Clinical application of reserved gastric tube in neuroendoscopic endonasal surgery for pituitary tumor.

BACKGROUND: The neuroendoscopic approach has the advantages of a clear operative field, convenient tumor removal, and less damage, and is the development direction of modern neurosurgery. At present, transnasal surgery for sphenoidal pituitary tumor is widely used. But it has been found in clinical practice that some patients with this type of surgery may experience post-operative nausea and vomiting and other discomforts. AIM: To explore the effect of reserved gastric tube application in the neuroendoscopic endonasal resection of pituitary tumors. METHODS: A total of 60 patients who underwent pituitary adenoma resection via the endoscopic endonasal approach were selected and randomly divided into the experimental and control groups, with 30 in each group. Experimental group: After anesthesia, a gastric tube was placed through the mouth under direct vision using a visual laryngoscope, and the fluid accumulated in the oropharynx was suctioned intermittently with low negative pressure throughout the whole process after nasal disinfection, during the operation, and when the patient recovered from anesthesia. Control group: Given the routine intraoperative care, no gastric tube was left. The number of cases of nausea/vomiting/aspiration within 24 h post-operation was counted and compared between the two groups; the scores of pharyngalgia after waking up, 6 h post-operation, and 24 h post-operation. The frequency of postoperative cerebrospinal fluid leakage and intracranial infection were compared. The hospitalization days of the two groups were statistically compared. RESULTS: The times of postoperative nausea and vomiting in the experimental group were lower than that in the control group, and the difference in the incidence of nausea was statistically significant (P < 0.05). After the patient woke up, the scores of sore throat 6 h after the operation and 24 h after operation were lower than those in the control group, and the difference was statistically significant (P < 0.05). The number of cases of postoperative cerebrospinal fluid leakage and intracranial infection was higher than that of the control group, but there was no statistically significant difference from the control group (P > 0.05). The hospitalization days of the experimental group was lower than that of the control group, and the difference was statistically significant (P < 0.05). CONCLUSION: Reserving a gastric tube in the endoscopic endonasal resection of pituitary tumors, combined with intraoperative and postoperative gastrointestinal decompression, can effectively reduce the incidence of nausea, reduce the number of vomiting and aspiration in patients, and reduce the complications of sore throat The incidence rate shortened the hospitalization days of the patients.

Comparison of the efficacy of neuronavigation-assisted intracerebral hematoma puncture and drainage with neuroendoscopic hematoma removal in treatment of hypertensive cerebral hemorrhage.

OBJECTIVE: To compare neuronavigation-assisted intracerebral hematoma puncture and drainage with neuroendoscopic hematoma removal for treatment of hypertensive cerebral hemorrhage. METHOD: Ninety-one patients with hypertensive cerebral hemorrhage admitted to our neurosurgery department from June 2022 to May 2023 were selected: 47 patients who underwent endoscopic hematoma removal with the aid of neuronavigation in observation Group A and 44 who underwent intracerebral hematoma puncture and drainage in control Group B. The duration of surgery, intraoperative bleeding, hematoma clearance rate, pre- and postoperative GCS score, National Institutes of Health Stroke Scale (NIHSS) score, mRS score and postoperative complications were compared between the two groups. RESULTS: The duration of surgery, intraoperative bleeding and hematoma clearance were significantly lower in Group B than in Group A (p < 0.05). Conversely, no significant differences in the preoperative, 7-day postoperative, 14-day postoperative or 1-month postoperative GCS or NIHSS scores or the posthealing mRS score were observed between Groups A and B. However, the incidence of postoperative complications was significantly greater in Group B than in Group A (p < 0.05), with the most significant difference in incidence of intracranial infection (p < 0.05). CONCLUSION: Both neuronavigation-assisted intracerebral hematoma puncture and drainage and neuroendoscopic hematoma removal are effective at improving the outcome of patients with hypertensive cerebral hemorrhage. The disadvantage of neuronavigation is that the incidence of complications is significantly greater than that of other methods; postoperative care and prevention of complications should be strengthened in clinical practice.

