High-mobility group box 1 protein activating nuclear factor-κB to upregulate vascular endothelial growth factor C is involved in lymphangiogenesis and lymphatic node metastasis in colon cancer

Li, Yan; He, Jia; Zhong, Dongdong; Li, Jianjun; Liang, Houjie

doi:10.1177/0300060515581671

Cited by 28 publications

(36 citation statements)

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“…BNIP3 immunohistochemistry of human samples was performed as previously described 10. In brief, 10% neutral formalin-fixed, paraffin-embedded tissues were cut into 5 to 6 μm thickness sections.…”

Section: Methodsmentioning

confidence: 99%

“…In brief, 10% neutral formalin-fixed, paraffin-embedded tissues were cut into 5 to 6 μm thickness sections. Immunohistochemistry was done according to the manual of SP-9000-D kits (Streptavidin-Biotin) (Beijing Zhongshan Jinqiao biotechnology Co., Ltd., China) 10. BNIP3 primary antibody was from Sigma-Aldrich (St Louis, MO, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Expression of BNIP3 was evaluated as previously described, based on the percentage and intensity of positively-stained cells 10. The percentage of positively-stained cells was scored as: 0, negative; 1, positive in ≤ 10%; 2, positive in 11~50%; 3, positive in 51~80%; 4, positive in > 80% of cells.…”

Section: Methodsmentioning

confidence: 99%

“…RT-PCR was performed as previously described 10. Total RNA of cells was extracted with Trizol reagent (Invitrogen, Carlsbad, CA, USA), and first-strand cDNA was synthesized using 2μg of total RNA.…”

Section: Methodsmentioning

confidence: 99%

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Chemoresistance of colorectal cancer to 5-fluorouracil is associated with silencing of the BNIP3 gene through aberrant methylation

He¹,

Li²,

Jiang³

et al. 2017

J. Cancer

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Purpose To investigate the correlation between chemoresistance of colorectal cancer to 5-fluorouracil and BNIP3 and the underlying mechanism.Methods BNIP3 protein in specimens was evaluated using immunohistochemistry. Semi-quantitative reverse transcription PCR and Western blot was employed to assay gene expression. The promoter methylation status of BNIP3 was examined by methylation-specific PCR. Drug sensitivity was assayed using MTT assay.Results Specimens from 81 patients with colorectal cancer receiving 5-fluorouracil-based chemotherapy were analyzed. BNIP3 expression was negative in 42 cancer samples. The mean score of BNIP3 in cancer was 1.8±0.2 and it was 3.7±0.5 in adjacent colorectum (p<0.05). The response rate of the BNIP3 positive group was 63.6% and that of the negative group was 36.4% (p=0.021). The median PFS of the BNIP3 positive group was 9.25 months and that of the BNIP3 negative group was 6.5 months (p=0.011). BNIP3 mRNA was not detectable in 4 of 8 colorectal cell lines and all these 4 cell lines displayed BNIP3 methylated allele only. Other 4 cell lines what expressed detectable BNIP3 displayed BNIP3 unmethylated allele only or both unmethylated and methylated alleles. 5-Aza dramatically increased BNIP3 expression. Knockdown of DNMT1 increased BNIP3. Knockdown of DNMT3B alone did not detectably change BNIP3 expression while knockdown of both DNMT1 and DNMT3B increased BNIP3 expression more than knockdown of DNMT1 alone. Knockdown of BNIP3 decreased chemosensitivity to 5-fluorouracil and increasing BNIP3 through demethylation increased chemosensitivity.Conclusion Chemoresistance of colorectal cancer to 5-fluorouracil is associated with silencing of the BNIP3 gene through aberrant methylation via DNMT1/DNMT3B.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Chemoresistance of colorectal cancer to 5-fluorouracil is associated with silencing of the BNIP3 gene through aberrant methylation

He¹,

Li²,

Jiang³

et al. 2017

J. Cancer

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“…Vascular endothelial growth factor (VEGF)-C is the best-characterized lymphangiogenic factor and reportedly plays a crucial role in lymphangiogenesis and lymphatic metastasis [14, 15]. In addition, many observations have noted that VEGF-C plays a pivotal role in various types of human cancers, such as colon [16], colorectal [17], acute myeloid leukemia [18], and lung cancer [19]. …”

