Background Hepatic ischemia-reperfusion injury (HIRI) is a pathophysiological process during liver transplantation, characterized by insufficient oxygen supply and subsequent restoration of blood flow leading to an overproduction of reactive oxygen species (ROS), which in turn activates the inflammatory response and leads to cellular damage. Therefore, reducing excess ROS production in the hepatic microenvironment would provide an effective way to mitigate oxidative stress injury and apoptosis during HIRI. Nanozymes with outstanding free radical scavenging activities have aroused great interest and enthusiasm in oxidative stress treatment. Results We previously demonstrated that carbon-dots (C-dots) nanozymes with SOD-like activity could serve as free radicals scavengers. Herein, we proposed that C-dots could protect the liver from ROS-mediated inflammatory responses and apoptosis in HIRI, thereby improving the therapeutic effect. We demonstrated that C-dots with anti-oxidative stress and anti-inflammatory properties improved the survival of L-02 cells under H 2 O 2 and LPS-treated conditions. In the animal model, Our results showed that the impregnation of C-dots could effectively scavenge ROS and reduce the expression of inflammatory cytokines, such as IL-1β, IL-6, IL-12, and TNF-α, resulting in a profound therapeutic effect in the HIRI. To reveal the potential therapeutic mechanism, transcriptome sequencing was performed and the relevant genes were validated, showing that the C-dots exert hepatoprotective effects by modulating the hepatic inflammatory network and inhibiting apoptosis. Conclusions With negligible systemic toxicity, our findings substantiate the potential of C-dots as a therapeutic approach for HIRI, thereby offering a promising intervention strategy for clinical implementation.

Background Hepatocellular carcinoma (HCC) is one of the most common and challenging cancers in the world. N6-methyladenosine (m 6 A) modification and long non-coding RNAs (lncRNAs) play critical roles in the progression of HCC. However, there are few reports on genome-wide screening and functional annotations of m 6 A-methylated lncRNAs in HCC. Methods The expression levels of m 6 A methyltransferase METTL3 and the association with the prognosis in HCC were determined by RT-qPCR, public dataset platforms. Then, RNA-seq, Pearson correlation analysis, MeRIP-qPCR, RNA half-life assay, gene site-directed mutation, RIP assay and RT-qPCR analysis were employed to determine the downstream target of METTL3 in HCC. Subsequently, the expression levels and roles of lncRNA glucosylceramidase beta pseudogene 1 (GBAP1) in HCC were determined by Kaplan–meier curves, RT-qPCR, in vitro functional experiments and in vivo tumorigenesis and lung metastasis models. Then, the downstream target and pathway of GBAP1 were explored by GO biological process, KEGG pathway enrichment, luciferase reporter assay, RIP assay and rescue experiments and so on. Results METTL3 was upregulated in HCC and closely related to HCC prognosis. And METTL3 induced GBAP1 expression by acting as the m 6 A writer of GBAP1 and IGF2BP2 worked as its m 6 A reader. Clinically, GBAP1 expression was significantly associated with tumor size, venous infiltration, TNM stage and prognosis of HCC, Functionally, GBAP1 promoted HCC metastasis and growth both in vitro and in vivo. Furthermore, GBAP1 acted as the molecular sponge for miR-22-3p to increase the expression of bone morphogenetic protein receptor type 1A (BMPR1A), which then activated BMP/SMAD pathway in HCC cells. Conclusions Our findings demonstrated that METTL3-induced GBAP1 promoted migration, invasion and proliferation of HCC cells via GBAP1/miR-22-3p/BMPR1A/SMAD axis. GBAP1 could be a potential prognosis indicator and therapeutic target for HCC.

