Molecular Engineering of Metal Complexes for Electrocatalytic Carbon Dioxide Reduction: From Adjustment of Intrinsic Activity to Molecular Immobilization.

The electrocatalytic CO2 reduction reaction (ECO2 RR) is one promising method for storing intermittent clean energy in chemical bonds and producing fuels. Among various kinds of catalysts for ECO2 RR, molecular metal complexes with well-defined structures are convenient for studies of their rational design, structure-reactivity relationships, and mechanisms. In this Review, we summarize the molecular engineering of several N-based metal complexes including Re/Mn bipyridine compounds and metal macrocycles, concluding with general modification strategies to devise novel molecular catalysts with high intrinsic activity. Through physical adsorption, covalent linking, and formation of a periodic backbone, these active molecules can be heterogenized into immobilized catalysts with more practical prospects. Finally, significant challenges and opportunities based on molecular catalysts are discussed.

Prolonging the Triplet State Lifetimes of Rhenium Complexes with Imidazole-Pyridine Framework for Efficient CO2 Photoreduction.

The photocatalytic reduction of CO2 into fuels offers the prospect for creating a new CO2 economy. Harnessing visible light-driven CO2 -to-CO reduction mediated by the long-lived triplet excited state of rhenium(I) tricarbonyl complexes is a challenging approach. We here develop a series of new mononuclear rhenium(I) tricarbonyl complexes (Re-1-Re-4) based on the imidazole-pyridine skeleton for photo-driven CO2 reduction. These catalysts are featured by combining pyridyl-imidazole with the aromatic ring and different pendant organic groups onto the N1 position of 1,3-imidazole unit, which display phosphorescence under Ar-saturated solution even at ambient conditions. By contrast, {Re[9-(pyren-1-yl)-10-(pyridin-2-yl)-9H-pyreno[4,5-d]imidazole)](CO)3 Cl} (Re-4) by introducing pyrene ring at the N1 position of pyrene-fused imidazole unit exhibits superior catalytic performance with a higher turnover number for CO (TONCO =124) and >99.9 % selectivity, primarily ascribed to the strong visible light-harvesting ability, long-lived triplet lifetimes (164.2 µs) and large reductive quenching constant. Moreover, the rhenium(I) tricarbonyl complexes derived from π-extended pyrene chromophore exhibit a long lifetime corresponding to its ligand-localized triplet state (3 IL) evidenced from spectroscopic investigations and DFT calculations.

Role of CARD9 in inflammatory signal pathway of peritoneal macrophages in severe acute pancreatitis.

Previous studies revealed that caspase recruitment domain protein 9 (CARD9) was involved in severe acute pancreatitis (SAP) inflammation and that interfering with its expression in vivo could inhibit inflammation. However, the specific mechanism is unknown. This study aimed to discover the related signal pathways of CARD9 in macrophages. SiRNA interference technology was used in vivo and in vitro to detect CARD9-related signal pathways in peritoneal macrophages. Furthermore, Toll-like receptor 4 (TLR4) and membrane-associated C-type lectin-1 (Dectin-1) pathways in macrophages were activated specially to looking for the upstream signal path of CARD9. Results showed up-regulation of CARD9 expression in peritoneal macrophages of SAP rats (P < .05). CARD9 siRNA alleviated inflammatory cytokines, and inhibited the phosphorylation of NF-κB and p38MAPK in peritoneal macrophages in vivo or in vitro. Meanwhile, CARD9 siRNA reduced the concentration of CARD9 and Bcl10 in peritoneal macrophages, and TLR4 and Dectin-1 took part in CARD9 signal pathways in macrophages. In conclusion, there is an inflammation signal pathway comprised of TLR4/Dectin-1-CARD9-NF-κB/p38MAPK activated in macrophages in SAP. Blockade of CARD9 expression in macrophages can effectively alleviate SAP inflammation.

CARD9 gene silencing with siRNA protects rats against severe acute pancreatitis: CARD9-dependent NF-κB and P38MAPKs pathway.

