Tumor heterogeneity has been associated with immunotherapy and targeted drug resistance in hepatocellular carcinoma (HCC). However, communications between tumor and cytotoxic cells are poorly understood to date. In the present study, thirty-one clusters of cells were discovered in the tumor tissues and adjacent tissues through single-cell sequencing. Moreover, the quantity and function exhaustion of cytotoxic cells was observed to be induced in tumors by the TCR and apoptosis signal pathways. Furthermore, granzyme failure of cytotoxic cells was observed in HCC patients. Importantly, the GZMA secreted by cytotoxic cells was demonstrated to interact with the F2R expressed by the tumor cells both in vivo and in vitro. This interaction induced tumor suppression and T cell-mediated killing of tumor cells via the activation of the JAK2/STAT1 signaling pathway. Mechanistically, the activation of JAK2/STAT1 signaling promoted apoptosis under the mediating effect of the LDPRSFLL motif at the N-terminus of F2R, which interacted with GZMA. In addition, GZMA and F2R were positively correlated with PD-1 and PD-L1 in tumor tissues, while the expressions of F2R and GZMA promoted PD-1 mAb-induced tumor suppression in both mouse model and HCC patients. Finally, in HCC patients, a low expression of GZMA and F2R in the tumor tissues was correlated with aggressive clinicopathological characteristics and poor prognosis. Collectively, GZMA-F2R communication inefficient induces deficient PD-1 mAb therapy and provide a completely novel immunotherapy strategy for tumor suppression in HCC patients.

The Apoptosis Stimulating Protein of p53 2 (ASPP2) is a heterozygous insufficient tumor suppressor; however, its molecular mechanism(s) in tumor suppression is not completely understood. ASPP2 plays an essential role in cell growth, as shown by liver hepatocellular carcinoma (LIHC) RNA-seq assay using the Cancer Genome Atlas (TCGA) and High-Throughput-PCR assay using ASPP2 knockdown cells. These observations were further confirmed by in vivo and in vitro experiments. Mechanistically, N-terminus ASPP2 interacted with Keratin 18 (k18) in vivo and in vitro. Interestingly, the RDIVpSGP motif of ASPP2 associates with 14-3-3 and promotes ASPP2/k18/14-3-3 ternary-complex formation which promotes MEK/ERK signal activation by impairing 14-3-3 and BRAF association. Additionally, ASPP2-rAd injection promotes paclitaxel-suppressed tumor growth by suppressing cell proliferation in the BALB/c nude mice model. ASPP2 and k18 were preferentially downregulated in Hepatocellular Carcinoma (HCC), which predicted poor prognosis in HCC patients. Overall, these findings suggested that ASPP2 promoted BRAF/MEK/ERK signal activation by promoting the formation of an ASPP2/k18/14-3-3 ternary complex via the RDIVpSGP motif at the N terminus. Moreover, this study provides novel insights into the molecular mechanism of tumor suppression in HCC patients.

A cDNA template with a high concentration is required to generate a high number of copies for accurate downstream high‑throughput reverse transcription‑quantitative PCR screening. However, with the traditional method, pre‑amplification is not widely available. In the present study, a novel strategy to resolve the pre‑amplification limitation has been developed. Total RNA was extracted using a commercially available RNeasy Micro kit then, the cDNA was synthesized using SuperScript® III First‑Strand Synthesis system. PCR inhibitors (proteins and soluble salt ions) in the enriched cDNA were removed using saturated phenol‑chloroform extraction. Finally, genes were evaluated using PCR amplification and the BioMark™ HD system. The positive detection rate of individual target gene expression reached 70.18%; however, it markedly decreased to 35.42% using PCR amplification without prior dilution. Next, the reverse transcription product was purified using saturated phenol‑chloroform extraction, and the positive detection rate increased to 97.04%. Notably, the positive detection rate of cDNA prepared using this method of high‑throughput and traditional PCR (97.04 vs. 96.6%) was not significantly different. In conclusion, the results demonstrate the novel method was an easy and reproducible method for performing robust and highly accurate targeted amplification.

