Direct Z-Scheme Heterostructure of Vertically Oriented SnS2 Nanosheet on BiVO4 Nanoflower for Self-Powered Photodetectors and Water Splitting.

The construction of nanostructured Z-scheme heterostructure is a powerful strategy for realizing high-performance photoelectrochemical (PEC) devices such as self-powered photodetectors and water splitting. Considering the band structure and internal electric field direction, BiVO4 is a promising candidate to construct SnS2 -based heterostructure. Herein, the direct Z-scheme heterostructure of vertically oriented SnS2 nanosheet on BiVO4 nanoflower is rationally fabricated for efficient self-powered PEC photodetectors. The Z-scheme heterostructure is identified by ultraviolet photoelectron spectroscopy, photoluminescence spectroscopy, PEC measurement, and water splitting. The SnS2 /BiVO4 heterostructure shows a superior photodetection performance such as excellent photoresponsivity (10.43 mA W-1 ), fast response time (6 ms), and long-term stability. Additionally, by virtue of efficient Z-scheme charge transfer and unique light-trapping nanostructure, the SnS2 /BiVO4 heterostructure also displays a remarkable photocatalytic hydrogen production rate of 54.3 µmol cm-2 h-1 in Na2 SO3 electrolyte. Furthermore, the synergistic effect between photo-activation and bias voltage further improves the PEC hydrogen production rate of 360 µmol cm-2 h-1 at 0.8 V, which is an order of magnitude above the BiVO4 . The results provide useful inspiration for designing direct Z-scheme heterostructures with special nanostructured morphology to signally promote the performance of PEC devices.

Strategies, Achievements, and Potential Challenges of Plant and Microbial Chassis in the Biosynthesis of Plant Secondary Metabolites.

Diverse secondary metabolites in plants, with their rich biological activities, have long been important sources for human medicine, food additives, pesticides, etc. However, the large-scale cultivation of host plants consumes land resources and is susceptible to pest and disease problems. Additionally, the multi-step and demanding nature of chemical synthesis adds to production costs, limiting their widespread application. In vitro cultivation and the metabolic engineering of plants have significantly enhanced the synthesis of secondary metabolites with successful industrial production cases. As synthetic biology advances, more research is focusing on heterologous synthesis using microorganisms. This review provides a comprehensive comparison between these two chassis, evaluating their performance in the synthesis of various types of secondary metabolites from the perspectives of yield and strategies. It also discusses the challenges they face and offers insights into future efforts and directions.

Whole genome sequence of mulberry crinivirus, a new member of the genus Crinivirus.

The whole genome sequence of mulberry crinivirus (MuCV), a novel member of the genus Crinivirus (family Closteroviridae) identified in mulberry (Morus alba L), was determined. The virus possesses a bipartite genome. RNA1 contains 8571 nucleotides (nt) with four open reading frames (ORFs). ORF1a encodes a putative polyprotein with papain-like protease, methyltransferase, and RNA helicase domains. ORF1b putatively encodes an RNA-dependent RNA polymerase (RdRp), which is probably expressed via a + 1 ribosomal frameshift. RNA2 consists of 8082 nt, containing eight ORFs that are similar in size and position to orthologous genes of other criniviruses. Phylogenetic analysis based on RdRp amino acid sequences of criniviruses placed MuCV in group 1.

Occurrence and Pathogenicity of Hop Stunt Viroid Infecting Mulberry (Morus alba) Plants in China.

