Thermally Activated Delayed Fluorescence with Nanosecond Emission Lifetimes and Minor Concentration Quenching: Achieving High-Performance Nondoped and Doped Blue OLEDs.

Simultaneously achieving a high photoluminescence quantum yield (PLQY), ultrashort exciton lifetime, and suppressed concentration quenching in thermally activated delayed fluorescence (TADF) materials is desirable yet challenging. Here, a novel acceptor-donor-acceptor type TADF emitter, namely, 2BO-sQA, wherein two oxygen-bridged triarylboron (BO) acceptors are arranged with cofacial alignment and positioned nearly orthogonal to the rigid dispirofluorene-quinolinoacridine (sQA) donor is reported. This molecular design enables the compound to achieve highly efficient (PLQYs up to 99%) and short-lived (nanosecond-scale) blue TADF with effectively suppressed concentration quenching in films. Consequently, the doped organic light-emitting diodes (OLEDs) base on 2BO-sQA achieve exceptional electroluminescence performance across a broad range of doping concentrations, maintaining maximum external quantum efficiencies (EQEs) at over 30% for doping concentrations ranging from 10 to 70 wt%. Remarkably, the nondoped blue OLED achieves a record-high maximum EQE of 26.6% with a small efficiency roll-off of 14.0% at 1000 candelas per square meter. By using 2BO-sQA as the sensitizer for the multiresonance TADF emitter ν-DABNA, TADF-sensitized fluorescence OLEDs achieve high-efficiency deep-blue emission. These results demonstrate the feasibility of this molecular design in developing TADF emitters with high efficiency, ultrashort exciton lifetime, and minimal concentration quenching.

Periampullary cancer and neurological interactions: current understanding and future research directions.

Periampullary cancer is a malignant tumor occurring around the ampullary region of the liver and pancreas, encompassing a variety of tissue types and sharing numerous biological characteristics, including interactions with the nervous system. The nervous system plays a crucial role in regulating organ development, maintaining physiological equilibrium, and ensuring life process plasticity, a role that is equally pivotal in oncology. Investigations into nerve-tumor interactions have unveiled their key part in controlling cancer progression, inhibiting anti-tumor immune responses, facilitating invasion and metastasis, and triggering neuropathic pain. Despite many mechanisms by which nerve fibers contribute to cancer advancement still being incompletely understood, the growing emphasis on the significance of nerves within the tumor microenvironment in recent years has set the stage for the development of groundbreaking therapies. This includes combining current neuroactive medications with established therapeutic protocols. This review centers on the mechanisms of Periampullary cancer's interactions with nerves, the influence of various types of nerve innervation on cancer evolution, and outlines the horizons for ongoing and forthcoming research.

Enhancing Reverse Intersystem Crossing in Triptycene-TADF Emitters: Theoretical Insights into Reorganization Energy and Heavy Atom Effects.

Thermally activated delayed fluorescence (TADF) emitters based on the triptycene skeleton demonstrate exceptional performance, superior stability, and low efficiency roll-off. Understanding the interplay between the luminescent properties of triptycene-TADF molecules and their assembly environments, along with their excited-state characteristics, necessitates a comprehensive theoretical exploration. Herein, we predict the photophysical properties of triptycene-TADF molecules in a thin film environment using the quantum mechanics/molecular mechanics method and quantify their substantial dependency on the heavy atom effects and reorganization energies using the Marcus-Levich theory. Our calculated photophysical properties for two recently reported molecules closely align with experimental values. We design three novel triptycene-TADF molecules by incorporating chalcogen elements (O, S, and Se) to modify the acceptor units. These newly designed molecules exhibit reduced reorganization energies and enhanced reverse intersystem crossing (RISC) rates. The heavy atom effect amplifies spin-orbit coupling, thereby facilitating the RISC process, particularly at a remarkably high rate of ∼109 s-1.

Evaluation of Multiple Liver Cancer Scoring Systems.

