Knockdown of the long non-coding RNA HOTTIP inhibits colorectal cancer cell proliferation and migration and induces apoptosis by targeting SGK1

Liu, Tianyou; Yu, Tao; Hu, Haiying; He, Keping

doi:10.1016/j.biopha.2017.12.064

Cited by 43 publications

(43 citation statements)

References 32 publications

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“…Accumulating studies reveal that HOTTIP has been up‐regulated in a multitude of diseases . However, we failed to detect an aberrant expression of HOTTIP in fibrotic livers.…”

Section: Discussioncontrasting

confidence: 73%

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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“…Accumulating studies reveal that HOTTIP has been up‐regulated in a multitude of diseases . However, we failed to detect an aberrant expression of HOTTIP in fibrotic livers.…”

Section: Discussioncontrasting

confidence: 73%

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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“…[13][14][15] Many factors have given rise to colon cancer, such as bad eating habits, environmental factors, and genetic factors. [13][14][15] Many factors have given rise to colon cancer, such as bad eating habits, environmental factors, and genetic factors.…”

Section: Discussionmentioning

confidence: 99%

E2F1‐mediated MNX1‐AS1‐miR‐218‐5p‐SEC61A1 feedback loop contributes to the progression of colon adenocarcinoma

Wang

et al. 2018

J of Cellular Biochemistry

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The long noncoding RNA MNX1‐AS1 has been reported to facilitate the progression of glioblastoma and ovarian cancer. Nevertheless, the biological roles and underlying mechanisms of MNX1‐AS1 in colon adenocarcinoma have not been studied until now. In the current study, MNX1‐AS1 was upregulated in colon adenocarcinoma. JASPAR prediction tool showed that E2F1 could bind to the promoter region of MNX1‐AS1. The chromatin immunoprecipitation assay and luciferase reporter assay were used to verify the interactions between MNX1‐AS1 and E2F1. Then functional assays revealed that downregulation of MNX1‐AS1 decreased cell proliferation, migration, and invasion in colon adenocarcinoma, but upregulation of E2F1 reversed the effects. Moreover, subcellular fractionation assay manifested that MNX1‐AS1 was enriched in the cytoplasm of colon adenocarcinoma cells, thus we speculated whether MNX1‐AS1 could function as a competing endogenous RNA (ceRNA) to play roles in colon adenocarcinoma. Bioinformatics analysis and luciferase reporter assay indicated that MNX1‐AS1 could sponge microRNA‐218‐5p (miR‐218‐5p). Furthermore, we discovered that SEC61A1 was downstream target of miR‐218‐5p, and MNX1‐AS1 acted as a ceRNA to upregulate the expression of SEC61A1 through sponging miR‐218‐5p. Finally, rescue assays confirmed that MNX1‐AS1 facilitated the progression of colon adenocarcinoma through regulating miR‐218‐5p/SEC61A1 axis. Taken together, we concluded that E2F1‐mediated MNX1‐AS1‐miR‐218‐5p‐SEC61A1 feedback loop contributed to the progression of colon adenocarcinoma.

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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%

“…13,14 Recently, studies have discovered that a series of lncRNAs are abnormally expressed and play vital roles in ischemic stroke. [19][20][21] A recent study demonstrated that HOTTIP expression is upregulated in coronary artery disease and in proliferating endothelial cells, and that it could promote endothelial cell proliferation and migration by activating the Wnt/β-catenin pathway. 14,16 Circulating H19 levels are higher in patients with stroke, compared with healthy controls.…”

mentioning

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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Knockdown of the long non-coding RNA HOTTIP inhibits colorectal cancer cell proliferation and migration and induces apoptosis by targeting SGK1

Cited by 43 publications

References 32 publications

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

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

E2F1‐mediated MNX1‐AS1‐miR‐218‐5p‐SEC61A1 feedback loop contributes to the progression of colon adenocarcinoma

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

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