To investigate the presence of hop stunt viroid (HSVd) in mulberry (Morus alba) plants in China, HSVd was detected by reverse transcription (RT)-PCR using dsRNAs extracted from symptomatic or asymptomatic mulberry leaf samples collected from a mulberry field located in Zhenjiang, China, as a template and the primer pairs for HSVd detection. The primer pairs were designed based on the conserved sequence of 25 HSVd variants deposited in the GenBank database. Four out of a total of 53 samples were HSVd-positive, confirming that HSVd is present in mulberry plants in China. The consensus full-length nucleotide (nt) sequence of two HSVd variants determined by sequencing the HSVd variants in these four HSVd-positive samples consisted of 296 nt and shared the highest nt identity of 96.8% with that from plum in Turkey but relatively low identity with those from mulberry in Iran (87.3 to 90.8%). Phylogenetic analysis showed that these HSVd variants clustered together with those of the HSVd-hop group. Analysis of the infectivity and pathogenicity to hosts by the constructed Agrobacterium-mediated dimeric head-to-tail HSVd cDNA infectious clones demonstrated that one of the HSVd variants identified in this study infects the natural host, mulberry plants, and also infects experimental plants, cucumber, and tomato. It probably induces stunting symptoms in HSVd-infected tomatoes but does not induce symptoms on mulberry leaves or in cucumbers. Although HSVd infecting mulberry has been found in Iran, Italy, and Lebanon, this is the first study to report this viroid in naturally infected mulberry plants in China.

Functional Characterization of a (E)-ß-Ocimene Synthase Gene Contributing to the Defense against Spodoptera litura.

Soybean is a worldwide crop that offers valuable proteins, fatty acids, and phytonutrients to humans but is always damaged by insect pests or pathogens. Plants have captured sophisticated defense mechanisms in resisting the attack of insects and pathogens. How to protect soybean in an environment- or human-friendly way or how to develop plant-based pest control is a hotpot. Herbivore-induced plant volatiles that are released by multiple plant species have been assessed in multi-systems against various insects, of which (E)-ß-ocimene has been reported to show anti-insect function in a variety of plants, including soybean. However, the responsible gene in soybean is unknown, and its mechanism of synthesis and anti-insect properties lacks comprehensive assessment. In this study, (E)-ß-ocimene was confirmed to be induced by Spodoptera litura treatment. A plastidic localized monoterpene synthase gene, designated as GmOCS, was identified to be responsible for the biosynthesis of (E)-ß-ocimene through genome-wide gene family screening and in vitro and in vivo assays. Results from transgenic soybean and tobacco confirmed that (E)-ß-ocimene catalyzed by GmOCS had pivotal roles in repelling a S. litura attack. This study advances the understanding of (E)-ß-ocimene synthesis and its function in crops, as well as provides a good candidate for further anti-insect soybean improvement.

Characterization of a strong constitutive promoter from paper mulberry vein banding virus.

Paper mulberry vein banding virus (PMVBV), a member of the genus Badnavirus in the family Caulimoviridae, infects paper mulberry (Broussonetia papyrifera), a dicotyledonous plant. Putative promoter regions in the PMVBV genome were tested using recombinant plant expression vectors, revealing that the promoter activity of three genome fragments was about 1.5-fold higher than that of the 35S promoter of cauliflower mosaic virus in Nicotiana benthamiana. In transformed transgenic Arabidopsis thaliana plants, these promoter constructs showed constitutive expression. Based on the activity and gene expression patterns of these three promoter constructs, a fragment of 384 bp (named PmVP) was deduced to contain the full-length promoter of the PMVBV genome. The results suggest that the PMVBV-derived promoter can be used for the constitutive expression of transgenes in dicotyledonous plants.

The influence of different proton pump inhibitors and potassium-competitive acid blockers on indomethacin-induced small intestinal injury.