Background:Serum albumin level and body mass index (BMI), acting as indicators of nutritional status, are commonly applied to predict surgical outcomes in cancer patients. This study aimed to evaluate the impact of preoperative serum albumin level and BMI on the operative outcomes of noncirrhotic patients with colorectal cancer liver metastasis who underwent hepatectomy. Methods:This was a retrospective study of medical records from the period between January 2013 and December 2022. Preoperative malnutrition was defined as hypoalbuminemia with a serum albumin level of <35 g/L before surgery or a BMI of <18.5 kg/m2 within 30 days before surgery. Multiple statistical methods were applied to analyze the data, including the two-independent sample t-test, analysis of variance, Chi-squared test, and multivariate analysis. Results:Among the 159 eligible patients, 42 (26.4%) were classified into the preoperative malnutrition group. The incidence of blood transfusion (45.24% vs. 18.80%, P = 0.040) was significantly higher in the malnutrition group. The drainage volume was significantly higher on the first day [65 (115) vs. 60 (80), P < 0.05] and the second day [50 (95) vs. 40 (79) P < 0.05] in the malnutrition group than that in the nonmalnutrition group. Postoperative hemoglobin levels were significantly lower in the malnutrition group (101.20 ± 2.43 vs. 108.76 ± 1.61, P = 0.015). Therefore, the incidence of grade Ⅱ or Ⅲ/Ⅳ complications was significantly higher in the malnutrition group (16.67% vs. 5.31% or 11.9% vs. 3.42%, P = 0.001), and the length of hospital stay was significantly extended [18 (12) vs. 15 (8), P = 0.002]. In the multivariate analysis, preoperative malnutrition [odds ratio (OR) = 5.548, 95% CI 1.508-20.413, p = 0.010] and operation time (OR = 1.009, 95% CI 1.002-1.016, P = 0.0011) were identified as independent predictors of postoperative complications. Conclusion:Preoperative malnutrition in patients who underwent hepatectomy for colorectal cancer liver metastasis was associated with worse surgical outcomes, especially aggrandizing the emergence of postoperative complications.

Hypoxic microenvironment plays a critical role in solid tumor growth, metastasis and angiogenesis. Hypoxia-inducible factors (HIFs), which are canonical transcription factors in response to hypoxia, are stabilized under hypoxia and they coordinate the process of hypoxia-induced gene expression leading to cancer progression. Increasing evidence has indicated that long noncoding RNAs (lncRNAs) which are closely associated with cancer play crucial roles in hypoxia-mediated HCC progression, while the mechanisms are largely unknown. Here, we identified a novel lncRNA SZT2-AS1 in HCC, which was induced by hypoxia in a HIF-1-dependent manner and promoted HCC growth, metastasis and angiogenesis. The clinical data indicated that SZT2-AS1 level was substantially upregulated in HCC and significantly associated with poor clinical outcomes, and acted as an independent prognostic predictor. Mechanistically, SZT2-AS1, in turn, recruited HIF-1α and HIF-1β to form the HIF-1 heterodimer. And SZT2-AS1 was required for the occupancy of HIF-1 to hypoxia response elements (HREs) and HIF target gene transcription. In addition, SZT2-AS1 was required for hypoxia-induced histone trimethylation (H3K4me3 and H3K36me3) at HREs. Through recruiting methyltransferase SMYD2, SZT2-AS1 promoted trimethylation modification of H3K4 and H3K36 in HCC cells. Taken together, our results uncovered a lncRNA-involved positive feedback mechanism under hypoxia and established the clinical value of SZT2-AS1 in prognosis and potential therapeutic strategy for HCC. Significance: LncRNA SZT2-AS1 involves in a positive feedback mechanism under hypoxia, which provides a therapeutic strategy for HCC.

Hypoxic microenvironment plays a critical role in solid tumor growth, metastasis and angiogenesis. Hypoxia-inducible factors (HIFs), which are canonical transcription factors in response to hypoxia, are stabilized under hypoxia and coordinate the process of hypoxia-induced gene expression, leading to cancer progression. Increasing evidence has uncovered that long noncoding RNAs (lncRNAs), which are closely associated with cancer, play crucial roles in hypoxia-mediated HCC progression, while the mechanisms are largely unknown. Here, we identified SZT2-AS1 as a novel lncRNA in HCC, which was induced by hypoxia in a HIF-1-dependent manner and promoted HCC growth, metastasis and angiogenesis both in vitro and in vivo. And SZT2-AS1 also mediated the hypoxia-induced HCC progression. Clinical data indicated that SZT2-AS1 level was substantially increased in HCC and closely associated with poor clinical outcomes, acting as an independent prognostic predictor. Mechanistically, SZT2-AS1 recruited HIF-1α and HIF-1β to form the HIF-1 heterodimer, and it was required for the occupancy of HIF-1 to hypoxia response elements (HREs) and HIF target gene transcription. In addition, SZT2-AS1 was required for hypoxia-induced histone trimethylation (H3K4me3 and H3K36me3) at HREs. Through recruiting methyltransferase SMYD2, SZT2-AS1 promoted trimethylation of H3K4 and H3K36 in HCC cells. Taken together, our results uncovered a lncRNA-involved positive feedback mechanism under hypoxia and established the clinical value of SZT2-AS1 in prognosis and as a potential therapeutic target in HCC.

