high mobility group box protein 1 release is inhibited by sodium salicylate in A549 lung adenocarcinoma cells

Low HMGB1 expression in non-small cell lung cancer may explain the poor therapeutical outcome during chemotherapy and radiotherapy.

Down-regulating HMGB1 gene expression by HMGB1 siRNA can inhibit the invasion and proliferation of human lung cancer cell.

Data suggest that determination of HMGB1, survivin and VEGF concentrations has no clinical significance in the prognosis of the survival time in lung cancer.

HMGB1 functions as a tumor promoter and it regulates the proliferation and invasion of lung cancer cells.

HMGB1-regulated autophagy is a significant contributor to docetaxel resistance in lung adenocarcinoma cells.

High HMGB1 expression is associated with non-small cell lung cancer.

These findings implied that miR-325-3p regulates cell invasion and proliferation via targeting HMGB1 and may be a potential prognostic marker for non-small cell lung cancer.

Suggest that miR-142-3p may function as a tumor suppressor through the downregulation of HMGB1 in non-small-cell lung carcinoma.

The repair capacity of lung cancer cell lines A549 and H1299 depends on HMGB1 expression level and the p53 status.

The relationship between HMGB1 expression and chemotherapy resistance in lung cancer cells was investigated. The expression level of HMGB1 was detected by western blotting analysis and the results revealed that HMGB1 levels were significantly higher in the cisplatin-resistant cell line, A549/DDP, compared with the cisplatin-sensitive cell line, A549, as well as the HMGB1 concentration in cultured medium.

These results demonstrated that miR-142-3p regulates starvation-induced autophagy of Non-small-cell lung cancer cells by directly downregulating HMGB1 and subsequently activating the PI3K/Akt/mTOR pathway.

High HMGB1 expression is associated with reduced chemosensitivity in the pleural effusion of non-small cell lung cancer.

CT or CC+CT heterozygotes of the HMGB1 rs1045411 polymorphism reduced the risks for lung cancer, while the G/T/C haplotypes of three HMGB1 SNPs (rs1360485, rs1045411 and rs2249825) also reduced the risk for lung cancer by almost half (0.486-fold) in the Chinese Han population.

miR-193a displayed its role in lung cancer via modulating the HMGB1 expression. This study demonstrated that UCA1 exerts oncogenes activity in lung cancer, acting mechanistically by upregulating HMGB1 expression through 'sponging' miR-193a.

The study indicated polymorphisms in HMGB1 may be a novel biomarker for female lung adenocarcinoma risk.

This review aims to encapsulate the relationship between HMGB1 and lung cancer, suggesting that HMGB1 plays a pivotal role in initiation, development, invasion, metastasis, and prognosis of lung cancer.

In lung cancer patients, circulating HMGB1-containing nucleosome is higher in those under chemotherapy, predicting poorly cancer cell differentiation state, enhanced cancer invasion and advanced TNM stages.

HMGB1 promoted lung cancer invasion and metastasis by upregulating the expression and activity of MMP-2 in an NF-kappaB-dependent manner.

effect that HMGB1 has on dendritic cell maturation and retention in lung cancers

NAC1/ HMGB1 signaling pathway is associated with the epithelial-mesenchymal transition (EMT), invasion, and metastasis of lung cancer cells.

These results demonstrate the general phenomenon that Rh-endostatin can induce HMGB1 suppression in a variety of non-small cell lung cancer cells. Rh-endostatin may suppress HMGB1 expression and release in A549 cancer cells, thus inhibiting cell proliferation.

LncRNA DSCAM-AS1 promotes non-small cell lung cancer progression via regulating miR-577/HMGB1 axis.