ breast cancers. This conflicts with other studies that have shown that these lncRNAs are TNBC-enriched [64,67].…”

Section: Are Breast Csc-associated Lncrnas Enriched In Tnbcs/basal-lisupporting

confidence: 93%

The Missing Lnc: The Potential of Targeting Triple-Negative Breast Cancer and Cancer Stem Cells by Inhibiting Long Non-Coding RNAs

Brown

Wasson

Marcato

2020

Cells

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Treatment decisions for breast cancer are based on staging and hormone receptor expression and include chemotherapies and endocrine therapy. While effective in many cases, some breast cancers are resistant to therapy, metastasize and recur, leading to eventual death. Higher percentages of tumor-initiating cancer stem cells (CSCs) may contribute to the increased aggressiveness, chemoresistance, and worse outcomes among breast cancer. This may be particularly true in triple-negative breast cancers (TNBCs) which have higher percentages of CSCs and are associated with worse outcomes. In recent years, increasing numbers of long non-coding RNAs (lncRNAs) have been identified as playing an important role in breast cancer progression and some of these have been specifically associated within the CSC populations of breast cancers. LncRNAs are non-protein-coding transcripts greater than 200 nucleotides which can have critical functions in gene expression regulation. The preclinical evidence regarding lncRNA antagonists for the treatment of cancer is promising and therefore, presents a potential novel approach for treating breast cancer and targeting therapy-resistant CSCs within these tumors. Herein, we summarize the lncRNAs that have been identified as functionally relevant in breast CSCs. Furthermore, our review of the literature and analysis of patient datasets has revealed that many of these breast CSC-associated lncRNAs are also enriched in TNBC. Together, this suggests that these lncRNAs may be playing a particularly important role in TNBC. Thus, certain breast cancer-promoting/CSC-associated lncRNAs could be targeted in the treatment of TNBCs and the CSCs within these tumors should be susceptible to anti-lncRNA therapy.

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Section: Are Breast Csc-associated Lncrnas Enriched In Tnbcs/basal-lisupporting

confidence: 93%

The Missing Lnc: The Potential of Targeting Triple-Negative Breast Cancer and Cancer Stem Cells by Inhibiting Long Non-Coding RNAs

Brown

Wasson

Marcato

2020

Cells

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“…Besides, NEAT1 sponged miR-124 in neuroblastoma [37], retinoblastoma [38], Alzheimer's disease [38] and nasopharyngeal carcinoma [39]. Furthermore, NEAT1 sponged miR-129 in esophageal squamous cell carcinoma [40] and hepatoblastoma [41]. NEAT1 also sponged miR-335 in hepatocellular carcinoma [42], acute lymphoblastic leukemia [43], gastric cancer [44] and pancreatic cancer [45].…”

Section: Discussionmentioning

confidence: 99%

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

et al. 2020

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Long noncoding RNAs (lncRNAs) were viewed as crucial participants in the pathogenesis of abdominal aortic aneurysm (AAA). LncRNA NEAT1 was recognized as an oncogenic gene in various diseases. However, its function and mechanism in AAA were not precisely documented. Here, we explored the functional role and molecular mechanism of NEAT1 in AAA. Functionally, the effect of NEAT1 on the proliferation was assessed by CCK-8 and EdU assay, while its impact on the apoptosis was evaluated through caspase-3/9 activity and TUNEL assays. As a result, we found that NEAT1 knockdown enhanced the proliferation and impaired the apoptosis of vascular smooth muscle cells (VSMCs). Reversely, overexpressed NEAT1 exerted anti-proliferation and pro-apoptosis effects in VSMCs. Mechanically, we found that STAT3 acted as a transcription factor and contributed to NEAT1 transcription by ChIP and luciferase reporter assays. In addition, NEAT1 was confirmed as a sponge of miR-4688 and thereby increase the expression of TULP3 in VSMCs via RIP assay and RNA pull-down assay. Rescue experiments indicted that TULP3 overexpressing countervailed the impact of NEAT1 depletion on AAA biological processes. Conclusively, lncRNA NEAT1 induced by STAT3 was identified as a ceRNA and facilitated AAA formation by targeting miR-4688/TULP3 axis.

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“…As known, lncRNAs can negatively regulate microRNAs (miRNAs), which can depress their miRNA targets (Xia et al, ). For example, NEAT1 can regulate esophageal squamous cell carcinoma (ESCC) progression through miR‐129/CTBP2 (Li, Chen, Gao, Li, & Shi, ). NEAT1 promotes HCC development by regulating miR‐129‐5p (Fang et al, ).…”

Section: Discussionmentioning

confidence: 99%

NEAT1 promotes colon cancer progression through sponging miR‐495‐3p and activating CDK6 in vitro and in vivo

Deng

Song

et al. 2019

Journal Cellular Physiology

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Recently, increasing evidence has indicated lncRNAs are powerful regulators in the progression of multiple tumors. Dysregulation of lncRNA NEAT1 has been recognized in many cancer types. Meanwhile, the studies on NEAT1 function have suggested that NEAT1 can serve as a crucial oncogene. Nevertheless, the investigation of NEAT1 in colon cancer is still few. In our study, the function of NEAT1 was studied in colon cancer. As we observed, NEAT1 level was obviously elevated in colon cancer cells.Then, HCT-116 and SW620 cells were stably infected with shRNA-NEAT1 for 48 hr.As exhibited, silence of NEAT1 could greatly repress colon cancer cell progression. Apoptosis of colon cancer cells was triggered and the cell cycle progression wasremarkably inhibited by downregulation of NEAT1. Interestingly, as exhibited, miR-495-3p was obviously decreased in colon cancer cells and it significantly suppressed colon cancer progression. Subsequently, miR-495-3p was predicted as a target of NEAT1. CDK6 was speculated as the target of miR-495-3p and miR-495-3p modulated its expression negatively. Finally, it was indicated that NEAT1 promoted colon cancer development through modulating miR-495-3p and CDK6 in vivo. Taken these together, we reported that NEAT1 could sponge miR-495-3p to contribute to colon cancer progression through activating CDK6. K E Y W O R D SCDK6, colon cancer, miR-495-3p, NEAT1

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LncRNA NEAT1 Regulates Cell Viability and Invasion in Esophageal Squamous Cell Carcinoma through the miR-129/CTBP2 Axis

Cited by 75 publications

References 40 publications

The Missing Lnc: The Potential of Targeting Triple-Negative Breast Cancer and Cancer Stem Cells by Inhibiting Long Non-Coding RNAs

The Missing Lnc: The Potential of Targeting Triple-Negative Breast Cancer and Cancer Stem Cells by Inhibiting Long Non-Coding RNAs

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

NEAT1 promotes colon cancer progression through sponging miR‐495‐3p and activating CDK6 in vitro and in vivo

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