Liver cancer is one of the most common malignant tumors in the world, and its incidence and mortality are increasing year by year. The prognosis of liver cancer depends on the stage of liver cancer, the treatment method, the liver function, and individual differences. The prognosis of liver cancer mainly worsens with the progression of the stage. The prediction and staging system of liver cancer prognosis plays a very important role in the outcome of liver cancer prognosis, providing some guidance for clinical practice and bringing benefits for patients. This article reports on the prediction models and staging systems that have been applied in the field of liver cancer in the past 5 years, objectively analyzes the advantages and disadvantages, applicable population of each model and staging system, and searches for other patient and clinical characteristics that need to be considered for successfully establishing a prediction model, aiming to improve the specificity, sensitivity, and accuracy of liver cancer prediction and increase the overall survival rate of liver cancer.

Efficient Tin-Based Perovskite Solar Cells Enabled by Precisely Synthesized Single-Isomer Fullerene Bisadducts with Regulated Molecular Packing.

Designing and synthesizing fullerene bisadducts with a higher-lying conduction band minimum is promising to further improve the device performance of tin-based perovskite solar cells (TPSCs). However, the commonly obtained fullerene bisadduct products are isomeric mixtures and require complicated separation. Moreover, the isomeric mixtures are prone to resulting in energy alignment disorders, interfacial charge loss, and limited device performance improvement. Herein, we synthesized single-isomer C60- and C70-based diethylmalonate functionalized bisadducts (C60BB and C70BB) by utilizing the steric-hindrance-assisted strategy and determined all molecular structures involved by single crystal diffraction. Meanwhile, we found that the different solvents used for processing the fullerene bisadducts can effectively regulate the molecular packing in their films. The dense and amorphous fullerene bisadduct films prepared by using anisole exhibited the highest electron mobility. Finally, C60BB- and C70BB-based TPSCs showed impressive efficiencies up to 14.51 and 14.28%, respectively. These devices also exhibited excellent long-term stability. This work highlights the importance of developing strategies to synthesize single-isomer fullerene bisadducts and regulate their molecular packing to improve TPSCs' performance.

Brucella infection-induced hemophagocytic syndrome with subsequent development of the probable vanishing bile duct syndrome: A case report and literature review.

Vanishing bile duct syndrome is a rare clinical manifestation, and many clinicians tend to classify vanishing bile duct syndrome as a surgical disease and perform emergency surgery, leading to poor prognosis for patients. In this report, we present a case of a patient initially diagnosed with probable vanishing bile duct syndrome. However, through a meticulous step-by-step investigation, we ultimately determined that the patient was suffering from Brucella infection-induced hemophagocytic syndrome, which contributed to the development of the probable vanishing bile duct syndrome. Once a definitive diagnosis was established, the patient underwent treatment following anti-Brucella and Hemophagocytic lymphohistiocytosis-2004 protocols, leading to an improvement in the patient's condition. We conducted a literature review on brucellosis, and it demonstrated the lack of specificity in diagnosing Brucella infections and the diverse range of clinical manifestations. Failure to arrive at a definitive diagnosis may result in clinical misdiagnosis and delayed treatment, thereby leading to grave consequences.

Physical activity, sedentary behavior and pancreatitis risk: Mendelian randomization study.