目的 构建血管内皮生长因子(VEGF)原核表达载体并诱导其表达蛋白,为后续迸行VEGF相关研究奠定基础.方法 通过逆转录聚合酶链式反应(RT-PCR)扩增得到目的片段,将DNA片段克隆至带组氨酸标签的pET-30a(+)载体上;构建的重组质粒经过菌液聚合酶链式反应(PCR)及测序方法鉴定;利用异丙基-β-D-硫代半乳糖苷(IPTG)诱导重组质粒表达,通过蛋白质印迹法(Western blot)迸行鉴定.结果 以HepG2细胞为模板扩增出大小正确的片段;构建的pET-30a-VEGF重组质粒经菌液PCR及DNA测序证实序列正确;考马斯亮蓝染胶和Western blot结果显示IPTG诱导表达的融合蛋白分子量正确且条带单一.结论 成功构建pET-30a-VEGF原核表达质粒,后续可迸行大量诱导表达用于肝癌的诊疗相关研究.

目的 通过收集乙型肝炎病毒(HBV)相关的肝癌患者的标本,分析各组织线粒体DNA D-LOOP区碱基的变化,探究HBV相关的肝癌线粒体DNA D-LOOP区的相关性.方法 选取2008年10月～2019年12月首都医科大学附属北京佑安医院就诊的慢性乙肝相关肝细胞癌(HCC)患者44例,其中31例患者的癌组织和对应的癌旁组织及外周血,7例患者的癌旁组织和相对应的外周血,5例患者有癌组织和对应的外周血,11例癌组织和对应的癌旁组织.同时选取了1 1例来自肝移植患者供体者的肝组织及对应的外周血作为对照.提取标本的线粒体DNA,设计引物和PCR反应获得线粒体D-LOOP区,对PCR产物进行一代测序.结果 一代测序数据结果显示长期慢性HBV肝炎可引起炎症肝组织和肝癌线粒体DNA D-LOOP区大量单碱基突变,肝癌组织和肝组织之间差异有统计学意义(P＜0.05).结论 长期慢性HBV肝炎可引起肝炎组织大量线粒体DNA D-LOOP区碱基突变,肝癌组织不同于正常肝组织的突变模式,对于肝癌的早期诊断具有提示意义.

Autophagy affects the pathological progression of non-alcoholic fatty liver disease (NAFLD); however, the precise role of autophagy in NAFLD remains unclear. In this study, we want to identify the role of autophagy including reticulophagy and mitophagy in NAFLD pathogenesis. When HepG2 cells were treated with 400 μM oleic acid (OA), increased reticulophagy was induced 8 h after treatment, which correlated with an anti-apoptotic response as shown by the activation of the PI3K/AKT pathway, an increase in BCL-2 expression, and the downregulation of OA-induced lipotoxicity. When treated with OA for 24 h, DRAM expression-dependent mitophagy resulted in increased apoptosis in HepG2 cells. Inhibition of reticulophagy aggravated and increased lipotoxicity-induced apoptosis 8 h after treatment; however, the inhibition of mitophagy decreased hepatocyte apoptosis after 24 h of OA treatment. Results from the analysis of patient liver samples showed that autophagic flux increased in patients with mild or severe NAFL. PI3K/AKT phosphorylation was observed only in samples from patients with low-grade steatosis, whereas DRAM expression was increased in samples from patients with high-grade steatosis. Together, our results demonstrate that reticulophagy and mitophagy are independent, sequential events that influence NAFLD progression, which opens new avenues for investigating new therapeutics in NAFLD.

流式细胞术在医学研究生的科研过程中应用广泛,学习和应用流式细胞术对培养研究生的科研能力具有重要作用.为了使初步接触流式细胞术的医学研究生对这门技术产生基本了解,并使对流式细胞仪具有潜在使用需求的医学研究生能够合理进行科研实验设计、顺利完成流式检测,文章从流式细胞术的基本理论、仪器操作、和常用实验等方面展开讨论,结合本单位的仪器条件以及研究生的科研方向,具体介绍了采用流式细胞术检测细胞周期的常用荧光染料、基本操作步骤和注意事项;并进一步介绍了分析流式数据文件的一般步骤,对通过应用流式细胞术来培养医学研究生的科研能力进行了探索分析.

