Non-small cell lung cancer is known as a malignant tumor with low survival rate and poor prognosis. Depression affects various diseases. However, the effect of depression on the progression of NSCLC remains unclear. In our current study, chronic mild stress (CMS) mice was used as depression animal model. Depression prompted the tumor progression in vivo analysis, including increasing tumor indexes and reducing survival rate. Serotonin secretion was observed to be remarkable elevation in both serum and tumor tissue, which was positively related with tumor progression. In vitro assays, serotonin promoted the proliferation of A549 cells. Ad -ditionally, we observed that miR-144 expression was significantly downregulated in serotonin stimulated group. Further loss-of- and gain-of-function assays verified that miR-144 was the downstream factor of serotonin underlying the condition of CMS. Taken to -gether, our research indicated that CMS-induced serotonin secretion accelerates NSCLC proliferation via inhibiting miR-144 expres sion, suggesting the potential therapeutic direction in NSCLC patients.

Objective. To evaluate the effect of p53 on pyroptosis and its inhibitory role on tumor growth in non-small-cell lung cancer (NSCLC). Methods. The correlation of p53 and pyroptosis was determined in tumor tissues of NSCLC patients. The pyroptotic level was detected in A549 cells to clarify the effect of p53 on pyroptosis. p53 overexpression A549 tumor-bearing mice were used to clarify the therapeutic target of p53 in NSCLC treatment. Results. p53 expression level was positively related to pyroptosis in NSCLC tissues. In in vitro assays, p53 directly regulated pyroptosis in A549 cells. p53-specific knockdown blocked lipopolysaccharide- (LPS-) induced pyroptosis. In in vivo assays, p53 overexpression in A549 markedly decreased tumor growth and death rate by increasing the pyroptotic level. Conclusions. Upregulation of p53 prompts pyroptosis to produce anti-NSCLC effects suggesting the potential of p53 on suppressing tumor growth in NSCLC patients.

非小细胞肺癌(NSCLC)患者进行靶向治疗前需要鉴定多种生物标志物,包括EGFR、ALK、ROS-1和PD-L1,通常经手术、 穿刺等途径获取样本.液体检测是目前新兴的肿瘤标记物检测方法,它可以从血浆中提取出循环系统中的肿瘤DNA(ctDNA),具有低风险、取样简单、术后不适感少等优点.常用的液体活检方法有定量聚合酶链反应(PCR)、数字PCR技术、新一代测序技术(NGS).本文简要地阐述了上述分析方法的研究进展及未来应用方向.

Acute lung injury (ALI) is a common severe clinical syndrome in intensive care unit. Inflammation has been reported to play a critical role in the development of ALI. Cordycepin, an active component isolated from Cordyceps militaris, has been reported to have anti-inflammatory effects. However, the anti-inflammatory effects of cordycepin on LPS-induced ALI remain unclear. Therefore, in the present study, we assessed whether cordycepin could attenuate ALI induced by LPS. The mice were conditioned with cordycepin 1 h before intranasal instillation of LPS. Lung wet/dry (W/D) ratio, MPO activity, MDA content, and inflammatory cytokines production were detected. The expression of NF-κB p65, I-κB, Nrf2, and HO-1 were detected by western blot analysis. We found that LPS significantly increased lung wet/dry (W/D) ratio, MPO activity, MDA content, and inflammatory cytokines production. However, the increases were significantly inhibited by treatment of cordycepin. LPS-induced NF-κB activation was also suppressed by cordycepin. In addition, cordycepin was found to up-regulate the expression of Nrf2 and HO-1 in a dose-dependent manner. In conclusion, our results demonstrated that cordycepin could attenuate LPS-induced ALI effectively, probably due to inhibition of inflammation and oxidative stress.

目的 探讨藤黄酸对非小细胞肺癌(NSCLC)A549细胞凋亡及B淋巴细胞瘤(Bcl)-2、Bcl-2相关X蛋白(Bax)、P53基因表达的影响.方法 体外常规培养NSCLC A549细胞,取对数生长期的A549细胞加入不同浓度的藤黄酸进行干预,藤黄酸干预24 h后采用流式细胞术检测A549细胞凋亡率,干预24、48、72 h后采用MTT分析A549细胞生长情况;采用Western印迹实验分析藤黄酸干预对Bcl-2、Bax、P53基因表达的影响,同时分析PUMA表达情况.结果 干预24 h后,A549细胞凋亡率随着藤黄酸浓度的增加而增加,均高于空白对照组(P<0.05).不同浓度的藤黄酸对A549的生长均有一定的抑制作用,且存在剂量、时间关系,不同浓度的藤黄酸干预组A549细胞存活率均显著低于空白对照组(P<0.05);随着时间的推移,各干预组A549细胞存活率降低(P<0.05).干预24 h后,P53、Bax、PUMA的相对表达量随着藤黄酸浓度的增加而增加,且不同浓度藤黄酸组均显著高于空白对照组(P<0.05);但Bcl-2的相对表达量显著低于空白对照组(P<0.05).结论 藤黄酸可抑制NSCLC A549细胞生长,促进其凋亡,其机制可能是通过活化促凋亡基因Bax、P53、PUMA表达和抑制抗凋亡基因Bcl-2表达实现.

Long noncoding RNAs (lncRNAs) have been illustrated as vital molecules in regulating human cancer by emerging evidence. LINC00163 is a novel lncRNA without functional definition. In this study, we investigated its role in the tumorigenesis of lung cancer. The results showed that LINC00163 level was significantly downregulated in lung cancer tissues and cell lines by bioinformatics and qRT-PCR analyses. Notably, we observed that LINC00163 expression was lower in metastatic tissues than in non-metastatic cases. Furthermore, higher expression of LINC00163 in patients with lung cancer predicted better prognosis. Gain-of-function assays illustrated that upregulation of LINC00163 dramatically suppressed the proliferation, migration and invasion of lung cancer cells in vitro, whereas promoting apoptosis. Consistently, LINC00163 overexpression impaired tumor propagation in vivo. Mechanical study revealed that LINC00163 recruited ARID1A to the promoter of TCF21 and initiated its expression. In conclusion, we concluded that LINC00163/ARID1A/TCF21 regulatory loop modulated the development of lung cancer, providing a new insight on the mechanism underlying lung cancer progression.