Micromorphology reformation of regenerated cellulose nanofibers from corn (Zea Mays) stalk pith in urea solution with high-speed shear induced.

Nanocellulose is a kind of renewable natural polymer material with high specific surface area, high crystallinity, and strong mechanical properties. RC nanofibers (RCNFs) have attracted an increasing attention in various applications due to their high aspect ratio and good flexibility. Herein, a novel and facile strategy for RCNFs preparation with high-speed shear induced in urea solution through "bottom-up" approach was proposed in this work. Results indicated that the average diameter and yield of RCNF was approach to 136.67 nm and 53.3 %, respectively. Meanwhile, due to the regular orientation RC chains and arrangement micro-morphology, RCNFs exhibited high crystallinity, strong mechanical properties, stable thermal degradation performance, and excellent UV resistance. In this study, a novel regeneration process with high-speed shear induced was developed to produce RCNFs with excellent properties. This study paved a strategy for future low-energy production of nanofibers and high value-added conversion applications of agricultural waste.

SLC25A3 negatively regulates NLRP3 inflammasome activation by restricting the function of NLRP3.

The NACHT, leucine-rich repeat, and pyrin domains-containing protein 3 (collectively known as NLRP3) inflammasome activation plays a critical role in innate immune and pathogenic microorganism infections. However, excessive activation of NLRP3 inflammasome will lead to cellular inflammation and tissue damage, and naturally it must be precisely controlled in the host. Here, we discovered that solute carrier family 25 member 3 (SLC25A3), a mitochondrial phosphate carrier protein, plays an important role in negatively regulating NLRP3 inflammasome activation. We found that SLC25A3 could interact with NLRP3, overexpression of SLC25A3 and knockdown of SLC25A3 could regulate NLRP3 inflammasome activation, and the interaction of NLRP3 and SLC25A3 is significantly boosted in the mitochondria when the NLRP3 inflammasome is activated. Our detailed investigation demonstrated that the interaction between NLRP3 and SLC25A3 disrupted the interaction of NLRP3-NEK7, promoted ubiquitination of NLRP3, and negatively regulated NLRP3 inflammasome activation. Thus, these findings uncovered a new regulatory mechanism of NLRP3 inflammasome activation, which provides a new perspective for the therapy of NLRP3 inflammasome-associated inflammatory diseases.

KIAA1549 promotes the development and chemoresistance of colorectal cancer by upregulating ERCC2.

Colorectal cancer (CRC) is the third most commonly diagnosed cancer worldwide. Chemotherapy is the mainstay of treatment for patients with CRC in II-IV stages. Resistance to chemotherapy occurs commonly, which results in treatment failure. Therefore, the identification of novel functional biomarkers is essential for recognizing high-risk patients, predicting recurrence, and developing new therapeutic strategies. Herein, we assessed the roles of KIAA1549 in promoting tumor development and chemoresistance in colorectal cancer. As a result, we found that KIAA1549 expression is up-regulation in CRC. Public databases revealed a progressive up-regulation of KIAA1549 expression from adenomas to carcinomas. Functional characterization uncovered that KIAA1549 promotes tumor malignant phenotypes and boosts the chemoresistance of CRC cells in an ERCC2-dependent manner. Inhibition of KIAA1549 and ERCC2 effectively enhanced the sensitivity to chemotherapeutic drugs oxaliplatin and 5-fluorouracil. Our findings suggest that endogenous KIAA1549 might function as a tumor development-promoting role and trigger chemoresistance in colorectal cancer partly by upregulating DNA repair protein ERCC2. Hence, KIAA1549 could be an effective therapeutic target for CRC and inhibition of KIAA1549 combined with chemotherapy might be a potential therapeutic strategy in the future.

Vortex array generation based on quasi-Talbot effects.

A lens-less method for generating vortex arrays with tunable parameters is proposed based on quasi-Talbot effects. By illuminating a two-dimensional periodic sinusoidal grating with a vortex beam carrying a fourth-order cross-phase, the continuous vortex array structure can be generated in the Fresnel diffraction region. Due to the shaping effect of the fourth-order cross-phase on the vortex beam, by changing the constant parameter of the fourth-order cross-phase, it is possible to shape the generation of optical vortex arrays at different positions. This will somewhat broaden the flexibility of the lens-free optical vortex array in terms of generation position. In addition, the generation of polygonal optical vortex arrays is achieved by higher-order cross-phases of different orders. This technique has potential applications in various fields such as optical tweezers, multi-particle screening, microscopic manipulation, etc.