Apoptosis stimulated protein of p53-2 (ASPP2) induces the transcription of p53-targeted genes to stimulates its pro-apoptosis function. The poor chemotherapeutic sensitivity is associated with the decreased ASPP2 expression in many human cancers. Here, multiple genes real-time RT-PCR array and western blotting analysis show that ASPP2 suppress the expression of X-linked inhibitor of apoptosis protein (XIAP), determinant of chemoresistance in cancer, in hepatocellular carcinoma (HCC) in a p53-independent manner. Further experiments with ASPP2-rAd and ASPP2-Lv confirmed that ASPP2 enhanced sensitivity of sorafenib to HCC via suppressing XIAP expression. XIAP mainly found on the cytoplasm and perinuclear areas of ASPP2 over-expressed HepG2 cells, while both cytoplasm and nucleus in ASPP2 shut down HepG2 cells. The association of poor sensitivity of sorafenib and XIAP expression was also found both in ASPP2 shut down and overexpress mice, where liver tissue with decreased or increased ASPP2 displayed less or more apoptosis, respectively. Finally, ASPP2 and XIAP expression analyzed in 43 hepatocellular carcinoma tumors and 44 adjacent normal tissues from 38 hepatocellular carcinoma patients for fully understand their expression within HCC patients. Compared with the tumor tissues, ASPP2 mRNA levels were increased, and XIAP levels decreased in the adjacent normal tissues. Taken together, XIAP suppressed ASPP2 increased tumor sensitivity to chemotherapy in a p53-independent manner, which was associated with chemotherapy resistance, suggesting that p53 activation and XIAP suppression were two independent ways that ASPP2 enhance the sensitivity of chemotherapy.

We have analyzed mutations in whole mitochondrial (mt) genomes of blood samples from HIV-1-infected children treated with long-term antiretroviral therapy (ART), who had an excellent virological response. HIV-1-infected children who have undergone ART for 4 y with an excellent virological response (group A; 15 children) and ten healthy children (controls) without HIV-1 infection were enrolled retrospectively. Peripheral blood mononuclear cells (PBMCs) were obtained and mt DNA mutations were studied. The total number of mtDNA mutations in group A was 3 H more than in the controls (59 vs. 19, P<0.001) and the same trend was seen in all mtDNA regions. Among these mtDNA mutations, 140 and 28 mutations were detected in group A and the controls, respectively. The D-loop, CYTB and 12s rRNA were the three most common mutation regions in both groups, with significant differences between the groups observed at nucleotide positions C309CC, T489C CA514deletion, T16249C and G16474GG (D-loop); T14783C, G15043A, G15301A, and A15662G (CYTB); and G709A (12s rRNA). G15043A and A15662G had been associated with mitochondrial diseases. Our findings suggest that mtDNA mutations occur frequently in long-term ART-treated, HIV-1-infected children who have an excellent virological response, although they did not have obvious current symptoms. The CYTB region may play an important role in mtDNA mutation during ART, which might contribute to the development of subsequent mitochondrial diseases.

目的 分析单独抗HIV治疗对HIV合并HBV感染者HBV病毒特征、病毒载量水平以及肝脏功能的影响.方法 纳入北京地区2010～2014年首都医科大学附属北京佑安医院收治的69例HIV感染且HBsAg阳性的患者,其中59例使用拉米夫定(3TC)加替诺福韦(TDF),10例使用3TC加齐多夫定(AZT)进行抗HIV治疗.收集患者的血浆和血清样本,检测其肝功能、HBV病毒载量,并分析了HBV逆转录酶区(RT)的耐药及突变.结果 33％的患者血清谷丙转氨酶(ALT》＞40 U/L,15％的患者血清谷草转氨酶(AST)＞40 U/L,并且传统的3TC+AZT与新的3TC+TDF相比,肝功异常的患者比例更多(P＜0.05);5例HBV病毒PCR扩增阳性的RT区测序结果显示,3TC+TDF和3TC+AZT都会导致大量的RT区和S抗原区突变,但是只有1例存在3TC耐药,2例存在S抗原逃逸.结论 HIV抗病毒治疗存在一定的肝脏损伤,可引起肝功ALT、AST水平增高,并可引起大量的RT区和S抗原区突变.是否会增强HBV耐药和病毒准种突变,有待对抗病毒治疗患者的动态检测分析.

Not all cognitive disorder/disease refers to Alzheimer’s disease, vascular dementia and other neurological related dementia (hereinafter referred to as neurologist dementia), AIDS can also cause cognitive impairment/dementia. However, its pathogenesis, clinical manifestation and treatment of various aspects are different from neurologist dementia. In this paper, the pathogenesis, pathological features and clinical manifestations of this disease were comprehensively expounded.

