RING finger protein 128 (RNF128) regulates malignant biological behaviors of colorectal cancer cells via PI3K/AKT signaling pathway.

This study was designed and conducted to clarify the impact of RNF128 expression on malignant biological behaviors of colorectal cancer (CRC) cells and the underlying mechanism. The expression of RNF128 in CRC tissues was analyzed using mRNA sequencing data of TCGA database and was validated by Western blot assay. The experimental studies on biological functions of RNF128 in vitro were conducted to assess its impact on the proliferation, apoptosis, and metastasis of CRC cells. Furthermore, tumor xenograft models in nude mice were established to investigate the relationship between RNF128 expression and tumor growth in vivo. The expression levels of both RNF128 mRNA and protein were significantly increased in CRC tissues (p < .001). The knockdown of RNF128 markedly suppressed the malignant phenotype of HCT116 and SW480 cells in vitro, including cell growth, antiapoptosis, migration, and invasion (p < .001). On the other hand, knockdown of RNF128 exerted a remarkable effect on the growth inhibition of tumor xenografts in vivo (p < .001). Further investigation revealed that RNF128 knockdown lead to a significant decrease in the expression of p-AKT and p-PI3K protein. More importantly, the proliferative, antiapoptotic, metastatic abilities of RNF128-knockdown cells were markedly increased by 740 Y-P treatment (p < .001). These findings further suggested that PI3K/AKT signaling pathway played a key role in RNF128-mediated aggressive phenotype of CRC cells. RNF128 functions as a tumor promoter in the pathogenesis of CRC via regulating PI3K/AKT pathway, and it could be a valuable target for CRC treatment.

LiDAR Intensity Completion: Fully Exploiting the Message from LiDAR Sensors.

Light Detection and Ranging (LiDAR) systems are novel sensors that provide robust distance and reflection strength by active pulsed laser beams. They have significant advantages over visual cameras by providing active depth and intensity measurements that are robust to ambient illumination. However, the systemsstill pay limited attention to intensity measurements since the output intensity maps of LiDAR sensors are different from conventional cameras and are too sparse. In this work, we propose exploiting the information from both intensity and depth measurements simultaneously to complete the LiDAR intensity maps. With the completed intensity maps, mature computer vision techniques can work well on the LiDAR data without any specific adjustment. We propose an end-to-end convolutional neural network named LiDAR-Net to jointly complete the sparse intensity and depth measurements by exploiting their correlations. For network training, an intensity fusion method is proposed to generate the ground truth. Experiment results indicate that intensity-depth fusion can benefit the task and improve performance. We further apply an off-the-shelf object (lane) segmentation algorithm to the completed intensity maps, which delivers consistent robust to ambient illumination performance. We believe that the intensity completion method allows LiDAR sensors to cope with a broader range of practice applications.

miR-487b and TRAK2 that form an axis to regulate the aggressiveness of osteosarcoma, are potential therapeutic targets and prognostic biomarkers.

To investigate the effect of microRNA-487b (miR-487b) as well as the underlying mechanism in osteosarcoma (OS). Data downloaded from the Gene Expression Omnibus (GEO) database were used to analyze the expression and prognostic value of miR-487b/TRAK2. Cell counting kit-8, colony formation, and transwell assays were performed to investigate the biological functions of miR-487b and TRAK2. Luciferase reporter assay was applied to confirm the interactions between miR-487b and TRAK2. miR-487b was overexpressed in OS tissues and was inversely associated with the prognosis of OS patients. We discovered that miR-487b could contribute to the proliferative, clonogenic, invasive, and migratory capabilities of OS cells. Through target prediction using miRWalk and differential expression analysis based on the GEO data set, trafficking kinesin protein 2 (TRAK2) was recognized as a potential target of miR-487b, which was further verified by luciferase reporter assay. The expression of TRAK2 was decreased in OS tissues compared with normal tissues and was positively correlated with the prognosis of OS patients. A negative relevance was presented between the expression of miR-487b and TRAK2 in OS cells. Of note, further mechanistic analyses indicated that TRAK2 was implicated in the regulatory effect of miR-487b on the cell malignant behaviors in OS. To sum up, these results demonstrated that miR-487b played an oncogenic role in OS progression via directly targeting TRAK2, which could advance the development of cancer treatment.

Expression of cyclin-dependent kinase 9 is positively correlated with the autophagy level in colon cancer.