We previously reported the up-regulation of caspase recruitment domain 9 (CARD9) expressions in severe acute pancreatitis (SAP) patients, but little is known about its regulation. In this study, small interfering RNA (siRNA) was used to reduce the levels of CARD9 expression in sodium taurocholate-stimulated SAP rats. CARD9 was overexpressed in SAP rats, which correlated with the severity of pancreatitis. When compared to the untreated group, the cohort that received the siRNA treatment demonstrated a significant reduction in pancreatic injury, neutrophil infiltration, myeloperoxidase activity and pro-inflammatory cytokines. Furthermore, siRNAs showed that the reduction of CARD9 in SAP rats down-regulated the expression of NF-κBp65 and P38MAPK which are involved in the transcription and release of a wide variety of inflammatory cytokines. These findings provide evidence that CARD9 is up-regulated in SAP rats and acts as a potential therapeutic target for the treatment thereof. Blocking the activation of NF-κB and P38MAPK via siRNA-mediated gene knock-down of CARD9 appears to reduce the inflammatory response in pancreatic tissue.

The role of Card9 overexpression in peripheral blood mononuclear cells from patients with aseptic acute pancreatitis.

Activated mononuclear cells are an early event in the course of severe acute pancreatitis (SAP). To date, the molecular mechanism triggering peripheral blood mononuclear cells (PBMCs) is poorly understood. The aim of this paper was to determine the potential role of Card9 in SAP. We collected data from 72 subjects between January 2013 and June 2014. Subsequently, PBMCs were isolated on day 1, 3 and 5 of pancreatitis. Immunofluorescence staining, quantitative real-time PCR, Western blotting, immunoprecipitation and ELISA were used to determine the role of Card9 in SAP. Microbial culture showed that SAP patients at the early period did not develop any bacteria and fungi infection. Card9 expression in SAP patients was higher than that in mild acute pancreatitis and volunteer healthy controls, up to the peak on day 1. The monocyte-derived cytokines interleukin (IL)-17, IL-1ß, IL-6 and tumour necrosis factor-α mediated by the induction of Card9 markedly increased in SAP patients compared with the control group. Furthermore, the inducible formation of Card9-Bcl10 complex was found in PBMCs, which may be involved in nuclear factor kappa B (NF-κB) and p38 activation in SAP. Receiver operating characteristic curve indicated that Card9 levels had a high sensitivity of 87.5% and specificity of 67.7%, showing the close correlation with SAP patients. Card9 overexpression was firstly found in aseptic SAP, which may be played an important role in NF-κB and p38 activation in PBMCs. It also provided the new insights into therapeutic interventions by targeting monocytes activation in SAP patients.

Central role of neutrophil in the pathogenesis of severe acute pancreatitis.

Severe acute pancreatitis (SAP) is an acute abdominal disease with the strong systemic inflammatory response, and rapidly progresses from a local pancreatic damage into multiple organ dysfunction. For many decades, the contributions of neutrophils to the pathology of SAP were traditionally thought to be the chemokine and cytokine cascades that accompany inflammation. In this review, we focus mainly on those recently recognized aspects of neutrophils in SAP processes. First, emerging evidence suggests that therapeutic interventions targeting neutrophils significantly lower tissue damage and protect against the occurrence of pancreatitis. Second, trypsin activation promotes the initial neutrophils recruitment into local pancreas, and subsequently neutrophils infiltration in turn triggers trypsin production. Finally, neutrophils have the unique ability to release neutrophil extracellular traps even in the absence of pathogens.

Concentration effects of grape seed extracts in anti-oral cancer cells involving differential apoptosis, oxidative stress, and DNA damage.

BACKGROUND: Grape seeds extract (GSE) is a famous health food supplement for its antioxidant property. Different concentrations of GSE may have different impacts on cellular oxidative/reduction homeostasis. Antiproliferative effect of GSE has been reported in many cancers but rarely in oral cancer. METHODS: The aim of this study is to examine the antioral cancer effects of different concentrations of GSE in terms of cell viability, apoptosis, reactive oxygen species (ROS), mitochondrial function, and DNA damage. RESULTS: High concentrations (50-400 µg/ml) of GSE dose-responsively inhibited proliferation of oral cancer Ca9-22 cells but low concentrations (1-10 µg/ml) of GSE showed a mild effect in a MTS assay. For apoptosis analyses, subG1 population and annexin V intensity in high concentrations of GSE-treated Ca9-22 cells was increased but less so at low concentrations. ROS generation and mitochondrial depolarization increased dose-responsively at high concentrations but showed minor changes at low concentrations of GSE in Ca9-22 cells. Additionally, high concentrations of GSE dose-responsively induced more γH2AX-based DNA damage than low concentrations. CONCLUSIONS: Differential concentrations of GSE may have a differentially antiproliferative function against oral cancer cells via differential apoptosis, oxidative stress and DNA damage.

HindIII polymorphism in the lipoprotein lipase gene and hypertensive intracerebral hemorrhage in the Chinese Han population.

