LncRNA HOTTIP modulates cancer stem cell properties in human pancreatic cancer by regulating HOXA9

Fu, Zhiqiang; Chen, Changhao; Zhou, Quanbo; Wang, Yinxue; Zhao, Yue; Zhao, Xiaohui; Li, Wenzhu; Zheng, Shusen; Ye, Huilin; Wang, Lin; He, Zonglin; Q, Lin; Li, Zhihua; Chen, Rufu

doi:10.1016/j.canlet.2017.09.019

Cited by 168 publications

(115 citation statements)

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“…20,21,24,28 Recently, Liao et al 22 demonstrated that HOTTIP expression is elevated in coronary artery disease and in tumor necrosis factor-α or platelet-derived growth factor-induced proliferating endothelial cells; moreover, ectopic expression of HOTTIP augments endothelial cell proliferation. Studies have revealed that HOTTIP is highly expressed in small-cell lung cancer, colorectal cancer, pancreatic cancer, and esophageal squamous cell carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA HOTTIP alleviates oxygen‐glucose deprivation‐induced neuronal injury via modulating miR‐143/hexokinase 2 pathway

Wang

Zhao

et al. 2018

J of Cellular Biochemistry

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HOXA transcript at the distal tip (HOTTIP), which is a long noncoding RNA, plays an important role in multiple cancers and in coronary artery disease. Elevated microRNA-143 (miR-143) expression causes impaired glucose uptake that is responsible for the ischemic cerebral injury. However, the role and mechanism of HOTTIP in ischemic stroke are still unknown. The expression of HOTTIP and miR-143 was first detected in mouse models of transient middle cerebral artery occlusion and in primary neurons exposed to oxygen-glucose deprivation (OGD). We used gain-of function and loss-of function approaches in vitro to investigate the effect and mechanism of HOTTIP on ischemic stroke by evaluating cell viability, apoptosis, and glycolytic metabolism of neurons exposed to OGD. The HOTTIP expression was decreased, whereas miR-143 increased in experimental ischemic stroke models. Overexpression of HOTTIP by the pcDNA3.1-HOTTIP plasmid significantly increased cell viability, glucose uptake, and the expression of hexokinase 2 (HK-2) and pyruvate kinase M2 that were reduced by OGD insult. The HOTTIP overexpression also diminished OGD induced the apoptosis and the caspase-3 activity of neurons. The miR-143 mimic reversed these effects, and anti-miR-143 enhanced them. In addition, we found that HOTTIP could function as a competing endogenous RNA for miR-143 to modulate HK-2 expression. In conclusion, the HOTTIP expression was reduced in ischemic stroke. The HOTTIP overexpression attenuated OGD-induced neuronal injury and imbalanced glycolytic metabolism by sponging miR-143, resulting in the de-repression of its endogenous target HK-2. Taken together, these findings improve understanding of the pathogenesis of ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA HOTTIP alleviates oxygen‐glucose deprivation‐induced neuronal injury via modulating miR‐143/hexokinase 2 pathway

Wang

Zhao

et al. 2018

J of Cellular Biochemistry

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“…Studies have found that the expression levels of HOTTIP are significantly increased in multiple PDAC cell lines and PDAC specimens (35). HOTTIP interacts with the WD repeat containing protein 5 (WDR5)/mixed lineage leukemia (MLL) complex to enhance the methylation of histone 3 on lysine 4 (H3K4) in order to modulate the proliferation and differentiation of PDAC cells (36,37). Up-regulation of HOTTIP promotes the secretion of IL-6 and expression of PD-L1 in neutrophils, thereby inhibiting the activity of T cells and promoting the immune escape of ovarian cancer cells (38).…”

Section: Hottipmentioning

confidence: 99%

Non-coding RNAs in Pancreatic Ductal Adenocarcinoma

Gong

Jiang

2020

Front. Oncol.

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“…Increasing evidence indicates that HOTTIP is overexpressed in prostate cancer, lung cancer, and pancreatic cancer . HOTTIP knockdown impedes cell viability, proliferation, invasion, and angiogenesis in human cancer cells, therefore it is been identified as an oncogenic long noncoding RNA (lncRNA).…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA HOTTIP mediates SRF expression through sponging miR‐150 in hepatic stellate cells

Zheng

Mao

Dong

et al. 2018

J Cellular Molecular Medi

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HOXA transcript at the distal tip (HOTTIP) has been shown to be up‐regulated in a variety of cancers and is identified as an oncogenic long noncoding RNA. However, the biological role of HOTTIP in liver fibrosis is unclear. Here, we reported that HOTTIP was specifically overexpressed in activated hepatic stellate cells (HSCs). HOTTIP knockdown suppressed the activation and proliferation of HSCs. Luciferase reporter assay showed that HOTTIP and serum response factor (SRF) were targets of miR‐150. RNA binding protein immunoprecipitation assay indicated the interaction between miR‐150 and HOTTIP. Further study revealed that HOTTIP increased SRF expression as a competing endogenous RNA for miR‐150, thus prompting HSC activation. Taken together, we provide a novel HOTTIP‐miR‐150‐SRF signalling cascade in liver fibrosis.

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LncRNA HOTTIP modulates cancer stem cell properties in human pancreatic cancer by regulating HOXA9

Cited by 168 publications

References 50 publications

Long noncoding RNA HOTTIP alleviates oxygen‐glucose deprivation‐induced neuronal injury via modulating miR‐143/hexokinase 2 pathway

Long noncoding RNA HOTTIP alleviates oxygen‐glucose deprivation‐induced neuronal injury via modulating miR‐143/hexokinase 2 pathway

Non-coding RNAs in Pancreatic Ductal Adenocarcinoma

Long noncoding RNA HOTTIP mediates SRF expression through sponging miR‐150 in hepatic stellate cells

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