BACKGROUND: Cyclin-dependent kinase 9 (CDK9) expression and autophagy in colorectal cancer (CRC) tissues has not been widely studied. CDK9, a key regulator of transcription, may influence the occurrence and progression of CRC. The expression of autophagy-related genes BECN1 and drug resistance factor ABCG2 may also play a role in CRC. Under normal physiological conditions, autophagy can inhibit tumorigenesis, but once a tumor forms, autophagy may promote tumor growth. Therefore, understanding the relationship between autophagy and cancer, particularly how autophagy promotes tumor growth after its formation, is a key motivation for this research. AIM: To investigate the relationship between CDK9 expression and autophagy in CRC, assess differences in autophagy between left and right colon cancer, and analyze the associations of autophagy-related genes with clinical features and prognosis. METHODS: We collected tumor tissues and paracarcinoma tissues from colon cancer patients with liver metastasis to observe the level of autophagy in tissues with high levels of CDK9 and low levels of CDK9. We also collected primary tissue from left and right colon cancer patients with liver metastasis to compare the autophagy levels and the expression of BECN1 and ABCG2 in the tumor and paracarcinoma tissues. RESULTS: The incidence of autophagy and the expression of BECN1 and ABCG2 were different in left and right colon cancer, and autophagy might be involved in the occurrence of chemotherapy resistance. Further analysis of the relationship between the expression of autophagy-related genes CDK9, ABCG2, and BECN1 and the clinical features and prognosis of colorectal cancer showed that the high expression of CDK9 indicated a poor prognosis in colorectal cancer. CONCLUSION: This study laid the foundation for further research on the combination of CDK9 inhibitors and autophagy inhibitors in the treatment of patients with CRC.

Role of deubiquitinase JOSD2 in the pathogenesis of esophageal squamous cell carcinoma.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a deadly malignancy with limited treatment options. Deubiquitinases (DUBs) have been confirmed to play a crucial role in the development of malignant tumors. JOSD2 is a DUB involved in controlling protein deubiquitination and influencing critical cellular processes in cancer. AIM: To investigate the impact of JOSD2 on the progression of ESCC. METHODS: Bioinformatic analyses were employed to explore the expression, prognosis, and enriched pathways associated with JOSD2 in ESCC. Lentiviral transduction was utilized to manipulate JOSD2 expression in ESCC cell lines (KYSE30 and KYSE150). Functional assays, including cell proliferation, colony formation, drug sensitivity, migration, and invasion, were performed, revealing the impact of JOSD2 on ESCC cell lines. JOSD2's role in xenograft tumor growth and drug sensitivity in vivo was also assessed. The proteins that interacted with JOSD2 were identified using mass spectrometry. RESULTS: Preliminary research indicated that JOSD2 was highly expressed in ESCC tissues, which was associated with poor prognosis. Further analysis demonstrated that JOSD2 was upregulated in ESCC cell lines compared to normal esophageal cells. JOSD2 knockdown inhibited ESCC cell activity, including proliferation and colony-forming ability. Moreover, JOSD2 knockdown decreased the drug resistance and migration of ESCC cells, while JOSD2 overexpression enhanced these phenotypes. In vivo xenograft assays further confirmed that JOSD2 promoted tumor proliferation and drug resistance in ESCC. Mechanistically, JOSD2 appears to activate the MAPK/ERK and PI3K/AKT signaling pathways. Mass spectrometry was used to identify crucial substrate proteins that interact with JOSD2, which identified the four primary proteins that bind to JOSD2, namely USP47, IGKV2D-29, HSP90AB1, and PRMT5. CONCLUSION: JOSD2 plays a crucial role in enhancing the proliferation, migration, and drug resistance of ESCC, suggesting that JOSD2 is a potential therapeutic target in ESCC.

Citrate Synthase Overexpression of Pseudomonas putida Increases Succinate Production from Acetate in Microaerobic Cultivation.

Acetate is an end-product of anaerobic biodegradation and one of the major metabolites of microbial fermentation and lingo-cellulosic hydrolysate. Recently, acetate has been highlighted as a feedstock to produce value-added chemicals. This study examined acetate conversion to succinate by citrate synthase (gltA)-overexpressed Pseudomonas putida under microaerobic conditions. The acetate metabolism is initiated with the gltA enzyme, which converts acetyl-CoA to citrate. gltA-overexpressing P. putida (gltA-KT) showed an ∼50% improvement in succinate production compared to the wild type. Under the optimal pH of 7.5, the accumulation of succinate (4.73 ± 0.6 mM in 36 h) was ∼400% higher than that of the wild type. Overall, gltA overexpression alone resulted in 9.5% of the maximum theoretical yield in a minimal medium with acetate as the sole carbon source. This result shows that citrate synthase is important in acetate conversion to succinate by P. putida under microaerobic conditions.