The phytoestrogenic potential of flavonoid glycosides from Selaginella moellendorffii via ERα-dependent signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Selaginella moellendorffii (SM) has been applied as an ethnic drug to treat conditions such as osteoporosis, idiopathic thrombocytopenic purpura, and chronic inflammation. It is known to be rich in flavonoids, including apigenin glycosides and unique elements of bioflavonoids. AIM OF THE STUDY: To investigate estrogen-like constituents of SM and the possible mechanism. MATERIALS AND METHODS: We identified the main components in liquid chromatography and liquid chromatography-mass spectrometry. The estrogenic effects were examined using a recombinant yeast screening assay, an E-screen cell proliferation assay, and an in vivo uterotrophic assay. RESULTS: Flavonoid glycosides extract, some flavonoid glycosides, and apigenin showed estrogen agonistic activity in the yeast screening assay. They also induced cell proliferation in estrogen receptor-positive (ER+) cells but not in estrogen receptor-negative (ER-) cells. Consistently, the protein expression of ERα, phosphorylation protein kinase B (p-AKT), phosphatidylinositol 3 kinase (PI3K), phosphorylation mammalian target of rapamycin (p-mTOR), phosphorylation 38,000-Da protein (p-P38), and phosphorylation extracellular-regulated kinase 1/2 (p-ERK1/2) elevated following treatment with flavonoid glycoside extract (P < 0.01 or P < 0.05). These effects could be blocked by ER antagonist or ERα antagonist but not be blocked by ERß antagonist. In vivo assay, flavonoid glycoside extract could significantly increase body weight, serum estradiol level, uterine wet weight, alter uterine morphology, and promote ERα protein expression (P < 0.01 or P < 0.05). CONCLUSIONS: ERα induction via mitogen-activated protein kinases (MAPK) and PI3K/Akt/mTOR pathways might be the possible mechanism underlying the phytoestrogen effect of SM, and the flavonoid glycosides might be the critical estrogenic constituents.

All-cellulose air filter composed with regenerated nanocellulose prepared through a facile method with shear-induced.

High-speed shear system is usually used for the dispersion improvement of slurry, nanomaterials preparation, and even two-dimensional materials production. However, there is barely study that focused on the regenerated cellulose (RC) which was coagulated with shear induced. In this work, a new type of all-cellulose air filter was fabricated through high-speed shear in aqueous regeneration system using parenchyma cellulose from corn stalk. The obtained RC were aggregated by ribbon-like fine cellulose and nanocellulose sheets. The study exhibited the micro-structure of RC displayed excellent unidirectional alignment and a relatively high crystallinity. All-cellulose air filter which was produced via RC presented excellent filtration efficiency (PM2.5 97.3 %, PM10.0 97.7 %) with slightly pressure drop (19 Pa). Therefore, this work provides a facile method to obtain a novel RC with nanocellulose particles used for air filtration, which gives an effective strategy application in the conversion of all-cellulose materials from agricultural waste.

The interplay of transcriptional coregulator NUPR1 with SREBP1 promotes hepatocellular carcinoma progression via upregulation of lipogenesis.

Nuclear protein 1 (NUPR1) is a transcriptional coregulator that has been implicated in the development of various cancer types. In addition, de novo fatty acid synthesis plays a pivotal role in hepatocellular carcinoma (HCC) development. However, little is currently known on the role of NUPR1 in hepatocellular carcinoma. In this study, bioinformatics analysis was conducted to analyze the expression level, prognosis value and enriched pathways of NUPR1 in Liver Hepatocellular Carcinoma (LIHC). We found that NUPR1 was significantly upregulated in human hepatocellular carcinoma cells compared with normal hepatocytes from LIHC patients in TCGA cohorts and our patients. Kaplan-Meier analysis and COX proportional hazard progression model showed that high expression of NUPR1 was correlated with a poor prognosis of LIHC patients. CCK-8, EdU and colony formation assays were performed to explore the effect of NUPR1 on the proliferation of HCC cells, then wound healing and transwell migration assays were performed to evaluate the effects of NUPR1 on cell migration. Furthermore, subcutaneous xenograft models were established to study tumor growth. Results showed that NUPR1 overexpression correlated with a highly proliferative and aggressive phenotype. In addition, NUPR1 knockdown significantly inhibited hepatocellular carcinoma cell proliferation and migration in vitro and hindered tumorigenesis in vivo. Mechanistically, endogenous NUPR1 could interact with sterol regulatory element binding protein 1 (SREBP1) and upregulated lipogenic gene expression of fatty acid synthase (FASN), resulting in the accumulation of lipid content. Moreover, pharmacological or genetic blockade of the NUPR1-SREBP1/FASN pathway enhanced anticancer activity in vitro and in vivo. Overall, we identified a novel function of NUPR1 in regulating hepatocellular carcinoma progression via modulation of SREBP1-mediated de novo lipogenesis. Targeting NUPR1-SREBP1/FASN pathway may be a therapeutic alternative for hepatocellular carcinoma.