Background: Bariatric surgeries, including the sleeve gastrectomy, have been recognized as the most effectively treatment strategy for severe obesity. Magnetic devices have been successfully used in bariatric surgeries. Here, we intended to evaluate the safety and efficiency of magnetic anchoring device assisted-laparoscopic sleeve gastrectomy (MLSG), and to make a comparison of the short-term results between conventional laparoscopic sleeve gastrectomy (CLSG) and MLSG. Methods: The retrospective cohort study was carried out by analyzing and summarizing the data from a database of routinely collected data. The cohort included the patients who underwent either CLSG (n = 120) or MLSG (n = 115) at a single center between January 2018 and December 2020 with a two-year follow-up. The effects of these two surgeries on the weight loss, resolution of comorbidities and quality of life (QOL) were analyzed. Results: The two groups were similar in gender, age, body mass index, abdominal girth, as well as the type and proportion of comorbidities. And the cases in MLSG group had a markedly shorter time of operation (MLSG, 72.59 min vs. CLSG, 76.67 min; P = 0.003). Length of stay in hospital was significantly shorter in the MLSG group than that in the CLSG group (MLSG, 5.59 days vs. CLSG, 5.96 days; P = 0.016). Neither fatal event nor conversion to open surgery happened among all cases. There were no differences in terms of the postoperative complications between the two groups. Magnetic device-related mild hepatic lacerations occurred and were handled by hemostatic treatments in 3 cases. The QOL of patients in MLSG was better at 6-month after surgery, but there was no significant difference between the two groups at 1-year or 2-year after surgery. Conclusion: Both MLSG and CLSG prove safe and effective, and the patients underwent MLSG have a shorter length of stay in hospital, and a better QOL during 6 months after surgery.

Abstract Objective: To determine the composition and influencing factors of hospital expenses of patients undergone laparoscopic Sleeve Gastrectomy (LSG) in an effort to reasonably control the hospital costs and reduce the economic burden of patients. Method: The inpatient expenses of 574 patients with LSG surgery from January 1, 2019, to December 31, 2022, in a tertiary hospital in China were retrospectively studied. Descriptive statistics were used to analyze the composition of inpatient expenses. The mean values between the two groups were compared using the independent t-test, and the mean values between multiple groups were compared using an ANOVA test. The effective results of Mono-factor analysis were further analyzed by multiple linear regression analysis. Result: (1) The result indicated an upward trend in hospital expenses among LSG patients over the past four years, with an average cost of 53241.87 RMB. The major components of hospital charge were: operation costs of 7109.60 RMB (13.35%) and disposable material costs of 13849.69 RMB (26.01%), accounting for 39.36% of the total hospital costs. (2) The results of multiple linear regression analysis were observed that F=33.478, P<0.05. Gender, complications, number of other diagnoses, year of discharge, age and length of stay were the important factors affecting hospital expenses. Hospitalization expenses were higher for male patients than female patients, which increased as comorbidities, age, postoperative complications, and length of stay increased. Conclusion: High operation costs and continuously rising material costs contribute to rising hospitalization expenses for LSG patients. Early operation to reduce weight, control of obesity-related comorbidities, reducing postoperative complication risk, reasonable control of hospitalization time, and more effective surgical costs management can significantly reduce hospitalization costs for this patient group.

Introduction: Dopamine is one of the most significant neurotransmitters and plays an important role in the management of cognitive functions such as learning, memory, and behavior. The disorder of dopamine is associated with many major mental diseases. It is necessary to develop selective methods for the detection of dopamine. Methods: In this work, carbon dots (CDs) were synthesized by a solvothermal route using glutathione, L-histidine, and formamide as sources. Results: Under light irradiation, The CDs convert dissolved oxygen to singlet oxygen ( 1 O 2 ), which could oxidize TMB. When reduced dopamine was present, it suppressed the catalysis of CDs, then the absorption of the CDs-coupled TMB complex at 652 nm was diminished. Furthermore, it was revealed that the surface groups including hydroxyl, amino, carbonyl, and carboxyl groups of CDs were related to their light-responsive catalytic activity by surface modification. In the range of 0.5-15 μM, the CDs could afford a LOD of 0.25 μM for dopamine detection with fine linearity, also showing good selectivity. Discussion: The results from fetal bovine serum indicated the good applicability of the CDs in the determination of dopamine.

