Dysregulation of miR-638 in hepatocellular carcinoma and its clinical significance

Cheng, Jiwen; Chen, Yanke; Zhao, Pengwei; Li, Na; Lu, Jianwen; Li, Jianhui; Liu, Zhengwen; Lv, Yi; Huang, Chen

doi:10.3892/ol.2017.5882

Cited by 15 publications

(11 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study, miR-454 was observed to be downregulated in GC tissues and cell lines. To clarify the clinical significance of miR-454 in GC, the median value (37,38) was used as the reference value to define the low/high expression of miR-454 expression in tumour tissues. The analysis showed that low miR-454 expression level in GC was correlated with lymph node metastasis, invasive depth and TNM stage.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-454 inhibits the malignant biological behaviours of gastric cancer cells by directly targeting mitogen-activated protein kinase 1

et al. 2017

View full text Add to dashboard Cite

Gastric cancer (GC) is the fifth most commonly diagnosed malignant disease and the third leading cause of cancer‑related deaths worldwide. Recently, numerous microRNAs (miRNAs) have been determined to contribute to GC initiation and progression, suggesting that miRNAs may be developed as effective diagnostic and prognostic molecular biomarkers and can be investigated as therapeutic targets for patients with this disease. Therefore, further investigation of the miRNAs involved in GC development represents an opportunity to improve the prognosis of GC patients. miRNA‑454 (miR‑454) is abnormally expressed in multiple types of human cancer. However, the expression pattern, biological roles and underlying mechanism of miR‑454 in GC remain unclear and require further investigation. In the present study, we assessed miR‑454 expression in GC tissues and cell lines. We also explored the effects of miR‑454 on the biological behaviours of tumour cells and the underlying molecular mechanisms of miR‑454. The results revealed that miR‑454 was significantly downregulated in GC tissues and cell lines. Low miR‑454 expression was positively associated with lymph node metastasis, invasive depth and TNM stage. Additionally, upregulation of miR‑454 inhibited cell proliferation and invasion and induced the apoptosis of the GC cells. Subsequently, mitogen‑activated protein kinase 1 (MAPK1) was identified as a direct target of miR‑454. MAPK1 was upregulated in GC tissues and was found to be negatively correlated with the miR‑454 expression level. Downregulation of MAPK1 also suppressed GC cell proliferation and invasion and increased apoptosis, thereby resembling the suppressive effects of miR‑454 overexpression in GC. Moreover, upregulation of MAPK1 reversed the tumour‑suppressive effects of miR‑454 in GC. Collectively, our data demonstrated that miR‑454 may play tumour‑suppressing roles in GC through the regulation of MAPK1, suggesting that miR‑454 may be a novel biomarker and therapeutic target for patients with this disease.

show abstract

Section: Discussionmentioning

confidence: 99%

MicroRNA-454 inhibits the malignant biological behaviours of gastric cancer cells by directly targeting mitogen-activated protein kinase 1

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Nineteen of the downregulated miRNAs in chronic patients were found to be associated with carcinogenesis in various organs and tissues, such as miR-1207 [ 40 ], miR-3162-5p [ 41 , 42 ], miR-3196 [ 43 , 44 ], miR-371b-5p [ 45 ], miR-574-5p [ 46 , 47 ], miR-1225-5p [ 48 ], miR-4485 [ 49 ], miR-572 [ 50 ], miR-4299 [ 51 ], miR-3679-5p [ 52 ], miR-3940-5p [ 53 ], miR-638 [ 54 , 55 ], miR-1202 [ 56 ], miR-5787 [ 57 ], miR-1973 [ 58 ], miR-4532 [ 59 ], miR-1275 [ 60 ], miR-4728-5p [ 61 ], and miR-1915-3p [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