Polydopamine/polypyrrole-modified graphite felt enhances biocompatibility for electroactive bacteria and power density of microbial fuel cell.

The interactions between the microbes and the surface of an anode play an important role in capturing the respiratory electrons from bacteria in a microbial fuel cell (MFC). The chemical and electrochemical characteristics of the carbon material affect biofilm growth and direct electron transfer in MFCs. This study examined the electrodeposition of polydopamine (PDA) and polypyrrole (PPY) on graphite felt electrode (GF). The MFC with the modified PDA/PPY-GF reached 920 mW/m2, which was 1.5, 1.17, and 1.18 times higher than those of the GF, PDA-GF, and PPY-GF, respectively. PDA has superior hydrophilicity and adhesive force biofilm formation, while PPY provides electrochemically active sites for microbial electron transfer. Raman spectroscopy, Fourier transform infrared spectroscopy, Brunauer-Emmett-Teller surface area measurements, and contact angle analysis revealed the enhanced physicochemical properties of the carbon electrode. These results show that co-doped PDA/PPY provides a strategy for electroactive biofilm development and improves the bioelectrochemical performance in realistic MFC reactors.

Prognostic value of ECOG performance status and Gleason score in the survival of castration-resistant prostate cancer: a systematic review.

Eastern Cooperative Oncology Group (ECOG) performance status and Gleason score are commonly investigated factors for overall survival (OS) in men with castration-resistant prostate cancer (CRPC). However, there is a lack of consistency regarding their prognostic or predictive value for OS. Therefore, we performed this meta-analysis to assess the associations of ECOG performance status and Gleason score with OS in CRPC patients and compare the two markers in patients under different treatment regimens or with different chemotherapy histories. A systematic literature review of monotherapy studies in CRPC patients was conducted in the PubMed database until May 2019. The data from 8247 patients in 34 studies, including clinical trials and real-world data, were included in our meta-analysis. Of these, twenty studies reported multivariate results and were included in our main analysis. CRPC patients with higher ECOG performance statuses (≥ 2) had a significantly increased mortality risk than those with lower ECOG performance statuses (<2), hazard ratio (HR): 2.10, 95% confidence interval (CI): 1.68-2.62, and P < 0.001. The synthesized HR of OS stratified by Gleason score was 1.01, with a 95% CI of 0.62-1.67 (Gleason score ≥ 8 vs <8). Subgroup analysis showed that there was no significant difference in pooled HRs for patients administered taxane chemotherapy (docetaxel and cabazitaxel) and androgen-targeting therapy (abiraterone acetate and enzalutamide) or for patients with different chemotherapy histories. ECOG performance status was identified as a significant prognostic factor in CRPC patients, while Gleason score showed a weak prognostic value for OS based on the available data in our meta-analysis.

Prognosis model of colorectal cancer patients based on NOTCH3, KMT2C, and CREBBP mutations.

BACKGROUND: Colorectal cancer (CRC) is one of the most common cancers. The aim of our study was to explore its related mutations, identify novel mutation markers, and construct predictive models for postoperative CRC patients, so as to provide evidence for the diagnosis, treatment, and prognosis of CRC. METHODS: A total 50 CRC patients were collected, and the mutations in tissue samples were detected through next-generation sequencing (NGS). Meanwhile, 246 CRC cases with complete mutation data were downloaded from The Cancer Genome Atlas (TCGA) database. Afterwards, the co-mutations in both clinical and TCGA cohorts were identified, and the high-frequency mutation genes were selected. Subsequently, functional enrichment analysis was performed, and overall survival (OS) and progression-free survival (PFS) predictive models were constructed. RESULTS: In all, 18 out of 238 co-mutation genes mutated in at least 20% of the samples and were selected out as common high-frequency mutation genes. They were significantly enriched in 460 Gene Ontology (GO) terms and 87 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways (P<0.05), which were closely related to the occurrence and development of CRC. Among the 18 genes, NOTCH3, histone lysine methyltransferase 2C (KMT2C), and cAMP-response element binding protein-BP (CREBBP) were respectively associated with tumor position, stage, and PFS (P<0.05), and could be considered as potential biomarkers of CRC. Finally, OS and PFS predictive models were constructed and verified using the 50 clinical cases, with both models demonstrating high fitting degrees useful for predicting the OS and PFS of CRC patients. CONCLUSIONS: NOTCH3, KMT2C, and CREBBP were found to be prospective biomarkers for the diagnosis and prognosis of CRC. The prognosis prediction models had high sensitivity and could be used to predict the OS and PFS of CRC patients.