Research on ACEI of Low-Molecular-Weight Peptides from Hirudo nipponia Whitman.

The renin-angiotensin system (RAS) is the primary pathway for regulating blood pressure in the body, and angiotensin-converting enzymes (ACEs) play a crucial role in it. Hirudo nipponia is an invertebrate that contains a variety of active peptides; however, there are no studies on the ACE inhibitory activity of hirudo. In the present study, our aim was to identify the active peptides in hirudo based on active peptide database analysis, unexpectedly filling the gap in hirudo ACE inhibitory activity research. Prep-HPLC was used to separate the part below 3 kD from hirudo. The peptide composition of the isolates was obtained based on Orbitrap LC-MS. The activity of each group of peptides was predicted by the database and the activity was determined by bioassay. Peptides with validation activity were screened through the database. In total, 337 peptides and 18 peptides matching the NCBI leech protein database were identified. All four fractions showed ACE inhibitory activity, and the IC50 was 0.8266, 0.2708, 0.4432, and 0.1764 mg/mL, respectively. Six screened peptides showed good affinity for ACE. This work reveals for the first time that low-molecular-weight peptides from H. nipponia have ACE inhibitory activity, which can provide a new explanation for leech treatment of hypertension.

TXN inhibitor impedes radioresistance of colorectal cancer cells with decreased ALDH1L2 expression via TXN/NF-κB signaling pathway.

BACKGROUND: Colorectal cancer (CRC) is prevalent worldwide and is often challenged by treatment failure and recurrence due to resistance to radiotherapy. Here, we aimed to identify the elusive underlying molecular mechanisms of radioresistance in CRC. METHODS: Weighted gene co-expression network analysis was used to identify potential radiation-related genes. Colony formation and comet assays and multi-target single-hit survival and xenograft animal models were used to validate the results obtained from the bioinformatic analysis. Immunohistochemistry was performed to examine the clinical characteristics of ALDH1L2. Co-immunoprecipitation, immunofluorescence and flow cytometry were used to understand the molecular mechanisms underlying radioresistance. RESULTS: Bioinformatic analysis, in vitro, and in vivo experiments revealed that ALDH1L2 is a radiation-related gene, and a decrease in its expression induces radioresistance in CRC cells by inhibiting ROS-mediated apoptosis. Patients with low ALDH1L2 expression exhibit resistance to radiotherapy. Mechanistically, ALDH1L2 interacts with thioredoxin (TXN) and regulates the downstream NF-κB signaling pathway. PX-12, the TXN inhibitor, overcomes radioresistance due to decreased ALDH1L2. CONCLUSIONS: Our results provide valuable insights into the potential role of ALDH1L2 in CRC radiotherapy. We propose that the simultaneous application of TXN inhibitors and radiotherapy would significantly ameliorate the clinical outcomes of patients with CRC having low ALDH1L2.

Antimicrobial cellulose hydrogels preparation with RIF loading from bamboo parenchyma cells: A green approach towards wound healing.

Wound healing is a challenged and complicated process due to the bacterial infections and frequent replacement in healing process. Hydrogels with properties of visibility and biocompatibility provided convenient and effective treatment during the wound healing process. Bamboo parenchyma cells have a great potential utilized on cellulosic materials fabrication for their high specific surface area and accessibility of chemical reagents. Herein, we present a simple and facile manufacture of transparent wound dressing from bamboo parenchymal cellulose via dissolution in DMAc/LiCl system. Rifampicin (RIF) was loaded on the hydrogel through immersion method. The result exhibited that the maximum drug loading efficiency of cellulose hydrogels was 82.13%. Hydrogel loaded RIF (HLR) showed that the inhibition zones against Gram-negative and Gram-positive bacteria were 19.11 mm and 36.93 mm, respectively. It was observed that the wound was healed more than 60% at 11th day in murine wound models. Meanwhile, RIF provided an exceptionally antibacterial property to hydrogels and promoted proliferation of epidermis cells in wound. As a result of observations, HLR demonstrating potential application in visual wound dressing materials for their excellent transparency, antibacterial effect, wound healing, and biocompatibility.