BACKGROUND AND AIM: The influence of gastric acid inhibitors (GAIs) on nonsteroidal anti-inflammatory drug (NSAID)-induced enteropathy is controversial. Herein, the influences of different GAIs on NSAID-induced intestinal injury and the underlying mechanisms are clarified. METHODS: Indomethacin (IND; 10 mg/kg/day) was administered to mice to induce small intestinal injury. Disease activity was examined macroscopically and histologically. The permeability of small intestine was evaluated by measuring plasma lipopolysaccharide levels. 16S rDNA sequencing was performed to determine the composition of intestinal flora. RESULTS: Among the four GAIs, ilaprazole (IPZ) significantly attenuated IND-induced small intestinal injury and maintained the integrity of the mucosal barrier. Omeprazole (OPZ) and vonoprazan (VPZ) ameliorated ulceration without significant differences, while rabeprazole (RPZ) failed to protect against the injury. To explore the potential mechanism, we investigated changes in the gut microbiota mediated by GAIs. After 5-day administration, GAIs significantly altered the composition of the gut microbiota. The IND group had a significant decrease in alpha diversity compared with the control group, and this decrease was reversed by OPZ and IPZ treatment, respectively. After IPZ treatment, the community membership was more assembled in the control group than the IND group. Further, we found that Lactobacillus was significantly increased in the groups of OPZ, IPZ, and VPZ, while Bacteroides was significantly increased in the RPZ group. CONCLUSION: Our results indicated that GAIs have different influences on the mucosal barrier, possibly by altering the composition of intestinal microbiota, and the impacts mediated by various GAIs in the IND-induced intestinal damage model seem different.

The Identification of Tautoneura mori as the Vector of Mulberry Crinkle Leaf Virus and the Infectivity of Infectious Clones in Mulberry.

Mulberry crinkle leaf virus (MCLV) is a novel geminivirus identified from mulberry. The pathogenicity and natural vector transmission of MCLV remain unknown. Here, infectious clones consisting of the complete tandem dimeric genome of MCLV in a binary vector were constructed and agroinoculated into young mulberry plants. The results showed that the infectious clones of MCLV were systemically infectious in mulberry, but the infected mulberry plants did not show any virus infection-like symptoms. The natural transmission vectors of MCLV were also identified from possible vector insects occurring on the MCLV-infected mulberry plants. The vector ability of Tautoneura mori was identified through an inoculation assay. Three of 21 (14.3%) plants inoculated with T. mori collected from MCLV-infected mulberry plants grown naturally were found to be MCLV-positive 50 days postinoculation. These MCLV-positive mulberry plants did not show any virus infection-like symptoms. Collectively, these results suggest that MCLV is infectious to mulberry plants but, by itself, does not induce infection symptoms. The leafhopper T. mori was experimentally determined to be a transmission vector of MCLV for the first time.

MYB transcription factors GmMYBA2 and GmMYBR function in a feedback loop to control pigmentation of seed coat in soybean.

Soybean has undergone extensive selection pressures for seed nutrient composition and seed color during domestication, but the major genetic loci controlling seed coat color have not been completely understood, and the transcriptional regulation relationship among the loci remains elusive. Here, two major regulators, GmMYBA2 and GmMYBR, were functionally characterized as an anthocyanin activator and repressor, respectively. Ectopic expression of GmMYBA2 in soybean hairy roots conferred the enhanced accumulation of delphinidin and cyanidin types of anthocyanins in W1t and w1T backgrounds, respectively, through activating anthocyanin biosynthetic genes in the reported loci. The seed coat pigmentation of GmMYBA2-overexpressing transgenic plants in the W1 background mimicked the imperfect black phenotype (W1/w1, i, R, t), suggesting that GmMYBA2 was responsible for the R locus. Molecular and biochemical analysis showed that GmMYBA2 interacted with GmTT8a to directly activate anthocyanin biosynthetic genes. GmMYBA2 and GmMYBR might form a feedback loop to fine-tune seed coat coloration, which was confirmed in transgenic soybeans. Both GmTT8a and GmMYBR that were activated by GmMYBA2 in turn enhanced and obstructed the formation of the GmMYBA2-GmTT8a module, respectively. The results revealed the sophisticated regulatory network underlying the soybean seed coat pigmentation loci and shed light on the understanding of the seed coat coloration and other seed inclusions.

The spatio-temporal biosynthesis of floral flavonols is controlled by differential phylogenetic MYB regulators in Freesia hybrida.

