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Insect group h chitinase is a promising target for designing non-target safe pesticides in that it is exclusively distributed in lepidopteran insects, over 80% of which are agricultural pests. In this work, lynamicin B was discovered to be an inhibitor of OfChi-h, the group h chitinase from the lepidopteran pest Ostrinia furnacalis. Lynamicin B was revealed to competitively inhibit OfChi-h with a Ki value of 8.76 μM and does not significantly inhibit other chitinases. The co-crystal structure of lynamicin B and OfChi-h revealed that the dichloroindolyl group of lynamicin B occupies an unexplored pocket below subsites +1 and +2 of the substrate-binding cleft, which is vital for its selectivity. Feeding experiments demonstrated that lynamicin B exhibited high insecticidal activities against other lepidopteran pests Mythimna separata and Spodoptera frugiperda besides O. furnacalis. Moreover, lynamicin B did not affect Trichogramma ostriniae, a natural enemy of O. furnacalis. This study provides a natural-derived potent pesticide for the control of lepidopteran pests, leaving its natural enemy unaffected.

Although great progress has been made in the early diagnosis and targeted therapy of lung adenocarcinoma (LUAD), the survival of patients with LUAD remains unsatisfactory. There is an urgent requirement for new biomarkers to guide the diagnosis, prognosis and treatment of LUAD. Following an initial bioinformatics screen, the present study focused on cyclin B1 (CCNB1) in LUAD. A total of 94 patients with LUAD from a single hospital were included in the study. CCNB1 protein expression was detected and scored in 94 LUAD samples and 30 normal tissue samples by immunohistochemistry. The associations between CCNB1 expression and the clinicopathological features of the patients with LUAD were analyzed. Furthermore, the relationship between prognosis and the CCNB1 expression level was analyzed using Cox regression and survival analyses. Weighted gene co-expression network analysis and RNA-sequencing were also applied to identify the potential molecular mechanisms of CCNB1 in LUAD. CCNB1 was highly expressed in patients with LUAD and was associated with poor prognosis. It may affect the expression of CPLX1, PPIF, SRPK2, KRT8, SLC20A1 and CBX2 genes and function via different pathways. CCNB1 has the potential to become a novel prognostic target for LUAD.

Tumor acidic microenvironment is the main feature of many solid tumors. As a part of the tumor microenvironment, it has a profound impact on the occurrence and development of tumors. However, the research on how tumor cells sense the changes of the external microenvironment and how the intracellular subcellular structures transmit the signals from extracellular to intracellular is unclear. In this study, we identify that the acidic microenvironment enhances cancer cell motility, and the expression of membrane-anchored membrane type 1-matrix metalloproteinase is also associated with cell motility, which indicates more degradation of the ECM under the acidic microenvironment. Moreover, the expression of cofilin is low in the acidic microenvironment, and the F-actin filaments are distributed more along the cells. The cytoskeletal F-actin changes are consistent with the potential of a high-invasive phenotype. Further study reveals the upstream control of the signal transductions from extracellular to intracellular, that is, the integrin β1 functions to trigger the biological responses under the acidic microenvironment. Our results demonstrate that the acidic microenvironment enhances cancer cell motility through the integrin β1/cofilin/F-actin signal axis. This study clearly shows the scheme of the signal transmissions from extracellular to intracellular and further reveals the cytoskeletal roles for the contributions of cancer cell motility under acidic microenvironment, which provides new targets for cancer intervention from the biochemical and biophysical perspectives.

