The role of High Mobility Group Box 1 (HMGB1) in colorectal cancer

Süren, Di̇nç; Yıldırım, Mustafa; Demirpençe, Özlem; Kaya, Vi̇ldan; Ali̇kanoğlu, Arsenal Sezgi̇n; Bülbüller, Nurullah; Yıldız, Mustafa; Sezer, Cem

doi:10.12659/msm.890531

Cited by 61 publications

(33 citation statements)

References 41 publications

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“…HMGB1 overexpression has a significant role in tumor progression (especially migration of tumor cells) and tumor ability to metastasize in colorectal cancers. Thus, it corroborates the idea that it might be an important prognostic factor [ 13 ]. Knockdown of HMGB1 inhibits growth and invasion of gastric cancer cells through the NF-κB pathway in vitro and in vivo [ 14 ].…”

Section: Introductionsupporting

confidence: 86%

RETRACTED ARTICLE: The microRNA-325 inhibits hepatocellular carcinoma progression by targeting high mobility group box 1

Huang

Luo

2015

Diagn Pathol

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BackgroundMicroRNAs (miRNAs) can serve as tumor suppressors and might provide an efficient strategy for annihilating tumor cells. Nevertheless, the potential role of miR-325 in hepatocellular carcinoma (HCC) is still unknown.MethodsUsing RT-PCR, immunoblots invasion assays and bioinformatics strategies, we investigated the potential role of miR-325 in HCC.ResultsWe showed that miR-325 was decreased and HMGB1 was increased in 99 patients with hepatocellular carcinoma. MiR-325 inhibition promoted cell invasion and proliferation, while miR-325 upregulation inhibited cell invasion and proliferation by using transwell and CCK8 assays. We further showed that HMGB1 might be a direct target of miR-325 and is negatively regulated by miR-325. Down-regulation of miR-325 predicts poor prognosis for HCC patients.ConclusionsThese findings implied that miR-325 regulates cell invasion and proliferation via targeting HMGB1 and may be a potential prognostic marker for HCC.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/4655707031717989

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Section: Introductionsupporting

confidence: 86%

RETRACTED ARTICLE: The microRNA-325 inhibits hepatocellular carcinoma progression by targeting high mobility group box 1

Huang

Luo

2015

Diagn Pathol

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“…HMGB1 is higher expressed in various types of tumors and is closely associated with the inflammatory response, angiogenesis, tumor cells growth, invasion and metastasis [20-22]. It has been manifested that HMGB1 overexpression inhibited cell apoptosis, induced cells growth and functions as an anti-apoptotic protein in leukemia [23].…”

Section: Introductionmentioning

confidence: 99%

MiR-34a Promotes Apoptosis and Inhibits Autophagy by Targeting HMGB1 in Acute Myeloid Leukemia Cells

Liu

Ren

Chen

2017

Cell Physiol Biochem

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Background: MiR-34a is identified as a tumor suppressor gene and involved in acute myeloid leukemia (AML) development. However, the regulatory mechanism of miR-34a in AML is unclear. Methods: The expression of miR-34a and HMGB1 in HL-60, THP-1 and HS-5 cells were detected by qRT-PCR and western blot. Lipofectamine 2000 was used to transfect with miR-34a mimics, miR-34a inhibitor, si-HMGB1, pcDNA 3.1-HMGB1, and corresponding controls. The apoptosis and autophagy of transfected AML cells were assessed by flow cytometry and western blot, respectively. Bioinformatics software and dual luciferase reporter assay were applied to predict and verify the target of miR-34a. The effects of miR-34a mimics or si-HMGB1 on chemotherapy-induced autophagy were further explored in HL-60 cells treated with all-trans retinoic acid (ATRA) along with lysosomal protease inhibitors E64d and pepstatin A. Results: MiR-34a was lower expressed and HMGB1 mRNA and proteins were both higher expressed in HL-60 and THP-1 cells compared with that in HS-5 cells. Higher expression levels of MiR-34 and lower expression levels of HMGB1 both significantly promoted apoptosis and inhibited autophagy in HL-60 and THP-1 cells. Dual luciferase reporter system confirmed that HMGB1 was a potential target of miR-34a. Moreover, overexpression of HMGB1 dramatically reversed the promotion of apoptosis and inhibition of autophagy mediated by higher expression level of miR-34a. Higher expression level of miR-34a and lower expression level of HMGB1 both inhibited chemotherapy-induced autophagy by stimulating the LC3 conversion. Conclusion: MiR-34a promoted cell apoptosis and inhibited autophagy by targeting HMGB1. Therefore, miR-34a may be a potential promising molecular target for AML therapy.

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“…In China, colorectal carcinoma has been ranked as the fifth most common human malignant disease, accounting for 6.51% of mortality in urban areas and 4.64% in rural areas [2]. The etiology of colorectal cancers is known to be heterogeneous and various mechanisms have been associated with the increased risk for development and progression of colorectal carcinoma, as well as the aggressive behaviors of the tumors [3–5]. Tumors at the invasive front appear morphologically more poorly differentiated and show different molecular characteristics [6].…”

Section: Introductionmentioning

confidence: 99%

Class III β-Tubulin in Colorectal Cancer: Tissue Distribution and Clinical Analysis of Chinese Patients

et al. 2016

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BackgroundClass III β-tubulin (βIII-tubulin) has been reported to express at the invasive margin of colorectal cancer. The present study aimed to investigate the clinical implication of βIII-tubulin expression at the invasive margin of colorectal cancer.Material/MethodsWe recruited 111 patients with surgically resected colorectal carcinoma for βIII-tubulin expression analysis. The cases with βIII-tubulin-positive tumor cells found only in the invasive front tumor area were assigned to the invasive front group, while the remaining cases were all assigned to the non-invasive front group. Clinical analysis of βIII-tubulin and other clinical data was performed.ResultsThe positive staining rates and staining intensity of βIII-tubulin were significantly different between the invasive and non-invasive front groups (p=0.001 and p=0.006), and there was a significant difference in tumor differentiation between the 2 groups (p=0.032). In the non-invasive front group, staining intensity of βIII-tubulin was significantly associated with positive staining rates and lymphatic metastasis (p<0.001 and p=0.048).ConclusionsOur data showed the tissue distribution of βIII-tubulin expression at invasive margin or diffuse distribution. Expression of βIII-tubulin was correlated with tumor differentiation and lymphatic metastasis, suggesting a potential role of βIII-tubulin in tumor differentiation and metastasis. This study may shed light on βIII-tubulin as a novel potential molecular target for a new anti-cancer drug.

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The role of High Mobility Group Box 1 (HMGB1) in colorectal cancer

Cited by 61 publications

References 41 publications

RETRACTED ARTICLE: The microRNA-325 inhibits hepatocellular carcinoma progression by targeting high mobility group box 1

RETRACTED ARTICLE: The microRNA-325 inhibits hepatocellular carcinoma progression by targeting high mobility group box 1

MiR-34a Promotes Apoptosis and Inhibits Autophagy by Targeting HMGB1 in Acute Myeloid Leukemia Cells

Class III β-Tubulin in Colorectal Cancer: Tissue Distribution and Clinical Analysis of Chinese Patients

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