The microRNA expression signature of CD4+ T cells in the transition of brucellosis into chronicity

et al. 2018

View full text Add to dashboard Cite

Brucellosis is a serious infectious disease that continues to be a significant cause of morbidity worldwide and across all ages. Despite early diagnosis and treatment, 10–30% of patients develop chronic brucellosis. Although there have been recent advances in our knowledge of Brucella virulence factors and hosts’ immune response to the infection, there is a lack of clear data regarding how the infection bypasses the immune system and becomes chronic. The present study investigated immunological factors and their roles in the transition of brucellosis from an acute to a chronic infection in CD4+ T cells. CD4+ T cells sorted from peripheral blood samples of patients with acute or chronic brucellosis and healthy controls using flow cytometry as well as more than 2000 miRNAs were screened using the GeneSpring GX (Agilent) 13.0 miRNA microarray software and were validated using reverse transcription polymerase chain reaction (RT-qPCR). Compared to acute cases, the expression levels of 28 miRNAs were significantly altered in chronic cases. Apart from one miRNA (miR-4649-3p), 27 miRNAs were not expressed in the acute cases (p <0.05, fold change> 2). According to KEGG pathway analysis, these miRNAs are involved in the regulation of target genes that were previously involved in the MAPK signalling pathway, regulation of the actin cytoskeleton, endocytosis, and protein processing in the endoplasmic reticulum. This indicates the potential role of these miRNAs in the development of chronic brucellosis. We suggest that these miRNAs can be used as markers to determine the transition of the disease into chronicity. This is the first study of miRNA expression that analyses human CD4+ T cells to clarify the mechanism of chronicity in brucellosis.

show abstract

“… 6 Previous studies suggest that miR-638 has an important clinical significance in HCC development. 7 , 8 Moreover, knockdown of miR-638 could promote HCC development by increasing cell growth, angiogenesis, migration and invasion. 9 , 10 In addition, miR-638 could be enriched in exosomes, and exosomal miR-638 plays a key role in human cancers.…”

Section: Introductionmentioning

confidence: 99%

<p>Exosomal miR-638 Inhibits Hepatocellular Carcinoma Progression by Targeting SP1</p>

Yang

Zhao

et al. 2020

OTT

View full text Add to dashboard Cite

Purpose Exosomal microRNAs (miRNAs) play essential roles in the development of hepatocellular carcinoma (HCC). Nevertheless, the role and mechanism of exosomal miR-638 in HCC development remain largely unknown. Methods Exosomes were isolated and confirmed via transmission electron microscopy and western blot. The abundances of miR-638 and specificity protein 1 (SP1) were measured via quantitative reverse transcription polymerase chain reaction or western blot. Cell proliferation was investigated by Cell Counting Kit-8, colony formation assay, apoptosis, cell cycle distribution and related protein expression. Cell migration and invasion were detected via transwell assay and western blot. Co-culture experiment was performed to assess exosome transfer from HCC cells to endothelial cells. The target correlation between miR-638 and SP1 was analyzed via dual-luciferase reporter and RNA immunoprecipitation assays. The subcutaneous xenograft experiment was conducted to test the function of miR-638 in vivo. Results The miR-638 level declined in exosomes from serum or HCC cell medium. miR-638 overexpression repressed HCC cell proliferation by decreasing viability and colony formation and inducing apoptosis and cell cycle arrest at G1 phase, and decreased abilities of migration and invasion. Exosomal miR-638 from HCC cells could transfer to human umbilical vein endothelial cells (HUVECs) and suppress HUVEC proliferation, migration and invasion. SP1 was a target of miR-638 and overexpression of SP1 reversed the effect of miR-638 on HCC cells. Overexpression of miR-638 reduced xenograft tumor growth via decreasing SP1. Conclusion Exosomal miR-638 inhibited HCC tumorigenesis by targeting SP1. This study indicated the potential clinical implications of miR-638 in HCC.

show abstract

Dysregulation of miR-638 in hepatocellular carcinoma and its clinical significance

Cited by 15 publications

References 39 publications

MicroRNA-454 inhibits the malignant biological behaviours of gastric cancer cells by directly targeting mitogen-activated protein kinase 1

MicroRNA-454 inhibits the malignant biological behaviours of gastric cancer cells by directly targeting mitogen-activated protein kinase 1

The microRNA expression signature of CD4+ T cells in the transition of brucellosis into chronicity

<p>Exosomal miR-638 Inhibits Hepatocellular Carcinoma Progression by Targeting SP1</p>

Contact Info

Product

Resources

About