BACKGROUND: Although observational studies have shown that physical activity is a protective factor for acute pancreatitis, the causal associations between PA/ sedentary behavior and acute pancreatitis (AP) and chronic pancreatitis (CP) remain unclear. METHODS: We used Mendelian randomization as a strategy to assess the causalities between exposures and outcomes by simulating randomized experiments with genetic variation. The collected genetic variants data of physical activity were from UK Biobank, the data on sedentary behavior were also from UK Biobank, and both of them could be found in the GWAS catalog, and the data on AP and CP were from FinnGen. There were three physical activity related activity patterns (moderate to vigorous physical activity [MVPA], accelerometer-based physical activity with average acceleration, [AccAve] and accelerometer-based physical activity with accelerations >425 milli-gravities, [Acc425]) and three sedentary behavior-related lifestyle patterns (Leisure screen time [LST], Sedentary commuting, Sedentary behavior at work). We used inverse variance weighted (IVW), weighted median and MR-Egger for the analysis of Mendelian randomization, followed by sensitivity tests with the Cochran Q test, MR-Egger intercepts analysis and MR-PRESSO. RESULTS: A causal relationship was found between LST and acute pancreatitis based on IVW analysis (odds ratios [OR] = 1.38, corresponding 95% confidence intervals [CI] = 1.16-1.64, p = 0.0002) and there were no causal relationships between physical activity/sedentary behavior and chronic pancreatitis. Sensitivity analysis showed no pleiotropy and heterogeneity of the results. CONCLUSIONS: Results show that reducing LST contributes to the prevention of acute pancreatitis, thereby reducing the health burden associated with it.

UXT at the crossroads of cell death, immunity and neurodegenerative diseases.

The ubiquitous expressed transcript (UXT), a member of the prefoldin-like protein family, modulates regulated cell death (RCD) such as apoptosis and autophagy-mediated cell death through nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), P53, P62, and methylation, and is involved in the regulation of cell metabolism, thereby affecting tumor progression. UXT also maintains immune homeostasis and reduces proteotoxicity in neuro-degenerative diseases through selective autophagy and molecular chaperones. Herein, we review and further elucidate the mechanisms by which UXT affects the regulation of cell death, maintenance of immune homeostasis, and neurodegenerative diseases and discuss the possible UXT involvement in the regulation of ferroptosis and immunogenic cell death, and targeting it to improve cancer treatment outcomes by regulating cell death and immune surveillance.

Optoelectronic performance of perovskite Cs2KMI6 (M = Ga, In) based on high-throughput screening and first-principles calculations.

Developing novel lead-free perovskite materials with suitable bandgaps and superior thermal stability is crucial to boost their applications in next-generation photovoltaic technologies. High throughput screening combined with the first principles method can accurately and effectively screen out promising perovskites. Herein, we select two lead-free all-inorganic halide double perovskite materials Cs2KMI6 (M = Ga, In) from 1026 compounds with the criteria including appropriate structure factors, positive decomposition energies, and suitable direct bandgaps. We investigated the thermal and mechanical stability, geometric and electronic structures, photoelectric properties, and defect formation energies for both perovskites Cs2KMI6 (M = Ga, In). They can exhibit excellent structural formability and stability through the analysis of structure factors, elastic constants, and stable chemical potential regions. In addition, we investigate the defect effects of Cs2KMI6 (M = Ga, In) on the photovoltaic performance by evaluating the defect formation energies and transition energy levels. Based on the HSE06 functional, we calculated the energy band structures of these two compounds and demonstrate the direct bandgaps of 1.69 eV (HSE06) and 2.16 eV (HSE06) for Cs2KGaI6 and Cs2KInI6, respectively. Moreover, we predicted excellent spectroscopic limited maximum efficiencies (SLMEs) of these two perovskites with high light absorption coefficients (around 105 cm-1), for instance, the SLME of Cs2KGaI6 can reach as high as 28.39%.

Fk506 Inhibit Liver Regeneration in HOC Model Rat.