Abstract Objective: To determine the composition and influencing factors of hospital expenses of patients undergone laparoscopic Sleeve Gastrectomy (LSG) in an effort to reasonably control the hospital costs and reduce the economic burden of patients. Method: The inpatient expenses of 574 patients with LSG surgery from January 1, 2019, to December 31, 2022, in a tertiary hospital in China were retrospectively studied. Descriptive statistics were used to analyze the composition of inpatient expenses. The mean values between the two groups were compared using the independent t-test, and the mean values between multiple groups were compared using an ANOVA test. The effective results of Mono-factor analysis were further analyzed by multiple linear regression analysis. Result: (1) The result indicated an upward trend in hospital expenses among LSG patients over the past four years, with an average cost of 53241.87 RMB. The major components of hospital charge were: operation costs of 7109.60 RMB (13.35%) and disposable material costs of 13849.69 RMB (26.01%), accounting for 39.36% of the total hospital costs. (2) The results of multiple linear regression analysis were observed that F=33.478, P<0.05. Gender, complications, number of other diagnoses, year of discharge, age and length of stay were the important factors affecting hospital expenses. Hospitalization expenses were higher for male patients than female patients, which increased as comorbidities, age, postoperative complications, and length of stay increased. Conclusion: High operation costs and continuously rising material costs contribute to rising hospitalization expenses for LSG patients. Early operation to reduce weight, control of obesity-related comorbidities, reducing postoperative complication risk, reasonable control of hospitalization time, and more effective surgical costs management can significantly reduce hospitalization costs for this patient group.

BACKGROUND:Long non-coding RNAs (lncRNAs) perform a vital role during the progression of hepatocellular carcinoma (HCC). Here, we aimed to identify a novel lncRNA involved in HCC development and elucidate the underlying molecular mechanism.METHODS:The RT-qPCR and TCGA dataset analysis were applied to explore the expressions of MRVI1-AS1 in HCC tissues and cell lines. Statistical analysis was applied to analyze the clinical significance of MRVI1-AS1 in HCC. The functions of MRVI1-AS1 in HCC cells metastasis and growth were explored by transwell assays, wound healing assay, MTT assay, EdU assay, the intravenous transplantation tumor model, and the subcutaneous xenograft tumor model. Microarray mRNA expression analysis, dual luciferase assays, and actinomycin D treatment were used to explore the downstream target of MRVI1-AS1 in HCC cells. RIP assay was applied to assess the direct interactions between CELF2 and MRVI1-AS1 or SKA1 mRNA. Rescue experiments were employed to validate the functional effects of MRVI1-AS1, CELF2, and SKA1 on HCC cells.RESULTS:MRVI1-AS1 was found to be dramatically upregulated in HCC and the expression was strongly linked to tumor size, venous infiltration, TNM stage, as well as HCC patients' outcome. Cytological experiments and animal experiments showed that MRVI1-AS1 promoted HCC cells metastasis and growth. Furthermore, SKA1 was identified as the downstream targeted mRNA of MRVI1-AS1 in HCC cells, and MRVI1-AS1 increased SKA1 expression by recruiting CELF2 protein to stabilize SKA1 mRNA. In addition, we found that MRVI1-AS1 expression was stimulated by hypoxia through a HIF-1-dependent manner, which meant that MRVI1-AS was a direct downstream target gene of HIF-1 in HCC.CONCLUSION:In a word, our findings elucidated that hypoxia-induced MRVI1-AS1 promotes metastasis and growth of HCC cells via recruiting CELF2 protein to stabilize SKA1 mRNA, pointing to MRVI1-AS1 as a promising clinical application target for HCC therapy.