Floral flavonols play specific pivotal roles in pollinator attraction, pollen germination and fertility, in addition to other functions in vegetative organs. For many plants, the process of flavonol biosynthesis in late flower development stages and in mature flower tissues is poorly understood, in contrast to early flower development stages. It is thought that this process may be regulated independently of subgroup 7 R2R3 MYB (SG7 MYB) transcription factors. In this study, two FLS genes were shown to be expressed synchronously with the flower development-specific and tissue-specific biosynthesis of flavonols in Freesia hybrida. FhFLS1 contributed to flavonol biosynthesis in early flower buds, toruses and calyxes, and was regulated by four well-known SG7 MYB proteins, designated as FhMYBFs, with at least partial regulatory redundancy. FhFLS2 accounted for flavonols in late developed flowers and in the petals, stamens and pistils, and was targeted directly by non SG7 MYB protein FhMYB21L2. In parallel, AtMYB21 and AtMYB24 also activated AtFLS1, a gene highly expressed in Arabidopsis anthers and pollen, indicating the conserved regulatory roles of MYB21 against FLS genes in these two evolutionarily divergent angiosperm plants. Our results reveal a novel regulatory and synthetic mechanism underlying flavonol biosynthesis in floral organs and tissues which may be exploited to investigate supplementary roles of flavonols in flowers.

[Effects of Long Non-coding RNA Plasmacytoma Variant Translocation 1 Gene on Inflammatory Response and Cell Migration in Helicobacter Pylori Infected Gastric Epithelial Cell Line].

Objective To investigate the mechanism of long non-coding RNA plasmacytoma variant translocation 1 (PVT1) in gastric cancer caused by helicobacter pylori (HP) infection. Methods The expression of PVT1 was detected by quantitative real-time polymerase chain reaction in HP-infected normal gastric epithelial cells GES-1. Gastric cancer cell line SGC-7901 was transfected with PVT1 small interfering RNA and co-cultured with HP,and then the inflammatory cytokines such as tumor necrosis factor-α (TNF-α),interleukin (IL) -1ß,IL-6 and IL-8 were detected. After PVT1 was knocked down,the effects of PVT1 on the proliferation and migration of gastric cancer cells were examined by cell scratch assay. RNA-pulldown combined with mass spectrometry was used to detect the protein binding to PVT1,and the result of mass spectrometry was verified by RNA-pulldown combined with Western blot. Results In HP-infected normal gastric epithelial cells GES-1,quantitative real-time polymerase chain reaction showed that PVT1 was significantly up-regulated (t=7.160,P=0.019). PVT1 was knocked down in gastric cancer cells,and then infected with HP. The expressions of inflammatory factors including TNF-α (t=3.899,P=0.011),IL-1ß (t=14.610,P=0.000),and IL-8 (t=6.557,P=0.001) were significantly inhibited. Although PVT1 knockdown had no significant effect on the proliferation ability of gastric cancer cells,it inhibited the migration of cells. PVT1 might interact with RPS8 protein. Conclusion PVT1 may act as a pro-inflammatory factor and regulate gastric cancer caused by HP infection.

The lncRNA SNHG5/miR-32 axis regulates gastric cancer cell proliferation and migration by targeting KLF4.