肝纤维化和肝硬化是肝脏损伤后的修复反应,其病理特征主要表现为细胞外基质的过度沉积,Ⅲ型前胶原蛋白[procollagen a1（Ⅲ）,cola1（Ⅲ）]是细胞外基质的主要成分[1]。通过检测血液或肝组织的表达量的变化可以观察肝纤维化及肝硬化的进展情况,指导临床诊疗和基础研究工作。因此,制备cola1（Ⅲ）单克隆抗体（mAb）对于肝纤维化和肝硬化的特异性检测具有重要意义。我们于2012年9月

血管生成是指在原有的血管结构基础上，内皮细胞以出芽方式，伴随内皮细胞的迁移、扩增、管腔化，形成新的血管的过程。血管生成可分为生理性和病理性两类，病理性血管生成见于以广泛、持续的炎症坏死和纤维化为特征的各种慢性肝脏疾病，包括：慢性乙型肝炎、慢性丙型肝炎、自身免疫性肝炎和原发性胆汁性肝硬化。新血管的形成与不同病因引起的慢性肝病纤维化发展模式紧密相关[1]，最终导致肝硬化组织异常血管结构的逐步形成。因此，在现代疾病进展的评价和治疗靶点的研究中，纤维化和血管生成的关系至关重要[2]。血管生成的程度可能会对疾病是否进展到肝硬化产生重要影响，并且是决定纤维化可否逆转的关键因素。

目的 探讨棕榈酸对肝癌HepG2细胞自噬和凋亡的影响.方法 采用含浓度为800 μmol/L棕榈酸的DMEM高糖培养基培养肝癌HepG2细胞24h,向HepG2细胞转染绿色荧光蛋白(GFP)-LC3质粒,通过观察LC3Ⅱ绿色荧光斑点确定自噬发生情况.利用BafA1抑制自噬后,采用M30免疫荧光检测细胞凋亡情况.结果 棕榈酸刺激24h明显增加自噬及凋亡细胞数量.阻断自噬,棕榈酸刺激引起的HepG2细胞凋亡水平明显增加.结论 棕榈酸可刺激自噬发生,该自噬对肝癌HepG2细胞有一定的保护作用.

Objective To investigate the role of Δ40P53 in apoptosis and cell cycle arrest after DNA damage in HCT116 p53-/-cell, to identify the difference between Δ40P53 and wild-type P53. Methods Luciferase reporter gene and immunoblotting were used to detect transcriptional activity and expression of Δ40P53 after DNA damage; flow cytometry was used to confirm cell cycle arrest after DNA damage, lactate dehydrogenase detection was used to analyze cell apoptosis after DNA damage, then biological functions of Δ40P53 was analyzed. Results The bax and p21 promoters activityhad 3-5 folds higher in MMS stress than no stress at HCT116 p53+/+. However, bax and p21 promoters activity had no significant difference between MMS and no-MMS stress at HCT116 p53-/-cells; immuno-blotting showed that Δ40P53 was keep in high level in both no-MMS and MMS stress and wtP53 was induced over expression by MMS; HCT116 p53-/-and HCT116 p53+/+ cells were treated with 50 μg/ml MMS for 24 h and then cell death was detected by LDH method,52.2% of HCT116 p53+/+cells died, while only 32.5% of HCT116 p53-/-cells died, with significant difference (t =84.2,P0.05); flow cytometry showed that 88% of HCT116 p53-/-cell went into G2/S phase after cells were treated by DNA damage agent-MMS, only 66% of HCT116 p53+/+ cell went into G2/S phase after cells were treated by DNA damage agent-MMS. Conclusion Δ40P53 in HCT116 p53-/-cells failed to induce cell apoptosis and cell cycle arrest following MMS stress.

ASPP2(apoptosis stimulating protein 2 of p53) binds to p53 specifically and enhance the pro-apoptotic function of p53,which plays a role in inhibiting tumor development.Adr-ASPP2 induces apoptosis through activating p53-DRAM-autophagy pathway.In this study,methyl methanesulfonate(MMS) was emplyed to stimulate Hep3B cells for 24 hours,then four different methods were used to detect autophage.Results: Adr-ASPP2 treatment induced autophagosome formation and expression of autophagy genes with and without MMS treatment.Moreover,ASPP2 combined with MMS induced higher autophagy level and higher level of gene expression.Both VPS34 and DRAM(damage-regulated autophagy modulator) siRNAs inhibited autophagy and blocked more ASPP2-or ASSP2 combined with MMS-induced apoptosis,indicating that ASPP2 induced DRAM-mediated autophagy involves in apoptotic death in Hep3B cells.The results showed that ASPP2 induces p53-independent DRAM expression-mediated autophagy,which promotes hepatocarcinoma death via apoptosis.Our results supply new idea in the field of gene therapy for liver cancer.