腹腔镜袖状胃切除术(laparoscopic sleeve gastrectomy, LSG)已经成为治疗肥胖及代谢性疾病的主要手术方式之一,因其创伤小、操作相对简单、手术时间短、治疗效果确切,越来越多的减重外科医生及患者选择该手术.据国际肥胖与代谢病外科联盟统计,2016年全球实施的减重手术总数为685874例;其中634897例(92.6%)为首次手术,50977例为修正性手术(7.4%).其中最主要的手术方式为LSG,占总数量的53.6%[1].据美国减肥及代谢外科学会统计,2017年美国的LSG手术比例已经达到59.39%[2].虽然LSG术后总的并发症只有7.5%～13%[3,4],但仍有部分严重的并发症可能导致患者休克、甚至死亡[4,5],胃漏就是其中之一,处理不当的话可能导致严重后果.由于LSG术后胃漏的治疗难度大、时间长,因此其往往是专科医师在临床中遇到的最大的困难与挑战.现报道一例袖状胃切除术后胃漏的诊治.

Objective:To measure the expression level of miR-886-5p in hepatocellular carcinoma(HCC),analyze the correlations of clinicopathological features with miR-886-5p expression,and explore the effects of miR-886-5p on invasion and migration of HCC cells.Methods:Real-time PCR was conducted to detect miR-886-5p expression in HCC tissues and cell lines.The correlations of clinicopathological features with miR-886-5p expression were analyzed by statistical analysis.Transwell assay was applied to explore the functions of miR-886-5p in migration and invasion of HCC cells.Results:miR-886-5p was significantly decreased both in HCC tissues and cell lines(P ＜ 0.05).miR-886-5p expression was remarkably associated with tumor nodules,vein invasion,Edmondson-Steiner grading and tumor-node-metastasis (TNM) stage (P ＜ 0.05).Transwell assay revealed that miR-886-5p could inhibit invasion and migration of HCC cells.Conclusion:miR-886-5p was down-regulated in HCC,and could inhibit migration and invasion of HCC cells.

Recently, it has been reported that miR-324-3p participates in regulation of the carcinogenesis and tumor progression in various cancers. However, the expression and function of miR-324-3p in hepatocellular carcinoma (HCC) remain unclear. In the current study, miR-324-3p expression was significantly up-regulated in HCC tissues and cell lines. HCC patients with high miR-324-3p level showed poor prognostic features and shorter overall survival and disease-free survival. And in vitro and in vivo experiments revealed that miR-324-3p promoted cell viability, colony formation, proliferation and cell cycle progression of HCC cells. Further studies demonstrated that miR-324-3p could directly target DACT1 (dishevelled binding antagonist of beta catenin 1) and negatively regulated its expression in HCC cells. And rescue experiments revealed that DACT1 could reverse the effects of miR-324-3p on HCC cells. Furthermore, the accumulation of both cytoplasmic and nuclear β-catenin as well as its downstream targets including c-Myc and cyclin D1 could be positively regulated by miR-324-3p. The regulatory effects of miR-324-3p on β-catenin, c-Myc and cyclin D1 levels could be reversed by DACT1. Overall, we concluded that miR-324-3p could promote tumor growth through targeting DACT1 and activation of Wnt/β-catenin pathway in HCC. MiR-324-3p may be a ponderable and promising therapeutic target for HCC.

OBJECTIVE:To detect the expression of BCL6 corepressor-like 1 (BCORL1) in tumor tissues of human non-small cell lung cancer (NSCLC) and determine the effect of BCORL1 on cell migration and invasion in A549 cells by knockdown of BCORL1.METHODS:Sixty-eight pairs of NSCLC and nontumor tissues were collected and the expressions of BCORL1 and E-cadherin in them were detected using immunohistochemical staining. The expression of BCORL1 was knocked down by siRNA in A549 cells. Transwell(TM) assays were performed to test NSCLC cell migration and invasion in vitro.RESULTS:The expression of BCORL1 in NSCLC was significantly higher than that in paired noncancerous tissues, while E-cadherin was down-regulated in NSCLC as compared with nontumor tissues. Pearson correlation coefficient analysis suggested that BCORL1 was negatively correlated with E-cadherin expression in NSCLC tissues. Clinical association analysis suggested that the elevated expression of BCORL1 was evidently associated with the higher incidence of lymph node metastasis and more advanced TNM stage. When the expression of BCORL1 was down-regulated by a specific siRNA, E-cadherin was up-regulated, and BCORL1 knockdown obviously inhibited cell migration and invasion in A549 cells.CONCLUSION:BCORL1 is overexpressed in NSCLC tissues and it is negatively correlated with E-cadherin expression. Its high expression is correlated with poor prognostic features. BCORL1 knockdown up-regulates E-cadherin expression and subsequently inhibits cell migration and invasion of lung cancer cells.