BACKGROUND: To investigate the relationship between the HindIII polymorphism and hypertensive intracerebral hemorrhage (HIH) and lipid metabolism. METHODS: A polymerase chain reaction-restriction fragment length polymorphism assay and the chain termination DNA sequencing method were used to determine the HindIII genotypes of 267 subjects, which included 120 cerebral hemorrhagic patients and 147 controls. The fasting levels of lipids and glucose in the plasma were used to measure the effect of genotype on HIH risk factors. RESULTS: The frequency of the T allele of the HindIII polymorphism in the HIH group was 90.8%. The frequency of the G allele was 9.2%. In the control group, the frequencies were 82.3% T and 17.7% G, which indicated that the proportion of the G allele in the HIH patient group was significantly lower than in the control group (P<.05). The frequency of GG+GT genotypes in HIH patients (P<.05) and the plasma triglyceride (TG) levels in these patients (P<.05) were also lower than in the control group. The levels of plasma TG, low-density lipoprotein cholesterol, glucose, systolic blood pressure, and diastolic blood pressure in the HIH group were higher than in the controls (P<.05). After controlling for risk factors related to HIH, the HindIII G allele was negatively correlated with the incidence of HIH (odds ratio=.417, 95% confidence interval: .193-.901). CONCLUSIONS: The HindIII G allele may be a protective factor against the development of HIH among the Han Chinese population.

Molecular Engineering of Copper Phthalocyanine for CO2 Electroreduction to Methane.

Efficient electrochemical CO2 reduction reaction (ECO2RR) to multi-electron reductive products remains a great challenge. Herein, molecular engineering of copper phthalocyanines (CuPc) was explored by modifying electron-withdrawing groups (EWGs) (cyano, sulfonate anion) and electron-donating groups (EDGs) (methoxy, amino) to CuPc, then supporting onto carbon paper or carbon cloth by means of droplet coating, loading with carbon nanotubes and coating in polypyrrole (PPy). The results showed that the PPy-coated CuPc effectively catalysed ECO2RR to CH4. Interestingly, experimental results and DFT calculations indicated EWGs markedly improved the selectivity of methane for the reason that the introduction of EWGs reduces electron density of catalytic active center, resulting in a positive move to initial reduction potential. Otherwise, the modification of EDGs significantly reduces the selectivity towards methane. This electronic effect and heterogenization of CuPc are facile and effective molecular engineering, benefitting the preparation of electrocatalysts for further reduction of CO2.

The power and the promise of synthetic lethality for clinical application in cancer treatment.

Synthetic lethality is a phenomenon wherein the simultaneous deficiency of two or more genes results in cell death, while the deficiency of any individual gene does not lead to cell death. In recent years, synthetic lethality has emerged as a significant topic in the field of targeted cancer therapy, with certain drugs based on this concept exhibiting promising outcomes in clinical trials. Nevertheless, the presence of tumor heterogeneity and the intricate DNA repair mechanisms pose challenges to the effective implementation of synthetic lethality. This review aims to explore the concepts, development, and ethical quandaries surrounding synthetic lethality. Additionally, it will provide an in-depth analysis of the clinical application and underlying mechanism of synthetic lethality.

Effects of peroxisome proliferator-activated receptor-γ activation on apoptosis in rats with acute pancreatitis.

PURPOSE: To investigate the effects and mechanisms of peroxisome proliferator-activated receptor-γ (PPAR-γ) activation on the induction of apoptosis in rats with acute pancreatitis. METHODS: Severe acute pancreatitis (SAP) and mild acute pancreatitis (MAP) were induced and pre-treated with pioglitazone, which is a ligand of PPAR-γ. The expression of inflammatory factors (TNF-α and IL6) of the pancreas was detected by ELISA. The apoptosis in pancreas were detected by TUNEL assay and the activity of caspase 3 was determined. Phosphorylation of p65 in pancreas of SAP or MAP was determined by western-blot. RESULTS: Expression levels of PPAR-γ proteins were elevated in the pancreases of SAP or MAP rats pre-injected with pioglitazone intraperitoneally. Downregulation of the expression TNF-α and IL6 and relief of pathological changes in the pancreas suggested that pioglitazone had protective effects on acute panceatitis. In pioglitazone pre-treated groups, a TUNEL assay indicated a high level of apoptosis in SAP but little apoptosis in MAP, showing pioglitazone could promote taurocholate-induced apoptosis but inhibit ceruleininduced apoptosis in pancraeatic aniniar cells. Furthermore, caspase 3 activity was high in SAP but low in MAP, implying that the apoptotic mechanism in pancreatic acinar cells of AP rats was correlated with caspase 3 activity. Phosphorylation of p65 was reduced in SAP or MAP group pretreated with pioglitazone, indicating that pioglitazone reduced the inflammation reaction by inhibiting the activation of the NF-κB. CONCLUSIONS: These results indicated that activation of PPAR-γ induced apoptosis in pancreatic acinar cells of SAP rats but inhibited apoptosis in pancraeatic acinar cells of MAP rats, which demonstrated that PPAR-γ may be an efficiently therapeutic target in pancreatic inflammation.