Spatiotemporal Controllable Sono-Nanovaccines Driven by Free-Field Based Whole-Body Ultrasound for Personalized Cancer Therapy.

Therapeutic cancer vaccines fail to produce satisfactory outcomes against solid tumors since vaccine-induced anti-tumor immunity is significantly hampered by immunosuppression. Generating an in situ cancer vaccine targeting immunological cold tumor microenvironment (TME) appears attractive. Here, a type of free-field based whole-body ultrasound (US)-driven nanovaccines are constructed, named G5-CHC-R, by conjugating the sonosensitizer, Chenghai chlorin (CHC) and the immunomodulator, resiquimod (R848) on top of a super small-sized dendrimeric nanoscaffold. Once entering tumors, R848 can be cleaved from a hypoxia-sensitive linker, thus modifying the TME via converting macrophage phenotypes. The animals bearing orthotopic pancreatic cancer with intestinal metastasis and breast cancer with lung metastasis are treated with G5-CHC-R under a free-field based whole-body US system. Benefit from the deep penetration capacity and highly spatiotemporal selectiveness, G5-CHC-R triggered by US represented a superior alternative for noninvasive irradiation of deep-seated tumors and magnification of local immune responses via driving mass release of tumor antigens and "cold-warm-hot" three-state transformation of TME. In addition to irradiating primary tumors, a robust adaptive anti-tumor immunity is potentiated, leading to successful induction of systemic tumor suppression. The sono-nanovaccines with good biocompatibility posed wide applicability to a broad spectrum of tumors, revealing immeasurable potential for translational research in oncology.

A General and Convenient Peptide Self-Assembling Mechanism for Developing Supramolecular Versatile Nanomaterials Based on The Biosynthetic Hybrid Amyloid-Resilin Protein.

Self-assembling peptides are valuable building blocks to fabricate supramolecular biomaterials, which have broad applications from biomedicine to biotechnology. However, limited choices to induce different globular proteins into hydrogels hinder these designs. Here, an easy-to-implement and tunable self-assembling strategy, which employs Ure2 amyloidogenic peptide, are described to induce any target proteins to assemble into supramolecular hydrogels alone or in combination with notable compositional control. Furthermore, the collective effect of nanoscale interactions among amyloid nanofibrils and partially disordered elastomeric polypeptides are investigated. This led to many useful macroscopic material properties simultaneously emerging from one pure protein material, i.e. strong adhesion to any substrates under wet conditions, rapidly self--assembling into robust and porous hydrogels, adaptation to remodeling processes, strongly promoting cell adhesion, proliferation and differentiation. Moreover, he demonstrated this supramolecular material's robust performance in vitro and vivo for tissue engineering, cosmetic and hemostasis applications and exhibited superior performance compared to corresponding commercial counterparts. To the best of his knowledge, few pure protein-based materials could meet such seemingly mutually exclusive properties simultaneously. Such versatility renders this novel supramolecular nanomaterial as next-generation functional protein-based materials, and he demonstrated the sequence level modulation of structural order and disorder as an untapped principle to design new proteins.

[Retracted] Isoquercitrin inhibits bladder cancer progression in vitro and in vivo by regulating the PI3K/Akt and PKC signaling pathways.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the agarose gel electrophoretic bands shown in Fig. 4A for PKC were strikingly similar to bands that had already appeared in another article written by different authors at different research institutes. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 36: 165­172, 2016; DOI: 10.3892/or.2016.4794].

"In situ bone flap" combined with vascular pedicled mucous flap to reconstruction of skull base defect.