Integration of glucose and cardiolipin anabolism confers radiation resistance of HCC.

BACKGROUND AND AIMS: Poor response to ionizing radiation (IR) due to resistance remains a clinical challenge. Altered metabolism represents a defining characteristic of nearly all types of cancers. However, how radioresistance is linked to metabolic reprogramming remains elusive in hepatocellular carcinoma (HCC). APPROACH AND RESULTS: Baseline radiation responsiveness of different HCC cells were identified and cells with acquired radio-resistance were generated. By performing proteomics, metabolomics, metabolic flux, and other functional studies, we depicted a metabolic phenotype that mediates radiation resistance in HCC, whereby increased glucose flux leads to glucose addiction in radioresistant HCC cells and a corresponding increase in glycerophospholipids biosynthesis to enhance the levels of cardiolipin. Accumulation of cardiolipin dampens the effectiveness of IR by inhibiting cytochrome c release to initiate apoptosis. Mechanistically, mammalian target of rapamycin complex 1 (mTORC1) signaling-mediated translational control of hypoxia inducible factor-1α (HIF-1α) and sterol regulatory element-binding protein-1 (SREBP1) remodels such metabolic cascade. Targeting mTORC1 or glucose to cardiolipin synthesis, in combination with IR, strongly diminishes tumor burden. Finally, activation of glucose metabolism predicts poor response to radiotherapy in cancer patients. CONCLUSIONS: We demonstrate a link between radiation resistance and metabolic integration and suggest that metabolically dismantling the radioresistant features of tumors may provide potential combination approaches for radiotherapy in HCC.

Antitumor Effects of Evodiamine in Mice Model Experiments: A Systematic Review and Meta-Analysis.

BACKGROUND: Evodiamine (EVO), an alkaloid extracted from the traditional Chinese medicine Euodia rutaecarpa, plays an important role in the treatment of cancer. This study was performed to clarify the effects of evodiamine in mice tumor model studies. METHODS: Electronic databases and search engines involved China Knowledge Resource Integrated Database (CNKI), Wanfang Database, Chinese Scientific Journal Database (CSJD-VIP), China Biomedical Literature Database (CBM), PubMed, Embase, Web of Science, and ClinicalTrials.gov databases, which were searched for literature related to the antitumor effects of evodiamine in animal tumor models (all until 1 October 2021). The evodiamine effects on the tumor volume and tumor weight were compared between the treatment and control groups using the standardized mean difference (SMD). RESULTS: Evodiamine significantly inhibited tumor growth in mice, as was assessed with tumor volume [13 studies, n=267; 138 for EVO and 129 for control; standard mean difference (SMD)= -5.99; 95% (CI): -8.89 to -3.10; I2 = 97.69%, p ≤ 0.00], tumor weight [6 studies, n=89; 49 for EVO and 40 for control; standard mean difference (SMD)= -3.51; 95% (CI): -5.13 to -3.90; I2 = 83.02%, p ≤ 0.00]. CONCLUSION: EVO significantly suppresses tumor growth in mice models, which would be beneficial for clinical transformation. However, due to the small number of studies included in this meta-analysis, the experimental design and experimental method limitations should be considered when interpreting the results. Significant clinical and animal studies are still required to evaluate whether EVO can be used in the adjuvant treatment of clinical tumor patients.

SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation.

Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation. N protein facilitates maturation of proinflammatory cytokines and induces proinflammatory responses in cultured cells and mice. Mechanistically, N protein interacts directly with NLRP3 protein, promotes the binding of NLRP3 with ASC, and facilitates NLRP3 inflammasome assembly. More importantly, N protein aggravates lung injury, accelerates death in sepsis and acute inflammation mouse models, and promotes IL-1ß and IL-6 activation in mice. Notably, N-induced lung injury and cytokine production are blocked by MCC950 (a specific inhibitor of NLRP3) and Ac-YVAD-cmk (an inhibitor of caspase-1). Therefore, this study reveals a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3 inflammasome activation and induces excessive inflammatory responses.

