HMGB1 released by irradiated tumor cells promotes living tumor cell proliferation via paracrine effect.
HMGB1 released by irradiated tumor cells promotes living tumor cell proliferation via paracrine effect.
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受辐射的肿瘤细胞释放的 HMGB1 通过旁分泌作用促进活肿瘤细胞增殖
DOI：
10.1038/s41419-018-0626-6
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发表时间：
2018-05-29
影响因子：
9
通讯作者：
Huang Q
中科院分区：
文献类型：
--
作者：
He S;Cheng J;Sun L;Wang Y;Wang C;Liu X;Zhang Z;Zhao M;Luo Y;Tian L;Li C;Huang Q
治疗过程中的肿瘤再增殖是治疗失败的重要原因。克服再增殖的策略与对潜在生物机制的理解的进展同时出现。在此，我们揭示了一种新的机制，即在放疗或化疗过程中死亡细胞释放的高迁移率族蛋白1（HMGB 1）可以刺激活肿瘤细胞增殖，抑制或基因切除HMGB 1抑制肿瘤细胞增殖。这种作用是由于HMGB 1与晚期糖基化终产物（Advanced Glycation End-products，ERK）成员受体结合，激活下游ERK和p38信号通路，促进细胞增殖。此外，肿瘤组织中HMGB 1的高表达与总生存率低相关，接受放射治疗的患者血清中检测到较高的HMGB 1浓度。总的来说，这项研究的结果表明，死亡细胞和存活细胞之间的相互作用可能会影响肿瘤的命运。HMGB 1可能是一种新的肿瘤促进剂，与癌症的治疗和预后相关。
Tumor repopulation during therapy is an important cause of treatment failure. Strategies to overcome repopulation are arising in parallel with advances in the comprehension of underlying biological mechanisms. Here, we reveal a new mechanism by which high mobility group box 1 (HMGB1) released by dying cells during radiotherapy or chemotherapy could stimulate living tumor cell proliferationInhibition or genetic ablation of HMGB1 suppressed tumor cell proliferation. This effect was due to binding of HMGB1with the member receptor for advanced glycation end-products (RAGE), which activated downstream ERK and p38 signaling pathway and promoted cell proliferation. Furthermore, higher HMGB1 expression in tumor tissue correlated with poor overall survival and higher HMGB1 concentration was detected in serum of patients who accepted radiotherapy. Collectively, the results from this study suggested that interaction between dead cells and surviving cells might influence the fate of tumor. HMGB1 could be a novel tumor promoter with therapeutic and prognostic relevance in cancers.
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影响因子：
14.9
作者：
Tang Z;Li C;Kang B;Gao G;Li C;Zhang Z
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Zhang Z
影响因子：
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Tang, Daolin
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影响因子：
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