As the backbone of highly active antiretroviral therapy (HAART), nucleoside reverse transcriptase inhibitors (NRTIs) have effectively improved outcomes for HIV-infected patients. However, long-term treatment with NRTIs can cause a series of pathologies associated with mitochondrial toxicity. To date, the status and mechanism of mitochondrial toxicity induced by NRTIs are still not clear, especially in HIV-infected children. As part of the national pediatric HAART program in China, our study focused on mitochondrial toxicity and its potential mechanism in HIV-1-infected children who were divided into two groups based on their duration of treatment with NRTIs: one group received treatment for less than 36 months and one group was treated for 36 to 72 months. The control group comprised age-matched non-HIV-infected children. Blood lactic acid and ATP levels in peripheral blood mononuclear cells (PBMCs) were measured to evaluate mitochondrial function, and mtDNA copies and mutations in PBMCs were determined for detecting mtDNA lesions. Simultaneously, TK2 and P53R2 gene expression in PBMC was measured. As compared with the control group, blood lactic acid levels in both NRTI treatment groups were significantly higher, whereas ATP levels and mtDNA mutation rates in PBMCs did not differ between the control and the two NRTI treatment groups. Both NRTI treatment groups exhibited significant mtDNA loss. N Moreover, we found that P53R2 mRNA expression and protein levels were significantly reduced in both treatment groups and that TK2 mRNA expression and protein levels were induced in the long-term NRTI treatment group. These results suggest that mitochondrial toxicity occurs in long-term HAART patients and that P53R2 and TK2 levels in PBMCs are useful biomarkers for detecting mitochondrial toxicity in patients on long-term treatment with NRTIs.

Objective To investigate the potential mitochondrial toxicity markers in peripheral blood mononuclear cells(PBMCs) of HIV-infected children who treated with anti-retroviral therapy(ART) and its associated mechanisms.Methods Sixty cases of HIV-infected children with ART and 20 normal children were enrolled to detect TK2 gene mRNA and protein expression in their PBMCs and then analyze the association of TK2 levels with treatment regimens and treatment duration.Results TK2 gene mRNA and protein expressions were significantly higher in PBMCs of HIV-infected children who treated with ART than those in control group(mRNA:2.45/1;protein:3.2/1).And increasement in TK2 protein levels was associated with the term of the d4T or AZT treatment(P < 0.05).Children were further grouped according to their baseline CD4+ T cell number,baseline viral load,sexual,age and route of HIV transmission to compare the differences.No statistical significances were found among each group(P > 0.05).Conclusion TK2 level in PBMCs could reflect the mitochondrial toxicity of ART in children.It is expected to be a new marker for mitochondrial toxicity.

