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Role of HDAC1 in the progression of gastric cancer and the correlation with lncRNAs.

ABSTRACT: Gastric cancer (GC) is a common life-threatening cancer type worldwide, with an increasing prevalence and a high rate of mortality. Due to limitations in clinical treatment, surgery has become the most efficient strategy for the treatment of GC. It is urgent to identify novel biomarkers, which are useful for the diagnosis of GC and for improving the survival rate of patients with GC. HDACs are multi-functional proteins and are involved in regulating gene expression, cell proliferation and the epigenetic regulation. However, the precise role of HDACs in the progression of GC remains unknown. The present study demonstrated that HDAC1 is involved in the promotion of GC cell proliferation, possibly by upregulating the expression of the lncRNAs, BC01600 and AF116637, in the tissues of patients with GC. Abnormal expression profiles of lncRNAs were observed in the tissues of patients with GC. lncRNAs were analyzed in the GSE64951 and GSE19826 databases, and it was revealed that BC01600 and AF116637 were two typically upregulated lncRNAs. Furthermore, it was revealed that BC01600 and AF116637 are regulated by HDAC1, as evidenced by decreased expression of these two lncRNAs in HDAC1-knockout SC-M1 cell lines, and by reduced expression of HDAC1 in these two lncRNA-knockout SC-M1 cell lines. Silencing of HDAC1 decreased the proliferation and increased the apoptosis of SC-M1 cell lines, but had no effect on the migration of the SC-M1 cell lines. The present study provided evidence of the importance of HDAC1 in the progression of SC-M1, and the association between HDAC1 and the expression of lncRNAs. The results of the present study indicated that HDAC1 may be a promising target for the clinical treatment of GC.

SUBMITTER: Yu Z

PROVIDER: S-EPMC6396103 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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Role of HDAC1 in the progression of gastric cancer and the correlation with lncRNAs.

Yu Zhiqiang Z Zeng Jun J Liu Hui H Wang Tian T Yu Ziqi Z Chen Jianyong J

Oncology letters 20190123 3

Gastric cancer (GC) is a common life-threatening cancer type worldwide, with an increasing prevalence and a high rate of mortality. Due to limitations in clinical treatment, surgery has become the most efficient strategy for the treatment of GC. It is urgent to identify novel biomarkers, which are useful for the diagnosis of GC and for improving the survival rate of patients with GC. HDACs are multi-functional proteins and are involved in regulating gene expression, cell proliferation and the ep ...[more]

PMID: 30867763

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Project description:An increasing number of studies indicate that adrenergic signalling plays a fundamental role in chronic stress-induced tumour progression and metastasis. However, its function in gastric cancer (GC) and its potential mechanisms remain unknown. The expression levels of β-adrenergic receptor (ADRB) in GC cell lines were examined by using real-time polymerase chain reaction (RT-PCR) and western blotting. The effects of β2 adrenergic receptor (ADRB2) activation and blockade were investigated in vitro in GC cells by using proliferation, migration, invasion, cell cycle and apoptosis assays. Chronic restraint stress (CRS) increased the plasma levels of catecholamines and cortisol and also induced progression and metastasis of GC in vivo. Furthermore, immunohistochemical staining and a TUNEL assay were employed to observe the regulation of cell viability in vivo. The expression levels of ADRB2 in 100 human GC samples were measured by RT-PCR and immunohistochemistry. The stress hormones epinephrine and norepinephrine significantly accelerated GC cell proliferation, invasion and viability in culture, as well as tumour growth in vivo. These effects were reversed by the ADRB antagonists propranolol and ICI118,551 (an ADRB2-specific antagonist). Moreover, the selective ADRB1 antagonist atenolol had almost no effect on tumour cell proliferation and invasion in vitro and in vivo. ADRB2 antagonists suppressed proliferation, invasion and metastasis by inhibiting the ERK1/2-JNK-MAPK pathway and transcription factors, such as NF-κB, AP-1, CREB and STAT3. Analysis of xenograft models using GC cells revealed that ADRB2 antagonists significantly inhibited tumour growth and metastasis, and chronic stress antagonized these inhibitory effects. In addition, chronic stress increased the expression of VEGF, MMP-2, MMP-7 and MMP-9 in transplanted tumour tissue, and catecholamine hormones enhanced the expression of metastasis-related proteins. The expression of ADRB2 was upregulated in tumour tissues and positively correlated with tumour size, histological grade, lymph node metastasis and clinical stage in human GC samples. Stress hormone-induced activation of the ADRB2 signalling pathway plays a crucial role in GC progression and metastasis. These findings indicate that ADRB2 signalling regulates GC progression and suggest β2 blockade as a novel strategy to complement existing therapies for GC.

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Role of HDAC1 in the progression of gastric cancer and the correlation with lncRNAs.

Publications

Role of HDAC1 in the progression of gastric cancer and the correlation with lncRNAs.

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