Mesenchymal stem cells regulate M1 polarization of peritoneal macrophages through the CARD9-NF-κB signaling pathway in severe acute pancreatitis.

BACKGROUND: Macrophages release large numbers of proinflammatory cytokines that trigger inflammatory cascade reactions, which promote the rapid development of severe acute pancreatitis (SAP) from local to systemic inflammation. The ability of mesenchymal stem cells (MSCs) to suppress inflammation is related to inhibition of M1 polarization of macrophages. Our previous studies revealed that caspase recruitment domain protein 9 (CARD9) was involved in SAP inflammation and activation of the CARD9-NF-κB signaling pathway plays an important proinflammatory role in SAP. At present, there is no effective treatment to control the inflammatory response in SAP. Therefore, the aim of the present study was to determine whether MSCs regulate the polarization of macrophages through the CARD9-NF-κB signaling pathway in SAP. METHODS: Short hairpin RNA interference technology and coculture in vitro were used to assess the activation status of the CARD9-NF-κB signal pathway in macrophages. Furthermore, flow cytometry was used to determine the polarization state of macrophages. RESULTS: The results showed MSCs inhibited CARD9 expression in vivo and in vitro (P < .05), alleviated inflammation induced by proinflammatory cytokines, and inhibited the phosphorylation of NF-κB in macrophages both in vivo and in vitro. Meanwhile, MSCs downregulated the CARD9-NF-κB signal pathway and inhibited M1 polarization of macrophages. CONCLUSION: In conclusion, MSCs regulate M1 polarization of peritoneal macrophages through the CARD9-NF-κB signaling pathway in SAP and transplantation of MSCs presents an effective treatment option for SAP.

Optimal threshold of urinary albumin-to-creatinine ratio (UACR) for predicting long-term cardiovascular and noncardiovascular mortality.

PURPOSE: Traditional cutoff values of urinary albumin-to-creatinine ratio (UACR) for predicting mortality have recently been challenged. In this study, we investigated the optimal threshold of UACR for predicting long-term cardiovascular and non-cardiovascular mortality in the general population. METHODS: Data for 25,302 adults were extracted from the National Health and Nutrition Examination Survey (2005-2014). Receiver operating characteristic (ROC) curve analysis was performed to assess the predictive value of UACR for cardiovascular and non-cardiovascular mortality. A Cox regression model was established to examine the association between UACR and cardiovascular and non-cardiovascular mortality. X-tile was used to estimate the optimal cutoff of UACR. RESULTS: The UACR had acceptable predictive value for both cardiovascular (AUC (95% CI) for 1-year, 3-year and 5-year mortality, respectively: 0.769 (0.711-0.828), 0.764 (0.722-0.805) and 0.763 (0.730-0.795)) and non-cardiovascular (AUC (95% CI) for 1-year, 3-year and 5-year mortality, respectively: 0.772 (0.681-0.764), 0.708 (0.686-0.731) and 0.708 (0.690-0.725)) mortality. The optimal cutoff values were 16 and 30 mg/g for predicting long-term cardiovascular and non-cardiovascular mortality, respectively. Both cutoffs of UACR had acceptable specificity (0.785-0.891) in predicting long-term mortality, while the new proposed cutoff (16 mg/g) had higher sensitivity. The adjusted hazard ratios of cardiovascular and non-cardiovascular mortality for the high-risk group were 2.50 (95% CI 1.96-3.18, P < 0.001) and 1.92 (95% CI 1.70-2.17, P < 0.001), respectively. CONCLUSIONS: Compared to the traditional cutoff value (30 mg/g), a UACR cutoff of 16 mg/g may be more sensitive for identifying patients at high risk for cardiovascular mortality in the general population.

Myofascial acupuncture versus routine acupuncture for mechanical neck pain: a protocol for a multicentre randomised controlled trial.