Esophageal squamous cell carcinoma (ESCC) is a kind of malignant tumor with high incidence and mortality in the digestive system. The aim of this study is to explore the function of lnc-ABCA12-3 in the development of ESCC and its unique mechanisms. RT-PCR was applied to detect gene transcription levels in tissues or cell lines like TE-1, EC9706, and HEEC cells. Western blot was conducted to identify protein expression levels of mitochondrial apoptosis and toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) signaling pathway. CCK-8 and EdU assays were carried out to measure cell proliferation, and cell apoptosis was examined by flow cytometry. ELISA was used for checking the changes in glycolysis-related indicators. Lnc-ABCA12-3 was highly expressed in ESCC tissues and cells, which preferred it to be a candidate target. The TE-1 and EC9706 cells proliferation and glycolysis were obviously inhibited with the downregulation of lnc-ABCA12-3, while apoptosis was promoted. TLR4 activator could largely reverse the apoptosis acceleration and relieved the proliferation and glycolysis suppression caused by lnc-ABCA12-3 downregulation. Moreover, the effect of lnc-ABCA12-3 on ESCC cells was actualized by activating the TLR4/NF-κB signaling pathway under the mediation of exosome. Taken together, the lnc-ABCA12-3 could promote the proliferation and glycolysis of ESCC, while repressing its apoptosis probably by regulating the TLR4/NF-κB signaling pathway under the mediation of exosome.

A genome-directed discovery strategy to identify new tetrahydroisoquinolines (THIQs) was applied to deep-sea derived Streptomyces niveus SCSIO 3406; 11 THIQs were found representing three THIQ clas...

Teratoma is a common type of mediastinal tumor, often located in the anterior mediastinum. Mediastinal teratomas often occur in young and middle-aged people, and account for 5–21.5% of mediastinal tumors. Mature cystic teratoma is a common type of mediastinal teratoma, its onset is slow, and most patients are asymptomatic. In a few patients, the tissue around the mediastinum is invaded or there is malignant transformation, which results in chest pain, chest tightness, a cough, and other symptoms. In this case, the patient had a giant teratoma, compressing large blood vessels and nerves, complicated by pleural and pericardial effusion. The 21-year-old female patient was misdiagnosed with tuberculous disease because of chronic cough and expectoration. Her initial symptoms improved after anti-tuberculosis treatment; however, an imaging examination showed that the lesion had enlarged some 9 months later. Surgery was performed at our hospital, as the tumor was squeezing blood vessels, and the trachea was seriously adhering to the surrounding tissue. To avoid damage to the peripheral blood vessels and nerves, many residual tissues were retained after the operation. The post-operative pathology results confirmed that the patient had a mature mediastinal cystic teratoma. One year after the operation, there was no recurrence, the peripheral blood vessels had basically returned, and the patient did not have any nerve injury. Effusion caused by mediastinal teratoma should be carefully differentiated from tuberculous diseases to avoid unnecessary damage to patients during treatment. Separation can be difficult in benign mediastinal tumors with severe adhesion. To avoid the trauma caused by the excessive separation of a tumor, it is our view that part of the residual tissue should be retained and left to be absorbed naturally.

Two new chlorinated bis-indole alkaloids, dionemycin (1) and 6-OMe-7',7″-dichorochromopyrrolic acid (2), along with seven known analogs 3-9, were isolated from the deep-sea derived Streptomyces sp. SCSIO 11791. Their structures were elucidated by extensive HRESIMS, and 1D and 2D NMR data analysis. In vitro antibacterial and cytotoxic assays revealed that, compound 1, shows anti-staphylococcal activity with an MIC range of 1-2 μg/mL against six clinic strains of methicillin-resistant Staphylococcus aureus (MRSA) isolated from human and pig. Additionally, compound 1 displayed cytotoxic activity against human cancer cell lines NCI-H460, MDA-MB-231, HCT-116, HepG2, and noncancerous MCF10A with an IC50 range of 3.1-11.2 μM. Analysis of the structure-activity relationship reveals that the chlorine atom at C-6″ could be pivotal for conferring their bioactivities, thus providing hints on chemical modifications on bis-indole alkaloid scaffold in drug design.

Baeyer–Villiger monooxygenases (BVMOs) play important roles in the biosynthesis of natural products. We describe here in vivo gene inactivation/complementation studies as well as in vitro enzyme as...