BACKGROUND: At present, neuroendoscopy technology has made rapid development, and great progress has been made in the operation of lesions in the saddle area of the skull base. However, the complications of cerebrospinal fluid and intracranial infection after the operation are still important and life-threatening complications, which may lead to poor prognosis. AIM: To investigate the method of in situ bone flap combined with nasal septum mucosal flap for reconstruction of enlarged skull base defect by endonasal sphenoidal approach and to discuss its application effect. METHODS: Clinical data of 24 patients undergoing transnasal sphenoidal endoscopic approach in the Department of Neurosurgery, Affiliated 2 Hospital of Nantong University from January 2019 to December 2022 were retrospectively analyzed. All patients underwent multi-layer reconstruction of skull base using in situ bone flap combined with nasal septum mucosa flap. The incidence of intraoperative and postoperative cerebrospinal fluid leakage and intracranial infection were analyzed, and the application effect and technical key points of in situ bone flap combined with nasal septum mucosa flap for skull base bone reconstruction were analyzed. RESULTS: There were 5 cases of high flow cerebrospinal fluid (CSF) leakage and 7 cases of low flow CSF leakage. Postoperative cerebrospinal fluid leakage occurred in 2 patients (8.3%) and intracranial infection in 2 patients (8.3%), which were cured after strict bed rest, continuous drainage of lumbar cistern combined with antibiotic treatment, and no secondary surgical repair was required. The patients were followed up for 8 to 36 months after the operation, and no delayed cerebrospinal fluid leakage or intracranial infection occurred during the follow-up. Computed tomography reconstruction of skull base showed satisfactory reconstruction after surgery. CONCLUSION: The use of in situ bone flap combined with vascular pedicled mucous flap to reconstruction of skull base defect after endonasal sphenoidal approach under neuroendoscopy has a lower incidence of cerebrospinal fluid leakage and lower complications, which has certain advantages and is worthy of clinical promotion.

Discovery of a Novel Ubenimex Derivative as a First-in-Class Dual CD13/Proteasome Inhibitor for the Treatment of Cancer.

The CD13 inhibitor ubenimex is used as an adjuvant drug with chemotherapy for the treatment of cancer due to its function as an immunoenhancer, but it has limitations in its cytotoxic efficacy. The proteasome inhibitor ixazomib is a landmark drug in the treatment of multiple myeloma with a high anti-cancer activity. Herein, we conjugated the pharmacophore of ubenimex and the boric acid of ixazomib to obtain a dual CD13 and proteasome inhibitor 7 (BC-05). BC-05 exhibited potent inhibitory activity on both human CD13 (IC50 = 0.13 µM) and the 20S proteasome (IC50 = 1.39 µM). Although BC-05 displayed lower anti-proliferative activity than that of ixazomib in vitro, an advantage was established in the in vivo anti-cancer efficacy and prolongation of survival time, which may be due to its anti-metastatic and immune-stimulating activity. A pharmacokinetic study revealed that BC-05 is a potentially orally active agent with an F% value of 24.9%. Moreover, BC-05 showed more favorable safety profiles than those of ixazomib in preliminary toxicity studies. Overall, the results indicate that BC-05 is a promising drug candidate for the treatment of multiple myeloma.

Positioning and design by computed tomography imaging in neuroendoscopic surgery of patients with chronic subdural hematoma.

BACKGROUND: Neuroendoscopy is a very useful technique to Chronic Subdural Hematoma (CSH). But how to achieve the goal of treatment more minimally invasive? AIM: To develop a simple, fast and accurate preoperative planning method in our way for endoscopic surgery of patients with CSH. METHODS: From June 2018 to May 2020, forty-two patients with CSH, admitted to our hospital, were performed endoscopic minimally invasive surgery; computed tomography (CT) imaging was employed to locate the intracerebral hematoma and select the appropriate endoscopic approach before the endoscopic surgery. The clinical data and treatment efficacy were analyzed. RESULTS: According to the learning of CT scanning images, the surgeon can accurately design the best minimally invasive neuroendoscopic surgical approach and realize the precise positioning and design of the drilling site of the skull and the size of the bone window, so as to provide the most effective operation space with the smallest bone window. In this group, the average operation time was only about 1 h, and the clearance rate of hematoma was about 95%. CONCLUSION: Patients with CSH can achieve good therapeutic effect by using our way to positioning and design to assist the operation of CSH according to CT scan and image, and our way is very useful and necessary.