BACKGROUND: Studies have shown that lymphocytes support hepatic oval cell (HOC)-dependent liver regeneration and FK506（Tacrolimus） is known as an immunosuppressor. Therefore, we studied the role of FK506 in HOC activation and/or proliferation to guide the clinical use of FK506. METHODS: Thirty male Lewis rats were randomly divided into 4 groups: (A) intervene in activation (n = 8), (B) intervene in proliferation (n = 8), (C) control HOC model (n = 8), and (D) pure partial hepatectomy (PH) (n = 6). The HOC model was established by 2AAF(2-acetylaminofluorene)/PH in groups A to C. FK506 (at a dose of 1 mg/kg/d) was given subcutaneously in group A except on operation day, and not until day 8 post-operation (PO) in group B. Half of the animals were euthanized on days 10 and 14 PO, respectively. The remnant liver was weighed and stained by hematoxylin and eosin and immunohistochemical staining of proliferating cell nuclear antigen and epithelial cell adhesion molecule enabled HOC proliferation analysis. RESULTS: FK506 intervention exacerbated liver damage and hindered the recovery of the HOC model rat. Weight gain was severely retarded or even negative. Liver weight and the liver body weight ratio were lower than control group. HE and immunohistochemistry showed pooer proliferation of hepatocytes and fewer HOC numbers in group A. CONCLUSION: FK506 inhibited HOC activation by affecting T and NK cells, ultimately blocking liver regeneration. Poor liver regeneration after auxiliary liver transplantation might be associated with the inhibition of HOC activation and proliferation caused by FK506 treatment.

Efficacy and safety of early enteral and intravenous fluid resuscitation in severe acute pancreatitis: a systematic review and meta-analysis.

OBJECTIVE: To compare the efficacy and safety of enteral fluid resuscitation (via nasointestinal tube or colorectal tube) and intravenous fluid resuscitation (via intravenous route) in the early treatment of severe acute pancreatitis. METHODS: In this study, 8 electronic databases (PubMed, Web of Science, Embase, Cochrane Library, Scopus, China HowNet database, Wanfang database, and VIP database) were searched to collect clinical studies from inception to June 12, 2022. After the quality evaluation and data extraction of the included studies, the RevMan 5.3 software was used for analysis. RESULTS: A total of seven studies including 580 patients were studied in this meta-analysis, in which 291 cases were treated with enteral fluid resuscitation and 289 cases were treated with intravenous fluid resuscitation. Compared with the intravenous route group, the enteral route resuscitation group reduced the incidence of new organ failure (OR = 0.23, 95% CI: 0.12-0.43, P < 0.00001), the incidence of persistent organ failure (OR = 0.38, 95% CI: 0.22-0.64, P = 0.0003), the incidence of mechanical ventilation (OR = 0.15, 95% CI: 0.03-0.69, P = 0.01), the incidence of ICU care (OR = 0.49, 95% CI: 0.27-0.88, P = 0.02), and the incidence of pancreatic infection (OR = 0.38, 95% CI: 0.17-0.83, P = 0.02). There were no statistically significant differences in mortality (OR = 0.77, 95% CI: 0.35-1.66, P = 0.50), surgical intervention rate (OR = 0.47, 95% CI: 0.19-1.18, P = 0.11), and incidence of localized ascites (OR = 0.65, 95% CI: 0.25-1.73, P = 0.39). CONCLUSION: Early enteral fluid resuscitation is safe and effective for in severe pancreatitis. But this conclusion needs to be verified by more additional multi-centre randomized controlled trials with large samples.

Circ_0003998 upregulates ARK5 expression to elevate 5-Fluorouracil resistance in hepatocellular carcinoma through binding to miR-513a-5p.

Chemoresistance has limited clinical treatment of cancer patients. This study aimed to research the regulatory function of circ_0003998 in 5-Fluorouracil (5-FU) resistance. Circ_0003998, microRNA-513a-5p (miR-513a-5p) and AMPK-Related Protein Kinase 5 (ARK5) levels were assayed via the quantitative reverse transcription-PCR. Colony formation ability was assessed by colony formation assay. Flow cytometry was performed for cell cycle and cell apoptosis analysis. Caspase-3 activity was detected using a caspase-3 activity assay. Target analysis was conducted via RNA pull-down assay, a dual-luciferase reporter assay, and an RNA immunoprecipitation assay. In-vivo assay was performed by establishing a xenograft model in mice. Circ_0003998 was upregulated in 5-FU-resistant hepatocellular carcinoma (HCC) tissues and cells. Circ_0003998 downregulation repressed 5-FU resistance and cancer progression in 5-FU-resistant HCC cells. Circ_0003998 interacted with miR-513a-5p. Inhibition of miR-513a-5p reversed the regulation of sh-circ_0003998 in 5-FU resistance. ARK5 was a target of miR-513a-5p, and ARK5 was regulated by circ_0003998 via targeting miR-513a-5p. Circ_0003998 regulated 5-FU resistance partly by upregulating ARK5 expression. 5-FU sensitivity was enhanced after circ_0003998 level reduction in vivo. These findings unraveled that circ_0003998 elevated 5-FU resistance in HCC by sponging miR-513a-5p to upregulate the level of ARK5, indicating that circ_0003998 might be used as a target to improve 5-FU therapy for HCC.