Section: Introductionmentioning

confidence: 99%

Basic fibroblast growth factor promotes VEGF-C-dependent lymphangiogenesis via inhibition of miR-381 in human chondrosarcoma cells

et al. 2016

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A chondrosarcoma is a common, primary malignant bone tumor that can grow to destroy the bone, produce fractures and develop soft tissue masses. Left untreated, chondrosarcomas metastasize through the vascular system to the lungs and ultimately lead to large metastatic deposits of the malignant cartilage taking over lung volume and function. Vascular endothelial growth factor (VEGF)-C has been implicated in tumor-induced lymphangiogenesis and elevated expression of VEGF-C has been found to correlate with cancer metastasis. bFGF (basic fibroblast growth factor), a secreted cytokine, regulates biological activity, including angiogenesis and metastasis. We have previously reported on the important role of bFGF in angiogenesis in chondrosarcomas. However, the effect of bFGF in VEGF-C regulation and lymphangiogenesis in chondrosarcomas is poorly understood. In this investigation, we demonstrate a correlation exists between bFGF and VEGF-C in tissue specimens from patients with chondrosarcomas. To examine the lymphangiogenic effect of bFGF, we used human lymphatic endothelial cells (LECs) to mimic lymphatic vessel formation. We found that bFGF-treated chondrosarcomas promoted LEC tube formation and cell migration. In addition, bFGF knockdown inhibited lymphangiogenesis in vitro and in vivo. We also found that bFGF-induced VEGF-C is mediated by the platelet-derived growth factor receptor (PDGFR) and c-Src signaling pathway. Furthermore, bFGF inhibited microRNA-381 expression via the PDGFR and c-Src cascade. Our study is the first to describe the mechanism of bFGF-promoted lymphangiogenesis by upregulating VEGF-C expression in chondrosarcomas. Thus, bFGF could serve as a therapeutic target in chondrosarcoma metastasis and lymphangiogenesis.

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HMGB1‐RAGE signaling facilitates Ras‐dependent Yap1 expression to drive colorectal cancer stemness and development

Qian

Xiao

Gai

et al. 2018

Molecular Carcinogenesis

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HMGB1-RAGE signaling plays an integral role in inflammation-driven carcinogenesis.In the present study, we showed that RAGE has direct association with K-Ras following HMGB1 exposure in colorectal cancer (CRC) cells. Immunofluorescence analysis revealed a significant co-localization between RAGE and K-Ras in HMGB1-exposed CRC cells. Moreover, we uncovered that HMGB1-mediated RAGE activation led to Yap1 accumulation in a Ras-dependent mechanism in CRC cells. HMGB1 activated the expression of Yap1 downstream stemness marker proteins CD44 and Sox2 in RAGEand Ras-dependent manners. Furthermore, HMGB1 exposure led to the proliferation of CRC cells and the expansion of CRC stem cells. RAGE, Yap1 and CD44 were overexpressed in CRC specimens. Linear regression analysis revealed that the expression of RAGE was positively correlated with Yap1 in clinical CRC specimens. Both of RAGE and Yap1 expression were correlated with advanced histological grades, lymph node metastasis and TNM stages. Finally, we revealed that both of RAGE and Yap1 expression could predicted unfavorable prognosis in CRC patients. These findings implicated that HMGB1-RAGE signaling may promote Yap1 activation and CRC progression, shedding new light on the mechanisms underlying inflammationdriven CRC development. K E Y W O R D S colorectal cancer, HMGB1, K-Ras, RAGE, stemness, Yap1

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High-mobility group box 1 protein activating nuclear factor-κB to upregulate vascular endothelial growth factor C is involved in lymphangiogenesis and lymphatic node metastasis in colon cancer

Abstract: HMGB1 immunohistochemical staining was significantly associated with lymphangiogenesis and lymphatic node metastasis in colon cancer. There was evidence that HMGB1 upregulates VEGF-C by activating NF-κB in a colon cancer cell line.

Cited by 28 publications

References 36 publications

Chemoresistance of colorectal cancer to 5-fluorouracil is associated with silencing of the BNIP3 gene through aberrant methylation

Chemoresistance of colorectal cancer to 5-fluorouracil is associated with silencing of the BNIP3 gene through aberrant methylation

Basic fibroblast growth factor promotes VEGF-C-dependent lymphangiogenesis via inhibition of miR-381 in human chondrosarcoma cells

HMGB1‐RAGE signaling facilitates Ras‐dependent Yap1 expression to drive colorectal cancer stemness and development

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