Discovery of [5,5'-bibenzo[d][1,3]dioxol]-6-substituted amine derivatives as potent proprotein convertase subtilisin/kexin type 9 inhibitors.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a promising therapeutic target for the treatment of hyperlipidemia. In discovery of novel small molecules that interfere PCSK9/LDLR protein-protein interaction (PPI), structural modification was performed based on our previously derived compounds. A series of [5,5'-bibenzo[d][1,3]dioxol]-6-amine analogs were designed and synthesized for the activity evaluation. In the PCSK9/LDLR PPI impairing test, molecules D28 and D29, exhibited remarkable inhibitory potency with IC50 values of 8.30 and 6.70 µM compared with SBC-115337 (17.89 µM), respectively. Molecular docking predicted the binding pattern of compounds D28 and D29 in the LDLR binding site of PCSK9. Hydrophobic interactions play an important role in the binding of aromatic molecular fragments to the pockets in the PCSK9/LDLR binding interface. Further LDLR expression and LDL uptake studies revealed that both D28 and D29 restored LDLR expression on the surface of hepatic HepG2 cells and improved extracellular LDL uptake in the presence of PCSK9. It is significant that molecules D28 and D29 exhibited potential for the treatment of hyperlipidemia in current in vitro investigations. Generally, lead compounds with novel structures were developed in the present study for further design of lipid-lowering molecules by targeting PCSK9/LDLR PPI.

Vermicomposting of Pleurotus eryngii spent mushroom substrates and the possible mechanisms of vermicompost suppressing nematode disease caused by Meloidogyne incognita.

The mushroom industry produces a large amount of spent mushroom substrate (SMS), which requires a large geographical footprint and causes pollution. Vermicomposting is a low-cost technology for its value in recycling of organic wastes and production of beneficial organic fertilizers. In this study, the changes of physicochemical properties was characterized during vermicomposting of Pleurotus eryngii SMS with cow dung (CD) as amendment. The efficiency and possible mechanisms of vermicompost suppressing disease induced by Meloidogyne incognita was also investigated. Six combinations with different ratios of SMS and cow dung (CD) was included in the vermicomposting using Eisenia fetida. Effect of vermicompost against disease induced by M. incognita on tobacco was conducted under greenhouse condition. And the possible mechanisms of vermicompost suppressing M. incognita was investigated by evaluated the species diversity of nematode-trapping fungi (NTF) in soil, and the defense response enzymes in tobacco. The combination of 65% SMS +35% CD was more suitable for vermicomposting, in which the highest vermicompost production (57%) and earthworm biomass increment (268%) were achieved. Additionally, the reduction in pH, total organic carbon, carbon: nitrogen ratio, and the pronounced elevation in four overall nutrient status were also observed. Soil amended with vermicompost (100:1 w/w) showed 61% control efficiency against nematode disease caused by M. incognita on tobacco, which significantly higher than that of the normal compost (24%). Comparing to the normal compost, the potential mechanism of vermicompost suppressing M. incognita could be rely on promoting species diversity of NTF in soil and enhancing the activities of the defense response enzymes in tobacco plant. Our findings indicate that vermicomposting is a promising technology for recycling of P. eryngii SMS, and the resulting vermicompost as organic fertilizer can be sued for management of the diseases caused by root-knot nematodes. This study establish a sustainable avenue for P. eryngii SMS disposal and a practical manner for controlling pathogens.

Design, Synthesis, and Anti-Cancer Evaluation of Novel Cyclic Phosphate Prodrug of Gemcitabine.