Long noncoding RNAs (lncRNAs) are emerging as important regulators in cellular processes, including the development, proliferation, and migration of cancer cells. We have demonstrated in a prior study that small nucleolar RNA host gene 5 (SNHG5) is dysregulated in gastric cancer (GC). To further explore the underlying mechanisms of SNGH5 function in the development of GC, in this study, we screened the microRNAs interacting with SNHG5 and elucidated their roles in GC. We showed that SNHG5 contains a putative miR-32-binding site and that deletion of this site abolishes the responsiveness to miR-32. Suppression of SNHG5 expression by miR-32 was found to be Argonaute (Ago)2-dependent. Immunoprecipitation showed that SNHG5 could be pulled down from the Ago-2 complex with miR-32. Furthermore, it was reported that Kruppel-like factor 4 (KLF4) is a target gene of miR-32. In agreement with SNHG5 being a decoy for miR-32, we showed that KLF4 suppression by miR-32 could be partially rescued by SNHG5 overexpression, whereas miR-32 mimic rescued SNHG5 overexpression-mediated suppression of GC cell migration. In addition, we identified a negative correlation between the expression of SNHG5 and miR-32 in GC tissues. Furthermore, KLF4 expression was significantly downregulated in GC specimens, and a negative correlation between miR-32 and KLF4 expression and a positive correlation between KLF4 and SNHG5 expression levels were detected. Overall, this study demonstrated, for the first time, that the SNHG5/miR-32/KLF4 axis functions as an important player in GC cell migration and potentially contributes to the improvement of GC diagnosis and therapy.-Zhao, L., Han, T., Li, Y., Sun, J., Zhang, S., Liu, Y., Shan, B., Zheng D., Shi, J. The lncRNA SNHG5/miR-32 axis regulates gastric cancer cell proliferation and migration by targeting KLF4.

MiR-382 inhibits cell growth and invasion by targeting NR2F2 in colorectal cancer.

Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide. MiR-382 has been found to have a decreased expression and the ability to suppress tumorigenesis in certain cancers. However, the role of miR-382 in CRC has not been sufficiently investigated. NR2F2 (also known as COUP-TFII), a member of the steroid/thyroid receptor superfamily, is often aberrantly activated in various tumors, but it is currently unclear whether NR2F2 may be a target of miR-382. In the present study, we investigated the role of miR-382 in CRC and identified the regulation of NR2F2 by miR-382. We observed that miR-382 was aberrantly downregulated in CRC. Transfection with miR-382 mimics impeded the growth, migration, and invasion of CRC cells. The direct binding of miR-382 to the 3' untranslated region (3' UTR) of NR2F2 was confirmed using a luciferase reporter gene assay. We showed that the relative expression levels of NR2F2 were significantly higher in CRC tissues compared with normal adjacent mucosa. A Kaplan-Meier analysis indicated that patients with high NR2F2 expression had a poor overall survival. Knockdown of NR2F2 inhibited CRC cell growth, migration, and invasion. Ectopic expression of NR2F2 mitigated miR-382 suppression of CRC cell proliferation, migration, and invasion. In conclusion, the present study describes a potential mechanism underlying a miR-382/NR2F2 link contributing to CRC development. Our results demonstrate that miR-382 represents a potential strategy against CRC. © 2016 Wiley Periodicals, Inc.

The long noncoding RNA colon cancer-associated transcript-1/miR-490 axis regulates gastric cancer cell migration by targeting hnRNPA1.

Colon cancer-associated transcript-1 (CCAT1) is a highly conserved long noncoding RNA that is deregulated in several cancers. However, its role in gastric carcinoma and its post-transcriptional regulation remain poorly understood. In this study, we provide the first evidence that CCAT1 regulates miR-490 in gastric cancer (GC) cells. Interestingly, miR-490 can also repress CCAT1 expression. CCAT1 expression was significantly upregulated, and miR-490 expression was downregulated in GC. The negative correlation between miR-490 and CCAT1 expression was observed in GC tissues. Importantly, CCAT1 contains a putative miR-490-binding site, and deletion of this binding site abolishes their miR-490 responsiveness. Post-transcriptional CCAT1 silencing by miR-490 significantly suppressed GC cell migration. Furthermore, miR-490 directly bound to the hnRNPA1 mRNA 3'-UTR to repress its translation. Inhibition of miR-490 rescued CCAT1 siRNA-mediated suppression of cell migration. hnRNPA1 expression was significantly upregulated in GC specimens, and there was a negative correlation between miR-490 and hnRNPA1 expression and also a positive correlation between hnRNAP1 expression level and CCAT1 level. Taken together, we show for the first time that the CCAT1/miR-490/hnRNPA1 axis promotes GC migration, and it may have a possible diagnostic and therapeutic potential in GC.

