High-Mobility Group Box 1 Protein Regulates Autophagy in LO2 Cells Following Anoxia-Reoxygenation Injury

Li, M; Peng, Guizhu; Ye, Q; Wang, Y; Xiong, Yan; R, Wang; Yang, Zhiqiang

doi:10.1016/j.transproceed.2018.03.002

Cited by 4 publications

(1 citation statement)

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“…High mobility group box 1 (HMGB1), a nonhistone nuclear protein known for its remarkable stability, is extensively distributed in the nucleus of each cell type, and it is present in small quantities in the cytoplasm and cytomembrane [3]. Studies have shown that HMGB1 is an essential factor in several diseases, such as sepsis, ischemia-reperfusion, neurodegeneration, and in particular, malignancy [4]. Recently, it was reported that HMGB1 is an early marker in ovarian carcinoma, non-small cell lung cancer [5], and colorectal carcinoma.…”

Section: Introductionmentioning

confidence: 99%

HMGB1-mediated-TLR4/MyD88 signaling regulates cell proliferation, migration and invasion in esophageal squamous cell carcinoma

Liang¹,

Ma²,

Zhang³

et al. 2023

Trop. J. Pharm Res

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Purpose: To study the effect of high mobility group box protein 1 (HMGB1)-mediated toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) on esophageal squamous cell carcinoma (ESCC). Methods: Cell viability was determined using CCK-8 test and colony formation assay, while cell migration and invasion were assessed by Transwell assay. Western blotting was used to determine protein and mRNA expression levels. The effect of TLR4/MyD88 signaling pathway on proliferation of ESCC cells was investigated via in vitro knockdown of HMGB1. Results: Data from in vitro experiments indicated that HMGB1 knockdown significantly decreased the proliferation, migration, and invasion of EC9706 cells in siHMGB1 group, when compared with siNC group (number of invasive cells in siHMGB1 vs. corresponding number in siNC: 26.7 ± 4.5 vs. 68.7 ± 2.5; p < 0.01), and also decreased proliferation, migration and invasion of TE-9 cells in siHMB1, relative to siNC group (number of invasive cells in siHMGB1 vs. corresponding number in siNC: 29.3 ± 3.5 vs. 55.7 ± 3.1; p < 0.01). Moreover, MGB1 knockdown via siTLR4 transfection significantly down-regulated the expressions of TLR4/MyD88 and epithelial-mesenchymal transition (EMT), but over-expression of TLR4 reversed the inhibition by HMGB1 knockdown on ESCC cells (p < 0.01). Conclusion: These findings suggest that HMGB1-mediated TLR4/MyD88 signal pathway is a potential treatment route for ESCC.

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Section: Introductionmentioning

confidence: 99%