ProTide and cyclic phosphate ester are two successful prodrug technologies to overcome the limitations of nucleoside drugs, among which the cyclic phosphate ester strategy has not been widely used in the optimization of gemcitabine. Herein, we designed a series of novel ProTide and cyclic phosphate ester prodrugs of gemcitabine. Cyclic phosphate ester derivative 18c exhibits much higher anti-proliferative activity than positive control NUC-1031 with IC50s of 3.6-19.2 nM on multiple cancer cells. The metabolic pathway of 18c demonstrates that 18c's bioactive metabolites prolong its anti-tumor activity. More importantly, we separated the two P chiral diastereomers of gemcitabine cyclic phosphate ester prodrugs for the first time, revealing their similar cytotoxic potency and metabolic profile. 18c displays significant in vivo anti-tumor activity in both 22Rv1 and BxPC-3 xenograft tumor models. These results suggest that compound 18c is a promising anti-tumor candidate for treating human castration-resistant prostate and pancreatic cancer.

Nanomedicine for Combination Urologic Cancer Immunotherapy.

Urologic cancers, particularly kidney, bladder, and prostate cancer, have a growing incidence and account for about a million annual deaths worldwide. Treatments, including surgery, chemotherapy, radiotherapy, hormone therapy, and immunotherapy are the main therapeutic options in urologic cancers. Immunotherapy is now a clinical reality with marked success in solid tumors. Immunological checkpoint blockade, non-specific activation of the immune system, adoptive cell therapy, and tumor vaccine are the main modalities of immunotherapy. Immunotherapy has long been used to treat urologic cancers; however, dose-limiting toxicities and low response rates remain major challenges in the clinic. Herein, nanomaterial-based platforms are utilized as the "savior". The combination of nanotechnology with immunotherapy can achieve precision medicine, enhance efficacy, and reduce toxicities. In this review, we highlight the principles of cancer immunotherapy in urology. Meanwhile, we summarize the nano-immune technology and platforms currently used for urologic cancer treatment. The ultimate goal is to help in the rational design of strategies for nanomedicine-based immunotherapy in urologic cancer.

1,25-D3 attenuates cerebral ischemia injury by regulating mitochondrial metabolism via the AMPK/AKT/GSK3ß pathway.

The brain injury caused by cerebral ischemia-reperfusion is related to mitochondrial damage. Maintaining the normal function of mitochondria, promoting angiogenesis, protecting neuronal cells, and resisting oxidative stress are the keys to functional recovery after acute ischemic stroke. In this study, we established a middle cerebral artery occlusion (MCAO) model and investigated the effects of 1α,25-dihydroxyvitamin D3 (VitD or 1,25-D3) on mitochondrial function via the adenosine 5'-monophosphate-activated protein kinase (AMPK)/protein kinase B (AKT)/glycogen synthase kinase-3ß (GSK-3ß) signaling pathway in rats with cerebral ischemia-reperfusion injury. The neurological function and infarct size were measured in each group. Hematoxylin-eosin, neuronal nucleus, and Nissl staining procedures were conducted to observe the morphology and number of the cerebral cortical neurons. Western blotting was then used to analyze p-AMPK, vitamin D receptor (VDR), p-GSK-3ß, p-AKT, P53, cytochrome C (CytC), TGF-ß, and vascular endothelial growth factor (VEGF) in mitochondria. Immunofluorescence staining was used to observe the expression of CytC and caspase-3. Succinate dehydrogenase, ATPase, reactive oxygen species, and malondialdehyde were detected by kits. RT-qPCR was used to analyze TGF-ß, VEGF, P53, and CytC mRNA. The results revealed that the cerebral infarct volume, neurological function score, apoptotic protein P53, CytC, caspase-3, reactive oxygen species, and malondialdehyde were significantly increased in MCAO rats. 1,25-D3 reduced the infarct size and neurological function score, activated VDR, upregulated TGF-ß, p-AMPK, p-AKT, p-GSK-3ß, VEGF, ATP, and succinate dehydrogenase, and downregulated P53, CytC, caspase-3, reactive oxygen species, and malondialdehyde. As an antagonist of VDRs, pyridoxal-5-phosphate could partially block the neuroprotective effect of 1,25-D3. In conclusion, 1,25-D3 activated AMPK/AKT/GSK-3ß signaling and VDRs, inhibited P53, CytC, and caspase-3, increased TGF-ß and VEGF, regulated mitochondrial metabolism, reduced neuronal apoptosis, promoted vascular growth, and exerted neuroprotective effects. These findings suggest that this signaling pathway may be an effective target for the treatment of ischemic stroke.