Two genes encoded by mulberry crinkle leaf virus (MCLV): The V4 gene enhances viral replication, and the V5 gene is needed for MCLV infection in Nicotiana benthamiana.

Mulberry crinkle leaf virus (MCLV) is a member of the genus Mulcrilevirus, family Geminiviridae. The expression and functions of the V4 and V5 genes encoded by the MCLV genome remain unknown. Here, we confirmed the expression of V4 and V5 by analyzing the V4 and V5 mRNAs and the promoter activity of individual ORFs upstream sequences. The functions of V4 and V5 were investigated by constructing Agrobacterium-mediated infectious clones of wild-type MCLV variant П (MCLV vII), MCLVwt and MCLV vП mutants, such as MCLVmV4 (start codon of V4 ORF mutated), MCLVdV4 (5'-end partial deletion of V4 ORF sequence) and MCLVmV5 (V5 ORF start codon mutated). Although MCLVwt, MCLVmV4, and MCLVdV4 could infect natural host mulberry and experimental tomato plants systematically, the replication of the MCLVmV4 and MCLVdV4 genomes was obviously reduced compared to MCLVwt in both mulberry and tomato plants. MCLV vП expressing V5 could infect Nicotiana benthamiana plants systematically, but MCLVmV5 could not, implying that V5 is needed for MCLV vП to infect N. benthamiana plants. Taken together, V4 is involved in replication of the MCLV genome in host plants, and V5 potentially might extend the host range. Our findings lay a foundation for in-depth insight into the functions of MCLV-encoded proteins and provide a novel perspective for the subsequent study of MCLV-host plant interactions.

EFHD2 suppresses intestinal inflammation by blocking intestinal epithelial cell TNFR1 internalization and cell death.

TNF acts as one pathogenic driver for inducing intestinal epithelial cell (IEC) death and substantial intestinal inflammation. How the IEC death is regulated to physiologically prevent intestinal inflammation needs further investigation. Here, we report that EF-hand domain-containing protein D2 (EFHD2), highly expressed in normal intestine tissues but decreased in intestinal biopsy samples of ulcerative colitis patients, protects intestinal epithelium from TNF-induced IEC apoptosis. EFHD2 inhibits TNF-induced apoptosis in primary IECs and intestinal organoids (enteroids). Mice deficient of Efhd2 in IECs exhibit excessive IEC death and exacerbated experimental colitis. Mechanistically, EFHD2 interacts with Cofilin and suppresses Cofilin phosphorylation, thus blocking TNF receptor I (TNFR1) internalization to inhibit IEC apoptosis and consequently protecting intestine from inflammation. Our findings deepen the understanding of EFHD2 as the key regulator of membrane receptor trafficking, providing insight into death receptor signals and autoinflammatory diseases.

Bi2 Te3 /Bi2 Se3 /Bi2 S3 Cascade Heterostructure for Fast-Response and High-Photoresponsivity Photodetector and High-Efficiency Water Splitting with a Small Bias Voltage.

Large-scale multi-heterostructure and optimal band alignment are significantly challenging but vital for photoelectrochemical (PEC)-type photodetector and water splitting. Herein, the centimeter-scale bismuth chalcogenides-based cascade heterostructure is successfully synthesized by a sequential vapor phase deposition method. The multi-staggered band alignment of Bi2 Te3 /Bi2 Se3 /Bi2 S3 is optimized and verified by X-ray photoelectron spectroscopy. The PEC photodetectors based on these cascade heterostructures demonstrate the highest photoresponsivity (103 mA W-1 at -0.1 V and 3.5 mAW-1 at 0 V under 475 nm light excitation) among the previous reports based on two-dimensional materials and related heterostructures. Furthermore, the photodetectors display a fast response (≈8 ms), a high detectivity (8.96 × 109 Jones), a high external quantum efficiency (26.17%), and a high incident photon-to-current efficiency (27.04%) at 475 nm. Due to the rapid charge transport and efficient light absorption, the Bi2 Te3 /Bi2 Se3 /Bi2 S3 cascade heterostructure demonstrates a highly efficient hydrogen production rate (≈0.416 mmol cm-2  h-1 and ≈14.320 µmol cm-2  h-1 with or without sacrificial agent, respectively), which is far superior to those of pure bismuth chalcogenides and its type-II heterostructures. The large-scale cascade heterostructure offers an innovative method to improve the performance of optoelectronic devices in the future.