Background Preoperative mediastinal staging is crucial for the optimal management of clinical stage I non-small cell lung cancer (NSCLC). Purpose To develop a deep learning signature for N2 metastasis prediction and prognosis stratification in clinical stage I NSCLC. Materials and Methods In this retrospective study conducted from May 2020 to October 2020 in a population with clinical stage I NSCLC, an internal cohort was adopted to establish a deep learning signature. Subsequently, the predictive efficacy and biologic basis of the proposed signature were investigated in an external cohort. A multicenter diagnostic trial (registration number: ChiCTR2000041310) was also performed to evaluate its clinical utility. Finally, on the basis of the N2 risk scores, the instructive significance of the signature in prognostic stratification was explored. The diagnostic efficiency was quantified with the area under the receiver operating characteristic curve (AUC), and the survival outcomes were assessed using the Cox proportional hazards model. Results A total of 3096 patients (mean age ± standard deviation, 60 years ± 9; 1703 men) were included in the study. The proposed signature achieved AUCs of 0.82, 0.81, and 0.81 in an internal test set (

It has been reported that tumor-associated macrophages (TAMs) participate in modulating the progression of cancer in the tumor microenvironment. However, the crosstalk between TAMs and non-small cell lung cancer (NSCLC) is still unclear.We investigated whether NSCLC-derived exosomes could affect TAMs, which feedback modulated progression of NSCLC.MiR-181b expression was measured by RT-PCR. Human THP-1 monocyte was differentiated into macrophages with phorbol myristate acetate, which were further identified by transmission electron microscopy and western blot. Macrophage M1 and M2 polarizations were detected by flow cytometry, RT-PCR and western blot. Proliferation, migration, and invasion of NSCLC cells treated with conditioned mediums were detected by EdU and Transwell assays.We demonstrated that miR-181b was up-regulated in exosomes derived from NSCLC patients' serum and NSCLC cells. MiR-181b could be transferred to macrophages via exosomes in the co-culture system of macrophages and NSCLC cells, which promoted macrophage M2 polarization. Further examinations revealed that exosomes derived from NSCLC cells could enhanced macrophage M2 polarizations by regulating miR-181b/JAK2/STAT3 axis, and silencing miR-181b in NSCLC cells and JAK2 inhibitor used in macrophages could reverse the effects. Importantly, the conditioned medium of macrophages treated with NSCLC cell-derived exosomes could promote NSCLC cell proliferation, migration, and invasion. Silencing miR-181b in NSCLC cells and JAK2 inhibitor used in macrophages could block the effects.All of these results indicated that exosomal miR-181b participated in the crosstalk between NSCLC cells and TAMs, providing potential therapeutic targets for NSCLC.

PurposeTo investigate the surgical prognosis and efficacy of adjuvant therapy in non-small cell lung cancer (NSCLC) with occult lymph node metastasis (ONM) defined by positron emission tomography-computed tomography (PET-CT).MethodsA total of 3537 NSCLC patients receiving surgical resection were included in this study. The prognosis between patients with ONM and evident nodal metastasis, ONM patients with and without adjuvant therapy were compared, respectively.ResultsONM was associated with significantly better prognosis than evident nodal metastasis whether for patients with N1 (5-year OS: 56.8% versus 52.3%, adjusted p value=0.267; 5-year RFS: 44.7% versus 33.2%, adjusted p value=0.031) or N2 metastasis (5-year OS: 42.8% versus 32.3%, adjusted p value=0.010; 5-year RFS: 31.3% versus 21.6%, adjusted p value=0.025). In ONM population, patients receiving adjuvant therapy yielded better prognosis comparing to those without adjuvant therapy (5-year OS: 50.1% versus 33.5%, adjusted p value

Macrophages are a heterogeneous group of phagocytes that play critical roles in inflammation, infection and tumor growth. Macrophages respond to different environmental factors and are thereby polarized into specialized functional subsets. Although hypoxia is an important environmental factor, its impact on human macrophage polarization and subsequent modification of the inflammatory microenvironment have not been fully established. The present study aimed to elucidate the effect of hypoxia exposure on the ability of human macrophages to polarize into the classically activated (pro-inflammatory) M1, and the alternatively activated (anti-inflammatory) M2 phenotypes. The effect on the inflammatory microenvironment and the subsequent modification of A549 lung carcinoma cells was also investigated. The presented data show that hypoxia promoted macrophage polarization towards the M2 phenotype, and modified the inflammatory microenvironment by decreasing the release of proinflammatory cytokines. Modification of the microenvironment by proinflammatory M1 macrophages under hypoxia reversed the inhibition of malignant behaviors within the proinflammatory microenvironment. Furthermore, it was identified p38 signaling (a major contributor to the response to reactive oxygen species generated by hypoxic stress), but not hypoxia-induced factor, as a key regulator of macrophages under hypoxia. Taken together, the data suggest that hypoxia affects the inflammatory microenvironment by modifying the polarization of macrophages, and thus, reversing the inhibitory effects of a proinflammatory microenvironment on the malignant behaviors of several types of cancer cell.