WY-14643 attenuates lipid deposition via activation of the PPARα/CPT1A axis by targeting Gly335 to inhibit cell proliferation and migration in ccRCC.

BACKGROUND: Histologically, cytoplasmic deposits of lipids and glycogen are common in clear cell renal cell carcinoma (ccRCC). Owing to the significance of lipid deposition in ccRCC, numerous trials targeting lipid metabolism have shown certain therapeutic potential. The agonism of peroxisome proliferator-activated receptor-α (PPARα) via ligands, including WY-14,643, has been considered a promising intervention for cancers. METHODS: First, the effects of WY-14,643 on malignant behaviors were investigated in ccRCC in vitro. After RNA sequencing, the changes in lipid metabolism, especially neutral lipids and glycerol, were further evaluated. Finally, the underlying mechanisms were revealed. RESULTS: Phenotypically, the proliferation and migration of ccRCC cells treated with WY-14,643 were significantly inhibited in vitro. A theoretical functional mechanism was proposed in ccRCC: WY-14,643 mediates lipid consumption by recognizing carnitine palmitoyltransferase 1 A (CPT1A). Activation of PPARα using WY-14,643 reduces lipid deposition by increasing the CPT1A level, which also suppresses the NF-κB signaling pathway. Spatially, WY-14,643 binds and activates PPARα by targeting Gly335. CONCLUSION: Overall, WY-14,643 suppresses the biological behaviors of ccRCC in terms of cell proliferation, migration, and cell cycle arrest. Furthermore, its anticancer properties are mediated by the inhibition of lipid accumulation, at least in part, through the PPARα/CPT1A axis by targeting Gly335, as part of the process, NF-κB signaling is also suppressed. Pharmacological activation of PPARα might offer a new treatment option for ccRCC.

Microenvironment immune response induced by tumor ferroptosis-the application of nanomedicine.

Ferroptosis is a non-apoptotic regulatory form of cell death that has sparked significant interest and research in cancer treatment and certain small chemical inducers have been used in the clinic. These inducers's weak water solubility, poor targeting, rapid metabolism; and other undesirable characteristics; however, for therapeutic approaches that combine immunotherapy and ferroptosis, challenges such as medication delivery, the complexity of the tumor microenvironment, and immunosuppression remain. The targeted, low toxicity, and efficient distribution benefits of nanotechnology have considerably enhanced the therapeutic efficacy of combining immunotherapy with ferroptosis. This paper describes the distinct mechanism of ferroptosis in tumor therapy and immunotherapy, as well as the application and benefits of nanotechnology in the combination of tumor immunotherapy and ferroptosis. Systematic review registration: http://clinicaltrials.gov/, NCT00941070.

Targeting feedback activation of signaling transduction pathways to overcome drug resistance in cancer.

Dysregulation or aberrant signaling transduction contributes to tumorigenesis. Targeting these abnormal signaling pathways becomes an effective anticancer strategy. However, feedback activation or crosstalk between signaling pathways drives adaptive drug resistance which causes failure of cancer therapy. In this review article, we summarized treatments that cause feedback activation of AKT, ERK, STAT3, EGFR, FGFR, and HER2/3 signaling pathways and the combination therapy to enhance anti-tumor effect or to overcome drug resistance, to explore the underlying mechanisms that define the protein molecules participated or regulated the feedback activation. In addition, we reviewed clinical trials that employ combination treatments to suppress feedback activation and improve therapeutic efficacy of cancer treatments.