Effectiveness of Hospital-Based Systemic Rehabilitation in Improving Ankle Function after Surgery in Chronic Ankle Instability Patients.

We investigated the therapeutic effect of a postoperative hospital-based systemic rehabilitation protocol on ankle function in chronic ankle instability (CAI) patients. Thirty-five patients who underwent a modified Broström procedure for CAI were recruited in this prospective randomized controlled trial. Fifty-minute sessions of hospital-based rehabilitation were performed three times weekly for 12 weeks in the intervention group. Education-based rehabilitation was conducted at home in the control group. The outcomes were evaluated at baseline (T0), 12 weeks (T1), and 16 weeks (T2). The primary outcome was the foot and ankle outcome score (FAOS). Ankle motor strength and spatiotemporal gait metrics were assessed as secondary outcomes. There were significant time and group interaction effects on the pain, symptoms, activities of daily living, sports activities, and quality of life (QOL) domains of the FAOS (P < 0.05, all). The patients in the intervention group showed larger improvements in all domains of the FAOS than did the control group at both T1 and T2 (P < 0.05, all). The time and group interaction effects on invertor and evertor strength were also significant (P = 0.047 and P = 0.044). Invertor and evertor strength improved significantly more in the intervention group than in the control group at T1 and T2 (P < 0.05, all). The preferred walking velocity, cadence, step length on the affected side, and double stance phase duration tended to improve over time. Postoperative hospital-based rehabilitation helped improve CAI pain, symptoms, independence in activities of daily living, sports activity levels, and QOL more effectively than did conventional rehabilitation at home.

Ectopic expression of CNN2 of colon cancer promotes cell migration.

BACKGROUND: Calponin is an actin filament-associated regulatory protein originally identified in smooth muscle cells. Three homologous have been identified in vertebrate species, but little functional characterization of potential activities in cancer has been performed. In this study, we determined the levels of CNN2 in colon cancer cell lines and determined the effects of this protein by increasing expression. METHODS: We used IHC and RT-PCR to measure CNN2 expression in colon cancer tissues and normal tissues and found increased expression levels in cancer tissues. We used viral vectors to decrease the level of CNN2 in the SW480 colon cancer cell line and found that silencing of CNN2 inhibited cell invasion. We detected potential protein interactions in signal pathways by western bolt analysis. To confirm the effect of CNN2 on cell invasion, we increased CNN2 expression in the SW620 cell line and observed increased invasion increased expression levels of associated proteins. RESULTS: High-expression levels of CNN2 were detected in cancer tissues. Silencing CNN2 inhibited cell invasion, down-regulated N-cadherin (N-CA) and C-myc proteins, and up-regulated E-cadherin (E-CA), suggesting that CNN2 promotes colon cancer cell invasion. Increasing CNN2 levels in the SW620 cell line showed the opposite results. CONCLUSIONS: CNN2 may act to promote colon cancer.

Small Current but Highly Productive Synthesis of 1,3-Propanediol from Glycerol by an Electrode-Driven Metabolic Shift in Klebsiella pneumoniae L17.

Electrofermentation actively regulates the bacterial redox state, which is essential for bioconversion and has been highlighted as an effective method for further improvements of the productivity of either reduced or oxidized platform chemicals. 1,3-Propanediol (1,3-PDO) is an industrial value-added chemical that can be produced from glycerol fermentation. The bioconversion of 1,3-PDO from glycerol requires additional reducing energy under anoxic conditions. The cathode-based conversion of glycerol to 1,3-PDO with various electron shuttles (2-hydroxy-1,4-naphthoquinone, neutral red, and hydroquinone) using Klebsiella pneumoniae L17 was investigated. The externally poised potential of -0.9 V vs. Ag/AgCl to the cathode increased 1,3-PDO (35.5±3.1 mm) production if 100 µm neutral red was used compared with non-bioelectrochemical system fermentation (23.7±2.4 mm). Stoichiometric metabolic flux and transcriptional analysis indicated a shift in the carbon flux toward the glycerol reductive pathway. The homologous overexpression of glycerol dehydratase (DhaB) and 1,3-PDO oxidoreductase (DhaT) enzymes synergistically enhanced 1,3-PDO conversion (39.3±0.8 mm) under cathode-driven fermentation. Interestingly, a small current uptake (0.23 mmol of electrons) caused significant metabolic flux changes with a concomitant increase in 1,3-PDO production. This suggests that both an increase in 1,3-PDO production and regulation of the cellular metabolic pathway are feasible by electrode-driven control in cathodic electrofermentation.