The Institute of Plasma Physics, Chinese Academy of Sciences (ASIPP), is in charge of the manufacturing and testing of the 60 high-temperature superconducting current lead series to be completed at the end of 2020 for the International Thermonuclear Experimental Reactor (ITER). This paper first summarizes the testing items and testing results of the ITER lead prototypes in 2015/2016, then, based on the prototypes experiences, discuss the final test piping and instrument diagram for the ITER lead series production testing. A new 5-K test platform to expedite the series testing is also introduced, and a new feature, the 30-kV high-voltage (HV) class insulation for the cryogenic temperature and voltage measurements to allow in situ HV testing, is introduced. The detailed test procedures and test items for the series are discussed finally.

Tumor‑associated macrophages (TAMs) are critical components of the tumor microenvironment that are tightly associated with malignancies in human cancers, including lung cancer. LGK‑974, a small molecular inhibitor of Wnt secretion, was reported to block Wnt/β‑catenin signaling and exert anti‑inflammatory effects by suppressing pro‑inflammatory gene expression in cancer cells. Although it was reported that Wnt/β‑catenin was critical in regulating TAMs, it is still largely unknown whether LGK‑974 regulates tumor malignancies by regulating TAMs. The present study firstly verified that the polarization of TAMs was regulated by LGK‑974. LGK‑974 increased M1 macrophage functional markers and decreased M2 macrophage functional markers. The addition of Wnt3a and Wnt5a, two canonical Wnt signaling inducers, reversed the decrease in M1 macrophage functional markers, including mannose receptor, IL‑10 and Arg1, by activating Wnt/β‑catenin signaling. Conditioned medium from LGK‑974‑modified TAMs inhibited the malignant behaviors in A549 and H1299 cells, including proliferation, colony formation and invasion, by blocking Wnt/β‑catenin signaling. LGK‑974‑modified TAMs blocked the cell cycle at the G1/G0 phase, which was reversed by the addition of Wnt3a/5a, indicating that LGK‑974 regulates the microenvironment by blocking Wnt/β‑catenin signaling. Taken together, the results indicate that LGK‑974 indirectly inhibited the malignant behaviors of A549 and H1299 cells by regulating the inflammatory microenvironment by inhibiting Wnt/β‑catenin signaling in TAMs.

A genome-directed discovery strategy to identify new tetrahydroisoquinolines (THIQs) was applied to deep-sea derived

Background Micropapillary/solid (MP/S) growth patterns of lung adenocarcinoma are vital for making clinical decisions regarding surgical intervention. This study aimed to predict the presence of a MP/S component in lung adenocarcinoma using radiomics analysis. Methods Between January 2011 and December 2013, patients undergoing curative invasive lung adenocarcinoma resection were included. Using the "PyRadiomics" package, we extracted 90 radiomics features from the preoperative computed tomography (CT) images. Subsequently, four prediction models were built by utilizing conventional machine learning approaches fitting into radiomics analysis: a generalized linear model (GLM), Naive Bayes, support vector machine (SVM), and random forest classifiers. The models' accuracy was assessed using a receiver operating curve (ROC) analysis, and the models' stability was validated both internally and externally. Results A total of 268 patients were included as a primary cohort, and 36.6% (98/268) of them had lung adenocarcinoma with an MP/S component. Patients with an MP/S component had a higher rate of lymph node metastasis (18.4% versus 5.3%) and worse recurrence-free and overall survival. Five radiomics features were selected for model building, and in the internal validation, the four models achieved comparable performance of MP/S prediction in terms of area under the curve (AUC): GLM, 0.74 [95% confidence interval (CI): 0.65-0.83]; Naive Bayes, 0.75 (95% CI: 0.65-0.85); SVM, 0.73 (95% CI: 0.61-0.83); and random forest, 0.72 (95% CI: 0.63-0.81). External validation was performed using a test cohort with 193 patients, and the AUC values were 0.70, 0.72, 0.73, and 0.69 for Naive Bayes, SVM, random forest, and GLM, respectively. Conclusions Radiomics-based machine learning approach is a very strong tool for preoperatively predicting the presence of MP/S growth patterns in lung adenocarcinoma, and can help customize treatment and surveillance strategies.