Analysis of miRNA expression profile in lung tissues of an intermittent hypoxia rat model.

We screened key miRNAs in an intermittent hypoxia rat model and explored the biological roles of downstream target genes and related regulatory pathways. We analyzed the expression profile of miRNAs in the lung tissues of rats in the 5 % (IH1), 7.5 % (IH2), 10 % (IH3), 12.5 % (IH4) oxygen concentration and negative control (NC) groups and identified common miRNAs. Multiple differentially expressed miRNAs were detected, and intersection of their expression profiles yielded 10 common miRNAs with 929 target genes mainly distributed in the nucleus. Molecular functions pertained mainly to the activation of transcription factors, while biological processes focused on cell interaction and signal transduction. Among signaling pathways, the top 5 included the LKB1 signaling, nectin adhesion, and S1P pathways. 8 of 10 common miRNAs had excellent diagnostic value for detecting intermittent hypoxia. The miRNAs binds to the target gene might play a key role in the pathophysiological process of OSA through the LKB1/AMPK and S1P/Akt/eNOS signaling pathways.

DENV NS1 and MMP-9 cooperate to induce vascular leakage by altering endothelial cell adhesion and tight junction.

Dengue virus (DENV) is a mosquito-borne pathogen that causes a spectrum of diseases including life-threatening dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Vascular leakage is a common clinical crisis in DHF/DSS patients and highly associated with increased endothelial permeability. The presence of vascular leakage causes hypotension, circulatory failure, and disseminated intravascular coagulation as the disease progresses of DHF/DSS patients, which can lead to the death of patients. However, the mechanisms by which DENV infection caused the vascular leakage are not fully understood. This study reveals a distinct mechanism by which DENV induces endothelial permeability and vascular leakage in human endothelial cells and mice tissues. We initially show that DENV2 promotes the matrix metalloproteinase-9 (MMP-9) expression and secretion in DHF patients' sera, peripheral blood mononuclear cells (PBMCs), and macrophages. This study further reveals that DENV non-structural protein 1 (NS1) induces MMP-9 expression through activating the nuclear factor κB (NF-κB) signaling pathway. Additionally, NS1 facilitates the MMP-9 enzymatic activity, which alters the adhesion and tight junction and vascular leakage in human endothelial cells and mouse tissues. Moreover, NS1 recruits MMP-9 to interact with ß-catenin and Zona occludens protein-1/2 (ZO-1 and ZO-2) and to degrade the important adhesion and tight junction proteins, thereby inducing endothelial hyperpermeability and vascular leakage in human endothelial cells and mouse tissues. Thus, we reveal that DENV NS1 and MMP-9 cooperatively induce vascular leakage by impairing endothelial cell adhesion and tight junction, and suggest that MMP-9 may serve as a potential target for the treatment of hypovolemia in DSS/DHF patients.

Long-term copper exposure promotes apoptosis and autophagy by inducing oxidative stress in pig testis.

Copper (Cu) is a heavy metal which is being used widely in the industry and agriculture. However, the overuse of Cu makes it a common environmental pollutant. In order to investigate the testicular toxicity of Cu, the pigs were divided into three groups and were given Cu at 10 (control), 125, and 250 mg/kg body weight, respectively. The feeding period was 80 days. Serum hormone results showed that Cu exposure decreased the concentrations of follicular stimulating hormone (FSH) and luteinizing hormone (LH) and increased the concentration of thyroxine (T4). Meanwhile, Cu exposure upregulated the expression of Cu transporter mRNA (Slc31a1, ATP7A, and ATP7B) in the testis, leading to increase in testicular Cu and led to spermatogenesis disorder. The Cu exposure led to an increased expression of antioxidant-related mRNA (Gpx4, TRX, HO-1, SOD1, SOD2, SOD3, CAT), along with increase in the MDA concentration in the testis. In LG group, the ROS in the testis was significantly increased. Furthermore, the apoptotic-related mRNA (Caspase3, Caspase8, Caspase9, Bax, Cytc, Bak1, APAF1, p53) and protein (Active Caspase3) and the autophagy-related mRNA (Beclin1, ATG5, LC3, and LC3B) expression increased after Cu exposure. The mitochondrial membrane potential in the testicular tissue decreased, while the number of apoptotic cells increased, as a result of oxidative stress. Overall, our study indicated that the Cu exposure promotes testicular apoptosis and autophagy by mediating oxidative stress, which is considered as the key mechanism causing testicular degeneration as well as dysfunction.