The role of UXT in tumors and prospects for its application in hepatocellular carcinoma.

UXT is widely expressed in human and mouse tissues and aberrantly expressed in various tumor tissues. UXT may play a pro-cancer or tumor suppressor role in different tumor types and microenvironments with different mechanisms of action. Studies have shown that UXT can interact with related receptors to exert its functions and affect tumor proliferation and metastasis, leading to a poor prognosis when the biological functions of these tumors are changed. Interestingly, the signaling pathways and mechanism-related molecules that interact with UXT are closely related to the occurrence of hepatocellular carcinoma (HCC) during disease progression. This article reviews the research progress of UXT and prospects for its application in HCC, with the aim of providing possible scientific suggestions for the basic research, diagnosis and treatment of HCC.

Patients with hepatocellular carcinoma (HCC) have a poor overall prognosis. Surgical resection is the preferred treatment option for HCC; however, most patients are already in the middle and late stages of the disease at the time of diagnosis. Surgical resection cannot achieve a therapeutic effect, and targeted therapy has become a feasible alternative. In this review we summarize the expression and mechanisms of action of the protein UXT in a variety of tumors and discuss its potential for future development as a therapeutic target to further improve the targeted therapy of HCC.

Overexpressing PLOD Family Genes Predict Poor Prognosis in Pancreatic Cancer.

Background: Pancreatic cancer is a common malignant tumor. Multiple studies have shown that procollagen lysyl-hydroxylase (PLOD) family genes were closely related to tumor progression and metastasis in a variety of human cancers. This study aimed to explore the prognosis and biological role of PLOD family genes in pancreatic adenocarcinoma (PAAD). Methods: GEPIA, GEO, HPA, CCLE, Kaplan-Meier plotter, cBioPortal, LinkedOmics, DAVID6.8, STRING, and TIMER were employed to determine the prognostic values and biological function of PLOD family members in PAAD. Results: The mRNA and protein expression patterns of PLOD family members were noticeably up-regulated in PAAD compared with normal tissues. PLOD family gene expression was also up-regulated in pancreatic cancer cell lines. PLOD1 was correlated with histological and pathological grades of pancreatic cancer. PLOD2 was related to histological grade. The high expression of PLOD1-2 was correlated with the poor overall survival rate and relapse-free survival rate in patients with PAAD. Additionally, PLODs showed high sensitivity and specificity in distinguishing pancreatic cancer from normal tissues. Through the functional enrichment analysis of PLOD-related genes in PAAD, we found that PLODs were enriched in collagen fiber tissue structure, lysine degradation, and collagen biosynthesis. Pathway analysis confirmed that PLODs regulated the proliferation, migration, and metastasis of pancreatic cancer through the RalGEF-Ral signaling pathway. Furthermore, the level of expression of PLOD1-2 was positively correlated with the activity of tumor-infiltrating immune cells, including CD8+T cells, neutrophils, macrophages, and dendritic cells. The level of expression of PLOD3 was inversely correlated with the level of infiltration of CD8+T cells. PLOD1 and PLOD2 were highly expressed in pancreatic cancer tissues with TP53 and KRAS mutations, respectively. However, the level of expression of PLOD3 in SMAD4 wild-type pancreatic cancer was increased. Conclusion: The findings showed that individual PLOD genes or PLOD family genes could be potential prognostic biomarkers for PAAD.