INTRODUCTION: Mechanical neck pain (MNP) is defined as pain in the area of the neck and/or neck-shoulder provoked by body mechanics and which adversely affects physical, psychological and social function. The treatments for MNP are limited. Previous studies and clinical experience have indicated that myofascial acupuncture might be a better treatment option for MNP, but the efficacy is controversial. Therefore, our aim is to compare the efficacy of myofascial acupuncture and routine acupuncture for MNP. METHODS AND ANALYSIS: The study is a multicentre, prospective randomised clinical trial. Patients will be recruited from four tertiary hospitals in China. A total of 438 participants with MNP will be randomly assigned into two groups, namely the 'Sancai-Tianbu' myofascial acupuncture group and the routine acupuncture group, at a ratio of 1:1. Each group will receive the acupuncture treatment twice a week for 21 days, totalling six sessions. The primary outcome will be the Visual Analogue Scale score. The secondary outcomes will be the Neck Disability Index, the cervical range of motion and the MOS 36-Item Short Form Health Survey. The assessments will be performed at baseline (immediately after allocation), pretreatment (5 min before every treatment), post-treatment (within 10 min after every treatment), postcourse (within 1 day after the course), and at 1, 3 and 6 months after the course. All patients will be included in the intent-to-treat analysis. Repeated-measure analysis of covariance will be used to determine the effects of the intervention on the outcome measures. ETHICS AND DISSEMINATION: Ethics approval was obtained from China Aerospace Science & Industry Corporation 731 Hospital, with permission number 2022-0204-01. Written informed consent will be obtained from the enrolled patients. Trial results will be disseminated in peer-reviewed publications. TRIAL REGISTRATION NUMBER: ChiCTR2200061453.

Corrigendum: Prevalence and Prognostic Significance of Malnutrition in Hypertensive Patients in a Community Setting.

[This corrects the article DOI: 10.3389/fnut.2022.822376.].

Highly Robust Rhenium(I) Bipyridyl Complexes Containing Dipyrromethene-BF2 Chromophores for Visible Light-Driven CO2 Reduction.

New rhenium bipyridyl complexes with dipyrromethene-BF2 chromophores (A-ReBDP-CZ, A-ReBDP2 , ReBDP-CZ, and ReBDP2 ) were developed for highly efficient photocatalytic carbon dioxide (CO2 ) reduction to carbon monoxide (CO). These catalysts consisted of two moderate electron-deficient groups (dipyrromethene-BF2 , BDP) as the visible-light-harvesting antenna as well as both electron donor (N-phenylcarbazole, CZ) and acceptor (BDP) on Re bipyridyl framework. Among ReBDP-CZ and ReBDP2 complexes, the ReBDP2 incorporating two electron-deficient BDP chromophores had a longer-lived photoexcited state (182.4 µs) and a twofold enhanced molar absorption coefficient (ϵ=157000 m-1 cm-1 ) compared with ReBDP-CZ. Thus, ReBDP2 achieved the superior photocatalytic reactivity and stability with a CO turnover number (TONCO ) value as high as 1323 and quantum yield (ΦCO ) up to 55 %, which was the most excellent photocatalysis efficiency among the single-active-site Re catalysts without additional photosensitizer. Furthermore, the acetylene-bridged linker was detrimental to the photoactivity and durability of the catalyst. In brief, two BDP-based Re bipyridyl systems with outstanding catalytic performance and significant visible-light-harvesting capabilities in the solar spectrum offer a promising strategy for solar-to-fuel conversion schemes.

Prevalence and Prognostic Significance of Malnutrition in Hypertensive Patients in a Community Setting.

Background: Malnutrition is a significantly poor prognostic factor for a variety of cardiovascular diseases. However, its prevalence and prognostic value in hypertensive patients is still unclear. The present study sought to determine the prevalence and prognostic value of malnutrition in hypertensive patients in a community setting. Methods: We included 9,949 hypertensive patients from the National Health and Nutrition Examination Survey (NHANES) (2005-2014). The Controlling Nutritional Status (CONUT) score, the Nutritional Risk Index (NRI), and the Naples Prognostic Score (NPS) were applied to assess the nutritional status of participants. A Cox regression model was established to examine the association between malnutrition and cardiovascular and all-cause mortality. Results: In all, 19.9, 3.9, and 82.9% hypertensive patients were considered to have malnutrition as evaluated by the CONUT, NRI, and NPS, respectively. Malnutrition assessed by CONUT and NRI was independently associated with cardiovascular mortality (HR [95% CI]) for mild and moderate-to-severe degree of malnutrition, respectively: 1.41 (1.04-1.91) and 5.79 (2.34-14.29) for CONUT; 2.60 (1.34-5.07) and 3.30 (1.66-6.56) for NRI (all P < 0.05), and for all-cause mortality (HR [95% CI]) for mild and moderate-to-severe degree of malnutrition, respectively: 1.48 (1.30-1.70) and 4.87 (3.40-6.98) for CONUT; 1.72 (1.24-2.39) and 2.60 (1.96-3.44) for NRI (all P < 0.01). Naples Prognostic Score could only independently predict all-cause mortality. Conclusions: Malnutrition was common among hypertensive patients and was closely associated with both long-term cardiovascular and all-cause mortality.