OBJECTIVE:To investigate the expression of microRNA-218 (miR-218) and its role in hepatocellular carcinoma (HCC). METHODS:Forty-six pairs of fresh surgical specimens of HCC and adjacent tissues were examined for miR-218 expression using qRT-PCR. A miR-218 mimic was transfected into HepG2 cells, and the cell viability and apoptosis were analyzed by MTT assay and flow cytometry, and the potential targets of miR-218 were detected by qRT-PCR and Western blotting. RESULTS:The expressions of miR-218 in HCC tissues were significantly down-regulated compared to those in the adjacent tissues (P<0.05). Down-regulation of miR-218 was found to correlate significantly with the tumor size (>5 cm) and an advanced TNM stage (III+IV) (P<0.05). Ectopic expression of miR-218 in HepG2 cells resulted in suppressed cell proliferation and enhanced cell apoptosis as well as the down-regulation of Bmi-1 and CDK6 mRNA and protein expressions (P<0.05). CONCLUSION:The low-expression of miR-218 is correlated with malignant clinicopathological characteristics of HCC, and miR-218 may inhibit cell proliferation and promote cell apoptosis by down-regulating Bmi-1 and CDK6 in HCC.

Objective Aim To compare the safety and efficacy between laparoscopic splenectomy and esophagogastric devascularization(LSED) and open splenectomy and esophagogastric devascularization(OSED) in treating portal hypertension with refractory variceal bleeding. Methods A retrospective analysis of clinical data and complications of 77 patients received OSED surgery and over the same period 67 patients received LSED surgery whom diagnosed of portal hypertension in our hospital from 2002.1—2012.7. Results The LSED group operation time and OSED groups had no significant difference(P=0.757). The LSED group blood loss, postoperative gastrointestinal function recovery time was significantly less than OSED group(P<0.001,P=0.019). The LSED group postoperative lab data ALT, AST and TBIL was significantly lower than OSED group(P =0.002,P =0.002,P =0.015). No significant difference in postoperative PLT, WBC and Hb between the two groups(P=0.786,P=0.056,P=0.973). The incidence of portal vein system thrombosis as the complications of the LSED group was higher than the OSED group, the other complications between the two groups had no significant difference. Conclusion The LSED surgery has the advantages of safe, less surgery trauma and effective in treating portal hypertension associated with refrctory variceal bleeding.

The Hedgehog (Hh) pathway is an evolutionarily conserved signaling mechanism that controls many aspects of cell differentiation and the development of tissues and organs during embryogenesis. Early investigations have focused on the effects of Hh activity on the development of organs including skin, gut, the nervous system and bone. However, in addition to normal developmental processes, these investigations also found that Hh signaling is involved in aberrant proliferation and malignant transformation. Consequently, the role of Hh in cancer pathology, and its modulation by environmental factors is the subject of many investigations. Numerous environmental toxins, alcohol, and hepatitis viruses can cause hepatocellular carcinoma (HCC), which is the most common form of liver cancer. Significant hyperactivation of Hh signaling has been observed in liver injury and cirrhosis which often leads to the development of HCC lesions. Moreover, Hh activity plays an important role in the progression of HCC. Here, we review findings relevant to our understanding of the role of Hh signaling in HCC pathogenesis.

OBJECTIVE:To investigate the expression of P300/CBP-associated factor (PCAF) in hepatocellular carcinoma (HCC) and its clinical significance.METHODS:Immunohistochemistry was performed to evaluate the expression of PCAF in HCC tissues and adjacent normal liver tissues of 35 HCC patients. We analyzed the correlation between the expression of PCAF and clinical data using chi-square test, and then anaylzed the factors which affected survival by Kaplan-Meier Log-rank test and multivariate Cox regression model.RESULTS:The expression of PCAF in the HCC tissues was significantly different from that in the adjacent liver tissues (P<0.05) and it was correlated with tumor TNM staging and tumor metastasis (P<0.05). Multivariate COX regression analysis showed that the independent factors predicting poor long-term HCC survival after radical liver resection included low PCAF expression, advanced TNM stage and tumor metastasis.CONCLUSION:PCAF expression is down-regulated in HCC and constitutes a promising biomarker for the prognosis after curative liver resection.