Piezoelectric Hysteresis Modeling of Hybrid Driven Three-Dimensional Elliptical Vibration Aided Cutting System Based on an Improved Flower Pollination Algorithm.

Three-dimensional elliptical vibration assisted cutting technology has been widely used in the past few years. The piezoelectric stack drive structure is an important part of the three-dimensional elliptical vibration aided cutting system. Its piezoelectric hysteresis characteristics affects the final output of the elliptical trajectory. Aiming at this problem, a piezoelectric hysteresis modeling method based on a generalized Bouc-Wen model is presented in this paper. An improved flower pollination algorithm (IFPASO) was used to identify Bouc-Wen model parameters. Standard test result shows that IFPASO has better algorithm performance. The model identification effect experiment proved that the Bouc-Wen model obtained by IFPASO identification, the highest modeling accuracy of the three axial subsystems, can reach 98.86%. Therefore, the model can describe the piezoelectric hysteresis characteristics of the three axial subsystems of the 3D-EVC system effectively and has higher modeling accuracy and fitting accuracy.

MicroRNA-203-3p inhibits the proliferation, invasion and migration of pancreatic cancer cells by downregulating fibroblast growth factor 2.

Aberrant expression of fibroblast growth factor 2 (FGF2) is a major cause of poor prognosis in patients with pancreatic cancer. MicroRNA (miRNA/miR) miR-203-3p is a newly identified miRNA that can affect the biological behavior of tumors. The present study investigated the function of miR-203-3p on the regulation of FGF2 expression, and its role in pancreatic cancer cell proliferation, apoptosis, invasion and migration. Reverse transcription-quantitative PCR was used to determine the mRNA expression levels of miR-203-3p and FGF2 in vitro. Cell Counting Kit-8, Annexin V-APC/7-AAD double-staining Apoptosis Detection kit, wound healing and Transwell assays were used to determine the proliferation, apoptosis, migration and invasion of pancreatic cancer cells. The binding of miR-203-3p to FGF2 was assessed by a luciferase reporter assay. The results demonstrated that miR-203-3p expression was downregulated in pancreatic cancer cells. Gain- and loss-of-function experiments indicated that miR-203-3p inhibited the proliferation, migration and invasion, and promoted the apoptosis of pancreatic cancer cells in vitro. In addition, it was found that alteration of miR-203-3p abolished the promoting effects of FGF2 on pancreatic cancer cells. The present study demonstrated that FGF2 significantly promoted the proliferation, invasion and migration of pancreatic cancer cells. The mechanism involved the binding of miR-203-3p to the 3'-untranslated region of FGF2 mRNA, resulting in the downregulation of FGF2. In conclusion, miR-203-3p inhibited FGF2 expression, regulated the proliferation and inhibited the invasion and migration of pancreatic cancer cells.

Analysis of CNOT Family Gene Expression, Clinicopathological Features, and Prognosis Value in Hepatocellular Carcinoma.

The carbon catabolite repressor 4-negative on TATA (CCR4-NOT) complex, abbreviated CNOT, has deadenylation and 3'-5' exonuclease activity, mediates deadenylation in the degradation of RNA, initiates the exonuclease degradation pathway, and participates in tumor gene regulation. CNOT proteins comprise a family of global transcriptional regulators that are evolutionarily conserved in eukaryotic cells. Several subunit types of the CNOT complex have been discovered; however, little is known about the role of different subunits in tumorigenesis and development. We observed overexpression of CNOT1-11 in liver cancer and correlations with clinicopathological characteristics. The expression of some CNOTs subunits was associated with histological grades, lymph node metastasis, and tumor stages in patients with hepatocellular carcinoma (HCC). Our data suggested that some CNOTs can be used as predictors of poor prognosis in HCC patients. At the same time, we conducted an analysis of CNOTs mutations in HCC patients. Moreover, we selected CNOT6, CNOT10, and CNOT11 for protein interaction network analysis and Gene Ontology enrichment analysis to investigate their related biological processes and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Finally, the results of western blot and quantitative reverse transcription-PCR (qRT-PCR) experiments were consistent with the database findings. Results of this study suggest that CNOT6, CNOT10, and CNOT11, acting as regulators of transcription, may play an important role in the development of HCC and may serve as biological markers in the diagnosis and prognosis of HCC.