A 26-year-old female was admitted to the emergency department of thoracic surgery complaining of chest tightness, shortness of breath, and a history of bilateral tuberculosis. A chest Computed Tomography (CT) scan showed bilateral pleural effusion. After that, the patient was implanted with bilateral intercostal drainage tubes. Further analysis of the pleural effusion was conducted to confirm the diagnosis of bilateral chylothorax. We initiated conservative treatment consisting of fasting and total parenteral nutrition. After the failure of conservative treatment, the patient underwent ligation of the thoracic duct by right-sided thoracotomy combined with talc slurry. On the first day postoperatively, the right pleural effusion had decreased significantly, while the left pleural effusion had not. Subsequently, talc slurry was injected into the left thoracic drainage tube of the patient. Bilateral pleural effusion was significantly reduced. Re-examination chest X-ray showed the disappearance of pleural effusion, and the patient was discharged good healthy. Chest X-rays were reexamined one month postoperatively, and the patient's lung was well dilated, with no recurrence of pleural effusion. In this case, it was shown that conservative treatment is the first choice for chylothorax. However, if this proves to be ineffective, early surgical treatment should be considered. Early diagnosis and timely surgical intervention are the key factors to improve the prognosis of patients.

Background Mitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatics tools. Results We found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD. Conclusions Consequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

Thoracic endometriosis is characterized by the presence of normal functioning endometrial tissues in normal pleural, diaphragm, or lung parenchyma, and main clinical symptoms include pneumothorax, menstrual hemothorax, menstrual hemoptysis, and pulmonary nodules. Chest X-ray (CXR), computed tomography (CT), magnetic resonance imaging (MRI), bronchoscopy, and surgical biopsy could be applied to the diagnosis of TE. Both drug therapy and surgical treatment were widely used to treat this disease, but no theory was used to guide the choice of treatment options. This paper introduces a case of menstrual hemoptysis due to endometriosis, and the final surgical treatment was chosen. The patient recovered well postoperatively and reported no hemoptysis during 2 months of follow-up. Reexamination of the chest through CT showed no ground-glass lesions or pulmonary exudative lesions. We make the following recommendations for patient selection when considering a surgical approach to the treatment of TE. Patients for whom surgery should be considered are those who (I) do not respond to drug therapy or relapse once drug therapy is withdrawn, (II) cannot tolerate drug therapy or who may wish to get pregnant in the near future (III) have limited lesions which are able to be completely removed during surgery. Patients in whom surgery is not recommended include those who have extensive lesions which cannot be surgically removed, including those with diaphragm or pleural involvement as the diseased tissues must be completely removed to avoid recurrence, and those who are unfit for surgery.

Background Spindle and kinetochore associated complex subunit 1/2/3 (SKA1/2/3), which stabilized spindle microtubules attaching to kinetochore (KT) in the middle stage of mitosis, were dysregulated, and closely related to prognosis in several malignant tumors. Nevertheless, the potential clinical value of SKA1/2/3, especially in terms of prognosis and development of NSCLC, had not been fully elucidated. Methods ONCOMINE, GEPIA, UALCAN, TCGA, STRING and other databases were used to analyze the expression of SKA1/2/3 in patients with lung adenocarcinoma (LUAD) and its clinical value, and to explore the possible regulatory mechanism of SKA in the occurrence and development of LUAD. Results In patients with LUAD, SKA1/2/3 mRNA expression level was significantly up-regulated, and AUC was 0.9558, 0.7034 and 0.9775, respectively. Increased SKA 1/2/3 expression was associated with smoking, tissue typing, and poor prognosis in LUAD patients. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) showed that SKA1/2/3 was mainly enriched in DNA replication, cell cycle, homologous recombination, p53 signaling pathway, etc. Hub genes in protein-protein interactions are CDK1, BUB1, CCNA2, CDC20, CCNB2, CCNB1, BUB1B, AURKB, TOP2A and MAD2L1. Hub gene expression in LUAD is increased, and its increased expression is related to poor prognosis of LUAD patients. Finally, the expression of SKA1/2/3 and its correlation with clinicopathological features were verified in 30 clinical LUAD samples. Conclusions SKA1/2/3 may serve as a potential prognostic biomarker and target for LUAD. In addition, SKA 1/2/3 may affect the prognosis of LUAD through DNA replication, cell cycle, homologous recombination and p53 signaling pathway.