A Purified Biflavonoid Extract From Selaginella moellendorffii Alleviates Gout Arthritis via NLRP3/ASC/Caspase-1 Axis Suppression.

Background: Activation of nucleotide oligomerization domain-like receptor protein 3 (NLRP3) inflammasome plays a crucial role in gout. Selaginella moellendorffii has been confirmed effective for the treatment of gout in hospital preparations. Flavonoids, such as amentoflavone (AM), are the main active components of this medicine. Purpose: We aimed to investigate the flavonoid extract (TF) and AM's effects on NLRP3 inflammasome in vitro and their preventive effects on gout in vivo. Methods: LC-MS method was employed to investigate the chemical profile of TF. The cellular inflammation model was established by lipopolysaccharide (LPS) or monosodium urate (MSU) stimulation. The cell membrane integrality and morphological characteristics were determined by using Lactate dehydrogenase (LDH) assay kits, propidium iodide (PI) stain, and scanning electron microscopy (SEM). The inflammatory cytokines and NLRP3 inflammasome activation were determined using enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (RT-PCR), immunofluorescence staining, and western blotting. The acute gout mouse model was induced by MSU injection into footpads, and then the paw edema, inflammatory mediators, and histological examination (HE) were analyzed. Results: The main constituents in TF are AM and robustaflavone. In the cellular inflammation model, TF down-regulated the levels of nitric oxide (NO), TNF-α, and LDH, suppressed NLRP3 inflammasome-derived interleukin-1ß (IL-1ß) secretion, decreased caspase-1 activation, repressed mature IL-1ß expression, inhibited ASC speck formation and NLRP3 protein expression. In an acute gout mouse model, oral administration of TF to mice effectively alleviated paw edema, reduced inflammatory features, and decreased the levels of IL-1ß in mouse foot tissue. Similarly, the characteristic constituent AM was also able to down-regulated the levels of NO, TNF-α, and LDH, down-regulate the mRNA expression of IL-1ß, TNF-α, caspase-1, and NLRP3. Besides, the foot thickness, lymphocyte infiltration, and IL-1ß level were also prevented by AM. Conclusion: The results indicated that TF and its main constituent AM alleviate gout arthritis via NLRP3/ASC/Caspase-1 axis suppression.

Factors influencing the short-term and long-term survival of hepatocellular carcinoma patients with portal vein tumor thrombosis who underwent chemoembolization.

BACKGROUND: The factors affecting the short-term and long-term prognosis of hepatocellular carcinoma (HCC) patients with portal vein tumor thrombosis (PVTT) receiving transarterial chemoembolization (TACE) are still unclear. AIM: To clarify the predictors correlated with the short-term and long-term survival of HCC patients with PVTT who underwent TACE. METHODS: The medical records of 181 HCC patients with PVTT who underwent TACE at the Second Affiliated Hospital of Chongqing Medical University from January 2015 to July 2019 were retrospectively analyzed. We explored the short-term and long-term prognostic factors by comparing the preoperative indicators of patients who died and survived within 3 mo and 12 mo after TACE. Multivariate analyses were conducted using logistic regression. The area under the receiver operating characteristic curve (area under curve) was used to evaluate the predictive ability of the factors related to the short-term and long-term prognosis. RESULTS: The median survival time was 4.8 mo (range: 2.5-8.85 mo). The 3 mo, 6 mo, and 12 mo survival rates were 68.5%, 38.7%, and 15.5%, respectively. In multivariable analysis, total bilirubin, sex, and aspartate aminotransferase (AST) were closely linked to short-term survival. When AST ≥ 87 U/L and total bilirubin ≥ 16.15 µmol/L, the 3-mo survival rate after TACE was reduced significantly (P < 0.05). AST had the best predictive ability, followed by total bilirubin, while sex had the worst predictive ability for short-term survival area under curve: 0.763 (AST) vs 0.707 (total bilirubin) vs 0.554 (sex)]. The long-term survival outcome was significantly better in patients with a single lesion than in those with ≥ three lesions (P = 0.009). Patients with massive block HCC had a worse long-term survival than patients with nodular and diffuse HCC (P = 0.001). CONCLUSION: AST, total bilirubin, and sex are independent factors associated with short-term survival. The number of tumors and the gross pathological type of tumor are related to the long-term outcome.