Abstract Background and Aims: Although Thymidine Kinase/Ganciclovir(TK/GCV) is a promising tumor-targeted chemotherapy by DNA damage, it is reported that tumor cells having wild-type p53 are more sensitive to chemotherapeutic agents. Furthermore some evidence have suggested approximately half of all cancers possess inactivated p53. Numerous studies have shown the key role of p53 as a tumor suppressor is blocking cell cycle progression and/or inducing apoptosis in response to high level of DNA damage. Given that TK/GCV results in DNA damage, exogenous wild-type p53 should enhance efficacy of adenovirus (adv)-mediated antitumor effect of TK/GCV on p53 −/- tumor cells. Thus, this article aims to determine whether p53 −/- cancer cells are sensitive at TK/GCV, whether coexpression of p53 and TK/GCV can actively kill p53−/- tumor cells and the main mechanisms responsible for TK/GCV tumor cell death. Methods:Hep3B cells (p53−/−) and HepG2(p53+/+) cells were infected with adv-p53 and adv-TK one day prior to GCV. The cellular growth inhibition was analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and immunofluorescent staining (PI and Calcein AM). Apoptosis and cell cycle arrest were measured using annexin V-FITC /PI double staining and PI by flow cytometry. p53,PUMA and p21 mRNA expression were analyzed using real-time quantitative PCR . The protein levels of p53,PUMA and p21 were detected by Western blotting. Results:The MTT results showed that cell viability (%) of HepG2 cell (p53+/+) treated with adv-TK(107/ml)/GCV(10ug/ml) were lower than Hep3B (p53−/−)(p<0.01). Growth inhibition of Hep3B treated with adv-p53 in combination with adv-TK/GCV was higher than adv-p53 and adv-TK/GCV alone (p<0.01). Annexin V-FITC/PI double staining and propidium iodide (PI) staining demonstrates that Hep3B cell treated with adv-p53 and adv-TK/GCV had significantly increased apoptosis compared to adv-p53 (p<0.01) and adv-TK/GCV(p<0.05) alone. The expression level of p53,p21 and PUMA mRNA and protein was significantly higher in Hep3B cell treated with adv-p53 and adv-TK/GCV compared to adv-p53 and adv-TK/GCV alone in a time-dependent manner. Conclusions:These results suggest that the p53−/- cancer cell is not sensitive to TK/GCV. p53 −/- tumor cells were actively killed by a combination adv- p53 with TK/GCV. p53-mediated apoptosis is the main mechanisms responsible for TK/GCV kill tumor cells. Citation Format: Kai Liu, Xiuhong Liu, Tao Wen, Feng Ren, Jiming Yin, Daojie Liu, Huiguo Ding, Ning Li, Dexi Chen. Adenovirus p53 enhances the antitumor effect of adenovirus thymidine kinase/ganciclovir on Hep3B cells by apoptosis. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 789. doi:10.1158/1538-7445.AM2013-789 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.

Abstract Background and Aims: ASPP2 (Apoptosis Stimulating Protein 2 of p53) binds to p53 and enhances p53 pro-apoptotic function. Autophagy may play a role in this process although the mechanisms remain to be clarified. Our aims were to explore the mechanisms by which the ASPP2-p53 pathway could promote apoptosis and autophagy in hepatocellular carcinoma cells in order to identify novel therapeutic targets in this disease. Methods: HepG2 cells were transfected with GFP-LC3 plasmid and then damaged with methyl methanesulfonate (MMS). Apoptosis was detected by cleavage of CK18 and PARP by immunocytochemical staining and Western blot. Real-time PCR and immunoblot were used to analyze changes in DRAM and LC3I/II expression. DRAM siRNA was used to inhibit DRAM function. Results: After MMS exposure for 24 hours, we identified more M30 positive cells and p85 formation in HepG2 cells compared to control cells. When HepG2 cells were transfected with a GFP-LC3 expression plasmid and then treated by MMS, we found that MMS treatment induced LC3 staining punctate structures, a marker for autophagy. Moreover, enforced expression of ASPP2 using adenovirus infection led to more autophagy and apoptosis in HepG2 after MMS treatment, under conditions where ASPP2 expressing adenovirus infection alone could not induce apoptosis and autophagy. Using real time PCR, we identified that MMS treatment could induce DRAM expression and that ASPP2 overexpression prior to MMS could further enhance DRAM expression compared to MMS alone. Immunoblot assay demonstrated that ASPP2 expression increased MMS-induced DRAM expression, LC3 II and p85 formation. Importantly, a DRAM specific siRNA blocked autophagy and apoptosis in HepG2 cells under these conditions when compared to a control siRNA. Conclusions: Our results suggest that ASPP2 can enhance MMS induced apoptosis via p53-dependent DRAM-mediated autophagy. Since DRAM is an important component of p53-mediated autophagy, our results demonstrate a new role for ASPP2 in this pathway. These findings open new avenues for investigation into the mechanisms of autophagy-based therapy in hepatocellular cancer (Supported by National Natural Science Foundation of China (30870853,30770742 and 30910103915), Beijing Municipal Natural Science Foundation (7092045 and 7101005) and Basic-Clinical Collaborative Research Fund, CCMU (12JL-L05)). Citation Format: Kai Liu, Tao Wen, Ming Ji Yin, Xin Lu Qiao, Ying Shi, Li Li, Jie Dao Liu, Chao Zhang, Ning Li, Charles Lopez, Xi De Chen. ASPP2 enhances DRAM induced autophagy to promote apoptosis in HepG2 cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1989. doi:10.1158/1538-7445.AM2013-1989