PD­L1/PD­1 axis serves an important role in natural killer cell­induced cytotoxicity in osteosarcoma.

Osteosarcoma is a serious malignancy in pediatric patients, which comprises 2.4% of fatal cancer in children and achieves 20% of all primary bone cancers. In the present study, we employed three human osteosarcoma cell lines MG­63, HOS and U2OS for susceptibility to cytolytic activity of freshly isolated healthy donor NK cells. Cells were lysed by NK cells in a dose dependent manner. MG­63 cells exhibited less susceptibility to NK cells than HOS and U2OS cells at all cell ratios. The specific mechanism underlying the effects of NK cells on osteosarcoma cells was determined by antibody blockage experiments. The results revealed that granzyme B was the key factor in the NK cell­induced cytotoxicity of human osteosarcoma cells. To the best of our knowledge, the present study is the first to investigate the expression of PD­L1 in MG­63, HOS and U2OS cells. The relative expression of the PD­L1 gene and protein in MG­63 cell was greater than HOS and U2OS cells. The specific lysis of human osteosarcoma cells induced by NK cells was enhanced when PD­L1/PD­1 was blocked by the PD­L1 antibody. The present study proposed that the PD­L1/PD­1 axis serves an important role in NK cell­induced cytotoxicity in osteosarcoma via granzyme B secretion. Our findings may contribute to the development of precise treatments for osteosarcoma based on the expression profile of PD­L1 in patients with this disease.

Sodium cantharidinate suppresses human osteosarcoma MG­63 cell proliferation and induces cell cycle arrest by inhibition of PI3K/AKT activation.

The function and mechanism of sodium cantharidininate (SC) underlying its suppression of human osteosarcoma (OS) MG­63 cells were investigated for the first time in the present study. MG­63 cell proliferation was determined by WST­1 assay post SC treatment at 0, 12, 24, 48 and 72 h. The results showed that SC effectively inhibited MG­63 cell proliferation and induced cell cycle arrest at the G0/G1 phase in a dose­dependent manner. Western blotting revealed that SC induced MG­63 cell cycle arrest at the G0/G1 phase by means of inhibition of cyclin D1, CDK4 and CDK6 expression. The expression of MAPK and AKT were evaluated using western blotting and FACS experiments to determine whether such signaling pathways are involved in the antiproliferative action of SC on MG­63 cells. SC significantly inhibited the phosphorylation of AKT, but not mTOR, JNK or P38. PI3K/AKT stimulator, IGF­1, reversed the SC­induced cell cycle arrest in the MG­63 cells. Collectively, our data indicate that the phosphorylation of AKT was inhibited by SC, consequently decreasing the expression of cyclin D1, CDK4 and CDK6 and inducing MG­63 cell G0/G1 phase arrest. SC has potential as a treatment agent for human osteosarcoma.

Danhong Injection Alleviates Mechanical Allodynia via Inhibiting ERK1/2 Activation and Elevates BDNF Level in Sciatic Nerve in Diabetic Rat.

Danhong injection (DHI) has been widely used in China for cardiocerebrovascular diseases treatments. And in this study, we demonstrated the therapeutic effect of DHI on experimental diabetic neuropathy for the first time. Methods. Streptozotocin- (STZ-) induced SD rats were used. In experiment 1, 4-week treatment with DHI or saline started 4 weeks after STZ injection; mechanical allodynia was measured before and every 2 weeks after STZ injection. In experiment 2, chronic intrathecal infusion of U0126 was conducted during the 8th week of diabetes. Phosphorylated and total ERK1/2 in spinal cord were analyzed by western blot. BDNF level in sciatic nerve was evaluated by ELISA. Results. DHI treatment significantly alleviated mechanical allodynia at the end of the study and downregulated the expression of phosphorylated ERK1/2 in spinal cord. In addition, DHI treatment also elevated brain-derived neurotrophic factor (BDNF) level in sciatic nerve of DPN rat. In experiment 2, inhibition of ERK1/2 activation was confirmed to result in the alleviation of mechanical allodynia. Conclusions. We demonstrated that DHI was able to alleviate mechanical allodynia in diabetic neuropathy rat through inhibiting the activation of ERK1/2. The reduction of BDNF content in sciatic nerve was also partially reversed by DHI treatment.