Cobalt Phthalocyanine Cross-Linked Polypyrrole for Efficient Electroreduction of Low Concentration CO2 To CO.

Immobilizing cobalt phthalocyanine (CoPc) onto the electrode surface is a significant approach to performing efficient electrochemical CO2 reduction reaction (ECO2 RR). Herein, sulfylphenoxy decorated CoPc cross-linked polypyrrole is prepared by in situ polymerization on the surface of carbon cloth. The synthesized N-rich catalyst exhibits above 95 % Faradaic efficiency toward CO (FECO ) at -0.9 V versus reversible hydrogen electrode (RHE) at least for 10 h in aqueous solution and even enables direct electrolysis at low CO2 concentrations, being potential for coupling ECO2 RR with CO2 capture. This facile in situ polymerization strategy would pave the way for developing efficient and practical electrocatalysis for ECO2 RR.

[Application of teaching method for the interpretation of acupoint names in the course of Science of Meridians and Acupoints].

The paper summarizes the valuable experience of the famous teachers of all generations in the teaching & research room of meridians and acupoints of Beijing University of CM. The shortcomings are presented when the acupoints are explained in accordance with the flowing route of meridians in classroom teaching of Science of Meridians and Acupoints. Hence, it is proposed that the acupoint names should be interpreted specially for the acupoints distributed on the same meridians or adjacent ones. It is suggested to emphasize the correlation of each acupoint with its adjacent ones from the perspective of the cultural connotation of acupoint names, and then, the differences and similarities in their clinical indications can be analyzed. Eventually, a new approach to the classroom teaching of Science of Meridians and Acupoints may be provided to guide the excavation of traditional cultural connotation and establish the cultural self-confidence and professional identity.

Lentivirus-mediated short hairpin RNA interference of CENPK inhibits growth of colorectal cancer cells with overexpression of Cullin 4A.

BACKGROUND: Colorectal cancer (CRC) is one of the most common malignant tumors worldwide. The identification of novel diagnostic and prognostic biomarkers for CRC is a key research imperative. Immunohistochemical analysis has revealed high expression of centromere protein K (CENPK) in CRC. However, the role of CENPK in the progression of CRC is not well characterized. AIM: To evaluate the effects of knockdown of CENPK and overexpression of Cullin 4A (CUL4A) in RKO and HCT116 cells. METHODS: Human colon cancer samples were collected and tested using a human gene expression chip. We identified CENPK as a potential oncogene for CRC based on bioinformatics analysis. In vitro experiments verified the function of this gene. We investigated the expression of CENPK in RKO and HCT116 cells using quantitative polymerase chain reaction (qPCR), western blot, and flow cytometry. The effect of short hairpin RNA (shRNA) virus-infected RKO cells on tumor growth was evaluated in vivo using quantitative analysis of fluorescence imaging. To evaluate the effects of knockdown of CENPK and overexpression of CUL4A in RKO and HCT116 cells, we performed a series of in vitro experiments, using qPCR, western blot, MTT assay, and flow cytometry. RESULTS: We demonstrated overexpression of CENPK in human colon cancer samples. CENPK was an independent risk factor in patients with CRC. The downstream genes FBX32, CUL4A, and Yes-associated protein isoform 1 were examined to evaluate the regulatory action of CENPK in RKO cells. Significantly delayed xenograft tumor emergence, slower growth rate, and lower final tumor weight and volume were observed in the CENPK short hairpin RNA virus infected group compared with the CENPK negative control group. The CENPK gene interference inhibited the proliferation of RKO cells in vitro and in vivo. The lentivirus-mediated shRNA interference of CENPK inhibited the proliferation of RKO and HCT116 colon cancer cells, with overexpression of the CUL4A. CONCLUSION: We indicated a potential role of CENPK in promoting tumor proliferation, and it may be a novel diagnostic and prognostic biomarker for CRC.