Background Upregulation of the six-transmembrane epithelial antigen of prostate-1 (STEAP1) is closely associated with prognosis of numerous malignant cancers. However, its role in lung adenocarcinoma (LUAD), the most common type of lung cancer, remains unknown. This study aimed to investigate the role of STEAP1 in the occurrence and progression of LUAD and the potential mechanisms underlying its regulatory effects. Methods STEAP1 mRNA and protein expression were analyzed in 40 LUAD patients via real-time PCR and western blotting, respectively. We accessed the clinical data of 522 LUAD patients from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) to investigate the expression and prognostic role of STEAP1 in LUAD. Further, we performed gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and gene set enrichment analysis (GSEA) to elucidate the potential mechanism underlying the role of STEAP1 in LUAD. The protein-protein interaction (PPI) network of STEAP1 was analyzed using the Search Tool for the Retrieval of Interacting Genes (STRING) database, and hub genes with significant positive and negative associations with STEAP1 were identified and their role in LUAD prognosis was predicted. Results STEAP1 was significantly upregulated in LUAD patients and associated with LUAD prognosis. Further, TCGA data indicated that STEAP1 upregulation is correlated with the clinical prognosis of LUAD. GO and KEGG analysis revealed that the genes co-expressed with STEAP1 were primarily involved in cell division, DNA replication, cell cycle, apoptosis, cytokine signaling, NF-kB signaling, and TNF signaling. GSEA revealed that homologous recombination, p53 signaling pathway, cell cycle, DNA replication, apoptosis, and toll-like receptor signaling were highly enriched upon STEAP1 upregulation. Gene Expression Profiling Interactive Analysis (GEPIA) analysis revealed that the top 10 hub genes associated with STEAP1 expression were also associated with the LUAD prognosis. Conclusion STEAP1 upregulation potentially influences the occurrence and progression of LUAD and its co-expressed genes via regulation of homologous recombination, p53 signaling, cell cycle, DNA replication, and apoptosis. STEAP1 is a potential prognostic biomarker for LUAD.

Streptomyces niveus SCSIO 3406 was isolated from a sediment sample collected from South China Sea at a depth of 3536 m. Four new sesquiterpenoid naphthoquinones, marfuraquinocins A-D, and two new geranylated phenazines, i. e. phenaziterpenes A and B, were isolated from the fermentation broth of the strain. Here, we present its genome sequence, which contains 7,990,492 bp with a G+C content of 70.46% and harbors 7088 protein-encoding genes. The genome sequence analysis revealed the presence of a 28,787 bp gene cluster encoding for 24 open reading frames including 1,3,6,8-tetrahydroxynaphthalene synthase and monooxygenase, seven phenazine biosynthesis proteins, two prenyltransferases and a squalene-hopene cyclase. These genes are known to be necessary for the biosynthesis of both marfuraquinocins and phenaziterpenes. Outside the gene cluster (and scattered around the genome), there are seven genes belonging to the methylerythritol phosphate pathway for the biosynthesis of the essential primary metabolite, isopentenyl diphosphate, as well as six geranyl diphosphate/farnesyl diphosphate synthase genes. The strain S. niveus SCSIO 3406 showed type I PKS, type III PKS and nonribosomal peptide synthetase cluster. The sequence will provide the genetic basis for better understanding of biosynthesis mechanism of the above mentioned six compounds and for the construction of improved strain for the industrial production of antimicrobial agents.