Following the publication of the above article, the authors drew to the Editor's attention that they has misclassified some of their original data, and this led to the erroneous compilation of the cell invasion and scratch wound assay data shown in Fig. 5A and B respectively on p. 604. Moreover, the authors realized that the same GAPDH control western blotting data had inadvertently been included in Fig. 4A and G on p. 603, where these data were correctly shown only for Fig. 4G. However, the authors had retained their original data for these figures, and the revised versions of Figs. 4 and 5, now showing the correct data for the GAPDH bands in Fig. 4A and the correct data for Fig. 5A and B, are shown on the next two pages. Note that the errors made in terms of the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for granting them this opportunity to publish a Corrigendum, and apologize to both the Editor and the readership for any inconvenience caused. [Oncology Reports 38: 598-606, 2017; DOI: 10.3892/or.2017.5667].

自噬是一种维持细胞内稳态的重要代谢过程.近年来研究发现,自噬与肿瘤的发生发展密切相关,参与调控肿瘤的形成、增殖、转移以及能量代谢等过程.并且自噬在肿瘤的发生发展中发挥着不同的作用,它能抑制早期肿瘤的生成,促进晚期肿瘤的发展.目前,自噬已成为肿瘤药物靶向研究中的一个新热点.许多草药,包括中草药,已作为现行药物的补充和替代药物、保健品和营养品,以减轻癌症治疗中化疗药物的毒副反应.此外,许多草药及天然产物均可通过诱导自噬,进而导致细胞衰老、凋亡非依赖性细胞死亡途径或补体介导的细胞凋亡途径的激活,最终发挥着抗肿瘤作用.据此,本文将回顾分析天然自噬诱导剂在癌症治疗中的潜在作用机制.同时,我们着重探讨白藜芦醇、姜黄素和16-羟基克罗烷-3,13-二烯-15,16-内酯这三种天然化合物作为候选自噬诱导剂在癌症治疗中的研究进展,旨在为研发靶向自噬的新型抗肿瘤药物提供方向.

长链非编码RNA(long non-coding RNAs,lncRNAs)是一类转录本长度超过200个核苷酸的非编码RNA(non-coding RNAs,ncRNAs),它们不编码蛋白质,而是以RNA的形式通过转录,转录后和表观遗传等多种调控机制发挥生物学功能,包括生长发育、骨髓造血、细胞凋亡和细胞增殖等生命进程中的一系列重要过程.肺癌是全球癌症死亡的主要原因,它是由不同病因引起的一系列疾病,可分为小细胞肺癌(small -cell lung cancer,SCLC)和非小细胞肺癌(non-small cell lung cancer,NSCLC)两种类型.肺癌的基本特征是基因组遗传和表观遗传发生改变;然而,肺癌发生的具体机制目前仍不明确.近年来的研究资料表明,lncRNAs的异常表达与包括肺癌在内的多种癌症的发生发展有关.本文着重研究lncRNAs在NSCLC中的表达和作用,并讨论其作为早期诊断,指导预后的生物标志物以及治疗靶点的潜在临床应用.

目的:以往研究表明,一种新型STAT3抑制剂牛蒡苷元(Arctigenin,Atn)在三阴性乳腺癌(triple negative breast cancer,TNBC)中能诱导显著的细胞毒性.本研究将进一步阐述Atn在TNBC细胞中通过下调蛋白磷酸酶2A (PP2A)的癌性抑制因子(cancerous inhibitor of protein phosphatase 2A,CIP2A)触发细胞毒性的新型分子机制.方法:Western blot法、实时荧光定量PCR法检测TNBC系中CIP2A的表达变化;Western blot法检测CIP2A下游分子Akt、ERK、PP2A的表达及活化;PP2A活性测定检测TNBC系中PP2A的活性;侵袭实验、划痕愈合实验检测TNBC的侵袭和迁移能力;siRNA干扰技术转染TNBC细胞系,检测转染后TNBC细胞侵袭能力.结果:Atn显著下调TNBC系CIP2A的表达;CIP2A下调导致PP2A活性增加和Akt的磷酸化水平下降;沉默CIP2A表达增强Atn对TNBC细胞转移行为的抑制作用;Atn通过重激活PP2A抑制TNBC增殖和侵袭.结论:研究发现Atn在TNBC中的新型作用机制,即Atn通过抑制CIP2A表达而活化PP2A,进而抑制Akt活化,从而抑制细胞的转移.

Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a human oncoprotein that is overexpressed in multiple kinds of tumors including gastric cancer (GC). Mammalian target of rapamycin complex 1 (mTORC1) over activation is detected in GC and many other cancers. Previous study found that CIP2A/mTORC1 controls cell growth and autophagy through direct association. CIP2A plays an 'oncogenic nexus' in several cancer types to participate in the tumorigenic transformation and chemoresistance. In the present study, we investigated whether Cucurbitacin B (CuB), a natural compound found in Cucurbitaceae, can be used in cisplatin (DDP)-resistant human GC cell line SGC7901/DDP. Results demonstrated that CuB treatment significantly suppressed SGC7901/DDP cell proliferation, induced caspase-dependent apoptosis, and autophagy. The activation of autophagy was mediated through CuB-induced inhibition of mTORC1. Furthermore, CuB inhibited mTORC1 via the activation of protein phosphatase 2A (PP2A) which is mediated by CIP2A inhibition. These findings indicated that CuB can inhibit the proliferation, induce caspase-dependent apoptosis, and autophagy of SGC7901/DDP cells by suppressing CIP2A/PP2A/mTORC1 signaling axis. Thus, CuB may be a novel effective candidate to treat DDP-resistant human GC cells.

Objective To explore the effects and mechanisms of natural compound (Cucurbitacin B,CuB) on reversing drug resistance to doxorubicirn (Dox)-resisted human breast cancer (MCF-7/Dox) cells.Methods Trypan blue dye staining,MTT and colony formation assay were used to detect the inhibitory effects of CuB on the growth of MCF-7/Dox cells.DAPI staining and Western blot were used to investigate the mechanisms of CuB on reversing Doxorubicin-resisted MCF-7/Dox cells.FResults CuB inhibited MCF-7/Dox cell proliferation,cell viability,and reversed chemoresistance to doxorubicin.CuB down-regulated the expression of P-glycoprotein,multidrug resistance-associated protein 1,and Cyclin D1.CuB also induced caspase-dependent apoptosis,and decreased phosphorylation of Akt (pAkt).The suppression of pAkt was mediated by CuB-induced activation of protein phosphatase 2A (PP2A) through the suppressing CIP2A.Conclusiorn The CIP2A/PP2A/Akt pathway may mediate the reversal effect of CuB on Doxorubicin-resisted MCF-7/Dox cells.

We have shown that a novel STAT3 inhibitor arctigenin (Atn) induces significant cytotoxicity in triple-negative breast cancer (TNBC) cells. This study further delineated molecular mechanisms where by Atn triggered cytotoxicity in TNBC cells. We found Atn can also inhibit metastasis in TNBC cells through cancerous inhibitor of protein phosphatase 2A (CIP2A) pathway. CIP2A is an endogenous inhibitor of protein phosphatase 2A (PP2A), which can increase the migration and invasion of various cancer cells. PP2A is a tumor suppressor, which is functionally defective in various cancers. Atn-induced metastasis inhibition was associated with reactivation of PP2A, downregulation of CIP2A and Akt phosphorylation. Silencing CIP2A enhanced Atn-induced metastasis inhibition and apoptosis in TNBCs. Furthermore, ectopic expression of CIP2A or inhibition of PP2A in TNBC cells abolished the effects of Atn. In conclusion, we found that enhancement of PP2A activity by inhibition of CIP2A, at least in part, promotes the anti-metastasis effect induced by Atn. Our findings disclose the novel therapeutic mechanism of this targeted agent, and suggest the therapeutic potential and feasibility of developing PP2A enhancers as a novel anticancer strategy.

SE translocation (SET) oncoprotein, an inhibitor of protein phosphatase 2A, is abnormally expressed in many cancers. In this study, SET was aberrantly upregulated in gastric cancer (GC) compared with control tissues. Clinicopathological analysis showed that SET expression was significantly correlated with pathological grade (p=0.002), lymph node stage (p=0.014), and invasive depth (p=0.022). Kaplan-Meier analysis indicated that patients with high SET expression showed poorer overall survival rates than those with low SET expression. Moreover, SET knockdown downregulated GC cell proliferation, colony formation, tumorigenesis, and metastasis. The biological effect of SET on proliferation and invasion was mediated by inhibition of protein phosphatase 2, which in turn, activated Akt. Taken together, our results suggested that SET overexpression is associated with GC progression, and it might be a potential diagnostic marker for GC, thereby a possible target for GC drug development.