Expression and clinical significance of HMGB1 in human liver cancer: Knockdown inhibits tumor growth and metastasis in vitro and in vivo

Dong, Yadong; Chen, Long; Peng, Chenghong; Cheng, Dongfeng; Han, Baosan; Huang, Fang

doi:10.3892/or.2012.2070

Cited by 47 publications

(41 citation statements)

References 29 publications

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“…HMGB1 can activate caspase-1 and contribute to hepatocellular carcinoma invasion and metastasis [34]. Moreover, knockdown of HMGB1 has clinical significance that inhibits human liver cancer growth and metastasis [35]. Our results were consistent with the above reports and suggested that silencing of HMGB1 inhibited lung cancer migration and invasion.…”

Section: Discussionsupporting

confidence: 82%

MiRNA-218, a new regulator of HMGB1, suppresses cell migration and invasion in non-small cell lung cancer

Zhang¹,

Ge²,

Hu³

et al. 2013

ABBS

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MicroRNAs (miRNAs) function as negative regulators of gene expression involved in cancer metastasis. The aim of this study is to investigate the potential roles of miR-218 in non-small cell lung cancer and validate its regulation mechanism. Functional studies showed that miR-218 overexpression inhibited cell migration and invasion, but had no effect on cell viability. Enhanced green fluorescent protein reporter assay, real-time polymerase chain reaction and western blot analysis confirmed that miR-218 suppressed the expression of high mobility group box-1 (HMGB1) by directly targeting its 3 0 -untranslated region. Accordingly, silencing of HMGB1 accorded with the effects of miR-218 on cell migration and invasion, and overexpression of HMGB1 can restore cell migration and invasion which were reduced by miR-218. In conclusion, these findings demonstrate that miR-218 functions as a tumor suppressor in lung cancer. Furthermore, miR-218 may act as a potential therapeutic biomarker for metastatic lung cancer patients.

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Section: Discussionsupporting

confidence: 82%

MiRNA-218, a new regulator of HMGB1, suppresses cell migration and invasion in non-small cell lung cancer

Zhang¹,

Ge²,

Hu³

et al. 2013

ABBS

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“…Extracellular HMGB1-induced chronic inflammation within the tumor microenvironment favors tumor survival, proliferation, metastasis and angiogenesis. Expression of HMGB1 is closely correlated with pathological grade and distant metastases of liver cancer, and knockdown of HMGB1 inhibits liver cancer growth and metastasis (75,76). Serum HMGB1 levels were significantly higher in HCC and HBV patients and were associated with clinicopathological features and outcome in HCC patients (64,77).…”

Section: Hmgb1 and Hepatocellular Carcinomamentioning

confidence: 95%

Emerging Role of High-Mobility Group Box 1 (HMGB1) in Liver Diseases

Chen

Hou

Zhang

et al. 2013

Mol Med

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Damage-associated molecular pattern (DAMP) molecules are essential for the initiation of innate inflammatory responses to infection and injury. The prototypic DAMP molecule, high-mobility group box 1 (HMGB1), is an abundant architectural chromosomal protein that has location-specific biological functions: within the nucleus as a DNA chaperone, within the cytosol to sustain autophagy and outside the cell as a DAMP molecule. Recent research indicates that aberrant activation of HMGB1 signaling can promote the onset of inflammatory and autoimmune diseases, raising interest in the development of therapeutic strategies to control their function. The importance of HMGB1 activation in various forms of liver disease in relation to liver damage, steatosis, inflammation, fibrosis, tumorigenesis and regeneration is discussed in this review.

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“…HMGB1 knockdown could suppress the ability of proliferation, migration, and invasion of HCC cells. HMGB1 overexpression could strengthen the ability of proliferation, migration, and invasion of HCC cells [15,22]. HMGB1 expression is significantly increased in laryngeal squamous cell carcinoma (LSCC) tissues, and HMGB1 overexpression is associated with a poorer prognosis [23].…”

Section: Introductionmentioning

confidence: 99%

HMGB1 promotes cellular proliferation and invasion, suppresses cellular apoptosis in osteosarcoma

et al. 2014

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Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. Unfortunately, treatment failures are common due to the metastasis and chemoresistance, but the underlying molecular mechanism remains unclear. Accumulating evidence indicated that the deregulation of DNA-binding protein high-mobility group box 1 (HMGB1) was associated with the development of cancer. This study aimed to explore the expression of HMGB1 in osteosarcoma tissues and its correlation to the clinical pathology of osteosarcoma and to discuss the role of HMGB1 in the development of osteosarcoma. The results from RT-PCR and Western blot showed that the expression rate of HMGB1 messenger RNA (mRNA) and the expression of HMGB1 in the osteosarcoma tissues were significantly higher than those in normal bone tissue (p < 0.05), the expression rate of HMGB1 mRNA and the expression of HMGB1 in the carcinoma tissues with positive lung metastasis were significantly higher than those without lung metastasis (p < 0.05), and with increasing Enneking stage, the expression rate of HMGB1 mRNA and the expression of HMGB1 also increased (p < 0.05). In order to explore the role of HMGB1 in osteosarcoma, the expression of HMGB1 in the human osteosarcoma MG-63 cell line was downregulated by the technique of RNA interference. Western blot results showed that the protein expression of HMGB1 was significantly decreased in the MG-63 cells from HMGB1-siRNA transfection group (p < 0.05), which suggested that HMGB1 was successfully downregulated in the MG-63 cells. Then the changes in proliferation, apoptosis, and invasion of MG-63 cells were examined by MTT test, PI staining, annexin V staining, and transwell chamber assay. Results showed that the abilities of proliferation and invasion were suppressed in HMGB1 knockdown MG-63 cells, and the abilities of apoptosis were enhanced in HMGB1 knockdown MG-63 cells. The expression of cyclin D1, MMP-9 was downregulated in HMGB1 knockdown MG-63 cells, and the expression of caspase-3 was upregulated in HMGB1 knockdown MG-63 cells. Taken together, the overexpression of HMGB1 in osteosarcoma might be related to the tumorigenesis, invasion, and metastasis of osteosarcoma, which might be a potential target for the treatment of osteosarcoma.

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Expression and clinical significance of HMGB1 in human liver cancer: Knockdown inhibits tumor growth and metastasis in vitro and in vivo

Cited by 47 publications

References 29 publications

MiRNA-218, a new regulator of HMGB1, suppresses cell migration and invasion in non-small cell lung cancer

MiRNA-218, a new regulator of HMGB1, suppresses cell migration and invasion in non-small cell lung cancer

Emerging Role of High-Mobility Group Box 1 (HMGB1) in Liver Diseases

HMGB1 promotes cellular proliferation and invasion, suppresses cellular apoptosis in osteosarcoma

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