Tanshinone IIA Improves Painful Diabetic Neuropathy by Suppressing the Expression and Activity of Voltage-Gated Sodium Channel in Rat Dorsal Root Ganglia.

Painful diabetic neuropathy (PDN) is one of the intractable complications of diabetes mellitus, which manifest as exaggerated pain perception. Previous studies showed that Tanshinone IIA (TIIA), one of the major bioactive extracts of Salvia miltiorrhiza Bunge, have obvious analgesic effect on different types of pain process, and the underlying analgesic mechanisms are not fully understood. The present study combined the behavioral, electrophysiological and biochemical methods to elucidate the analgesic mechanism of TIIA, using streptozotocin (STZ)-induced PDN rat models. Intraperitoneal injection (i.p.) of TIIA for 3 weeks in PDN rats significantly improved mechanical allodynia and thermal hyperalgesia. Patch clamp recordings showed that the excitability of dorsal root ganglion (DRG) nociceptive neuron was increased in diabetic state, and TIIA treatment effectively recovered the subnormality, which was achieved by preventing augments of both Tetrodotoxin-sensitive (TTX-resistant) and Tetrodotoxin-sensitive (TTX-S) sodium currents. Further, the protein expressions of voltage-gated sodium channels (VGSCs) α-subunits Nav1.3, Nav1.7 and Nav1.9 increased in DRG of diabetic rats and were normalized by TIIA application. In conclusion, this study provides evidence that the TIIA attenuated PDN by effecting VGSCs activities and expressions, indicating that the TIIA could be a promising agent for PDN treatment.

Targeting BCRP/ABCG2 by RNA interference enhances the chemotherapy sensitivity of human colon cancer side population cells.

Relapse and metastasis are frequent in colon cancer and may be linked to stem cell characteristics. This study isolated side population (SP) cells from a colon cancer cell line (Colo-320) and examined their self-renewal and differentiation abilities. Compared to non-SP (NSP) cells, SP colon cancer cells were more tumorigenic in vivo and exhibited more invasive characteristics and a greater ability to form colonies. Additionally, more cells were in G0/G1 phase and more highly expressed the multidrug resistance protein BCRP/ABCG2. We achieved enhanced chemotherapy sensitivity by transfecting SP cells with a hairpin-like, small interfering RNA (siRNA) eukaryotic expression plasmid targeting BCRP/ABCG2.

Adjuvant interferon for early or late recurrence of hepatocellular carcinoma and mortality from hepatocellular carcinoma following curative treatment: A meta-analysis with comparison of different types of hepatitis.

Adjuvant interferon (IFN) therapy following curative treatment for hepatocellular carcinoma (HCC) has been extensively investigated; however, the clinical benefits with different hepatitis backgrounds remain unclear. Medline, Embase, PubMed and the Cochrane Library databases were searched to identify randomized trials and cohort studies that enrolled HCC patients who received curative surgery or ablation therapy followed by IFN and control subjects; the studies were required to include data on early or late recurrence and mortality rates of HCC. Hepatitis B virus (HBV) associated with HCC (HBV-HCC) and hepatitis C virus (HCV) associated with HCC (HCV-HCC) were separately analyzed and recurrence, mortality and clinicopathological factors were compared. A total of 14 studies (9 randomized trials and 5 cohort studies, including 1,385 patients in total) were eligible for meta-analysis. IFN was found to decrease mortality and early recurrence rates, but exerted no effect on late recurrence rate. The effect of IFN differed between HBV-HCC and HCV-HCC cases. In HCV-HCC, IFN significantly reduced mortality as well as recurrence rates. However, in HBV-HCC patients, IFN reduced mortality rather than recurrence rates, although it also reduced the recurrence rate in certain subgroups. In conclusion, the effect of adjuvant IFN on postoperative recurrence differed between HBV-HCC and HCV-HCC cases; therefore, different strategies with adjuvant IFN should be used to treat HCC with different hepatitis backgrounds.