Enhanced UV-Vis photodetector performance by optimizing interfacial charge transportation in the heterostructure by SnS and SnSe2.

Optimizing interfacial charge transfer in type-II heterostructures, is one promising solution to improve efficiency of the solar energy conversion in photodetectors and solar cells. Herein, the SnS/SnSe2/ITO and SnSe2/SnS/ITO heterostructures are prepared by two-step physical vapor epitaxial growth. X-ray photoelectron spectroscopy confirms the SnS/SnSe2 heterostructure belongs to type-II band-alignment. The SnS/SnSe2 based photodetector shows higher photoresponsivity, which is approximately 2, 9, and 14 times larger than that of SnSe2/SnS, SnSe2, and SnS, respectively. The improvement of SnS/SnSe2 in photoelectric response mainly comes from high light harvesting and efficient charge transportation than individual SnSe2 and SnS, which is verified by UV-Vis absorption spectra. Electrochemical impedance spectroscopy, open circuit potentials, and Mott-Schottky characterization results further confirm that the better photodetection performance of SnS/SnSe2/ITO than that of SnSe2/SnS/ITO heterostructure is from the appropriate energy level cascade facilitating electron transport. These results provide an effective way to further improve the performance of heterostructure-based optoelectronic devices by an appropriate interface design.

CYP24A1 Involvement in Inflammatory Factor Regulation Occurs via the Wnt Signaling Pathway.

OBJECTIVE: While the upregulation of cytochrome P450 family 24 subfamily A member 1 (CYP24A1) gene expression has been reported in colon cancer, its role in tumorigenesis remains largely unknown. In this study, we aimed to investigate the involvement of CYP24A1 in Wnt pathway regulation via the nuclear factor kappa B (NF-κB) pathway. METHODS: The human colon cancer cell lines HCT-116 and Caco-2 were subjected to stimulation with interleukin-6 (IL-6) as well as tumor necrosis factor alpha (TNF-α), with subsequent treatment using the NF-κB pathway-specific inhibitor ammonium pyrrolidinedithiocarbamate (PDTC). Furthermore, CYP24A1 expression was subjected to knockdown via the use of small interfering RNA (siRNA). Subsequently, NF-κB pathway activation was determined by an electrophoretic mobility shift assay, and the transcriptional activity of ß-catenin was determined by a dual-luciferase reporter assay. A mouse ulcerative colitis (UC)-associated carcinogenesis model was established, wherein TNF-α and the NF-κB pathway were blocked by anti-TNF-α monoclonal antibody and NF-κB antisense oligonucleotides, respectively. Then the tumor size and protein level of CYP24A1 were determined. RESULTS: IL-6 and TNF-α upregulated CYP24A1 expression and activated the NF-κB pathway in colon cancer cells. PDTC significantly inhibited this increase in CYP24A1 expression. Additionally, knockdown of CYP24A1 expression by siRNA could partially antagonize Wnt pathway activation. Upregulated CYP24A1 expression was observed in the colonic epithelial cells of UC-associated carcinoma mouse models. Anti-TNF-α monoclonal antibody and NF-κB antisense oligonucleotides decreased the tumor size and suppressed CYP24A1 expression. CONCLUSION: Taken together, this study suggests that inflammatory factors may increase CYP24A1 expression via NF-κB pathway activation, which in turn stimulates Wnt signaling.