CNOT7 depletion reverses natural killer cell resistance by modulating the tumor immune microenvironment of hepatocellular carcinoma.

A major obstacle to effective cancer immunotherapy is the tumor immune microenvironment. Natural killer (NK) cell resistance has been suggested as a primary cause of poor prognosis in hepatocellular carcinoma (HCC), which seemingly correlates with CNOT7 overexpression. CNOT7, a cytoplasmic mRNA deadenylase that is highly expressed in HCC, may regulate cytokine transforming growth factor-ß1 (TGF-ß1) secretion by controlling nuclear factor-κB subunit p65 trafficking. CNOT7 depletion suppresses TGF-ß1 secretion in HCC and promotes interferon-γ (IFN-γ) secretion by NK cells, and we previously demonstrated that CNOT7 depletion reversed IFN-γ resistance in HCC cells. Therefore, we hypothesized that CNOT7 depletion might reverse NK cell resistance by influencing the tumor immune microenvironment of HCC. To test this hypothesis, we examined the correlation between CNOT7, STAT1, TGF-ß1 and IFN-γ expression with hepatitis B virus-related cirrhosis and HCC with hepatitis B virus-related cirrhosis. We found that modulation of CNOT7 expression alters TGF-ß1 secretion in HCC and IFN-γ secretion in NK cells. We also examined the effects of NK cells in HepG2 cells with CNOT7 knockdown, which showed that NK cell surface CD107a expression is up-regulated and caspase-3 expression is significantly enhanced in CNOT7-deficient HepG2 cells. Overall, our results show that knockdown of CNOT7 expression reverses NK cell resistance in HCC cells. Therefore, CNOT7 depletion has potential as a new adjuvant therapy in immunotherapy for HCC.

The HPA/SDC1 axis promotes invasion and metastasis of pancreatic cancer cells by activating EMT via FGF2 upregulation.

Pancreatic cancer is characterized by the absence of early specific clinical symptoms, accompanied with rapid metastasis and invasion. It is one of the most prevalent types of cancer and more importantly, one of the most common types of malignant cancer with the highest mortality rate of all cancer types. The heparanase (HPA)/syndecan-1 (SDC1) axis has been reported to promote tumor growth, invasion, metastasis and angiogenesis in a variety of cancer types; however, studies into the role and mechanism of the HPA/SDC1 axis in pancreatic cancer are limited. The present study aimed to investigate the biological function and clinical significance of the HPA/SDC1 axis in pancreatic cancer. The results demonstrated that HPA is elevated in pancreatic cancer tissues and cell lines, and that its high expression was associated with poor prognosis. HPA was revealed to mediate an increase in fibroblast growth factor 2 (FGF2) expression by upregulating the expression of SDC1. Conversely, silencing HPA mediated the suppression of FGF2 expression. Furthermore, upregulated FGF2 was observed to increase the expression of downstream Palladin proteins by activating the PI3K/Akt signaling pathway and also lead to the activation of epithelial-mesenchymal transition (EMT). Subsequently, EMT was found to promote the migration and invasion of pancreatic cancer cells. In summary, the HPA/SDC1 axis was revealed to serve an important role in the regulation of FGF2, and was found to promote the invasion and metastasis of pancreatic cancer cells. These findings indicated that the HPA/SDC1 axis may be used as an effective therapeutic target for pancreatic cancer.