Clinical value and molecular mechanism of AQGPs in different tumors.

Aquaglyceroporins (AQGPs), including AQP3, AQP7, AQP9, and AQP10, are transmembrane channels that allow small solutes across biological membranes, such as water, glycerol, H2O2, and so on. Increasing evidence suggests that they play critical roles in cancer. Overexpression or knockdown of AQGPs can promote or inhibit cancer cell proliferation, migration, invasion, apoptosis, epithelial-mesenchymal transition and metastasis, and the expression levels of AQGPs are closely linked to the prognosis of cancer patients. Here, we provide a comprehensive and detailed review to discuss the expression patterns of AQGPs in different cancers as well as the relationship between the expression patterns and prognosis. Then, we elaborate the relevance between AQGPs and malignant behaviors in cancer as well as the latent upstream regulators and downstream targets or signaling pathways of AQGPs. Finally, we summarize the potential clinical value in cancer treatment. This review will provide us with new ideas and thoughts for subsequent cancer therapy specifically targeting AQGPs.

Nocardioides nematodiphilus sp. nov., isolated from rhizosphere of Arabidopsis thaliana.

An actinobacterial strain, designated R-N-C8T, was isolated from the rhizosphere soil of Arabidopsis thaliana collected in Yunnan Province, south-west China. Based on the results of 16S rRNA gene sequence analysis, strain R-N-C8T had highest similarity to Nocardioides terrae CGMCC 1.7056T (96.5%), Nocardioides opuntiae KCTC 19804T (96.3%) and Nocardioides currus IB-3T (96.1%), and lower than 96.0 % similarity to other members of the genus Nocardioides. Phylogenetic trees based on 16S rRNA gene sequences indicated that strain R-N-C8T formed an isolated branch with N. terrae CGMCC 1.7056T and N. opuntiae KCTC 19804T. The polar lipids contained phosphatidylglycerol, diphosphatidylglycerol, one unidentified phosphoglycolipid and four unidentified phospholipids in the cellular membrane. The major fatty acids were identified as iso-C16 : 0, anteiso-C17 : 0, iso-C17 : 0, summed feature 9 (iso-C17 : 1 ω9c and/or C16 : 0 10-methyl) and iso-C15 : 0. The predominant respiratory quinone was MK-8(H4) and ll-diaminopimelic acid was the diagnostic diamino acid in the cell-wall peptidoglycan. The genomic DNA G+C content was 70.9 mol%. The orthologous average nucleotide identiy values between N. terrae CGMCC 1.7056T, N. currus IB-3T and strain R-N-C8T were 77.1 and 75.1 %, respectively. DNA-DNA hybridization values between N. terrae CGMCC 1.7056T, N. currus IB-3T and strain R-N-C8T were 20.7 and 19.9 % respectively. Data from phenotypic and genotypic analyses supported that strain R-N-C8T represents a new species of Nocardioides, for which the name Nocardioides nematodiphilus sp. nov. is proposed. The type strain is R-N-C8T (=CGMCC 1.18723T= KCTC 49528T).

ZBTB7A, a miR-144-3p targeted gene, accelerates bladder cancer progression via downregulating HIC1 expression.

BACKGROUND: Zinc finger and BTB domain-containing 7A (ZBTB7A) is a member of the POK family of transcription factors that plays an oncogenic or tumor-suppressive role in different cancers depending on the type and genetic context of cancer. However, the function and molecular mechanism of ZBTB7A in bladder cancer (BC) remain elusive. METHODS: The role of ZBTB7A in bladder cancer was detected by colony formation, transwell, and tumor formation assays. The expression levels of ZBTB7A, HIC1, and miR-144-3p were analyzed by qRT-PCR and Western blot. Bioinformatics analysis and a dual-luciferase reporter assay were used to assess the effect of ZBTB7A on the promoter activity of HIC1. RESULTS: The present study revealed that knockdown of ZBTB7A suppressed BC cell growth and migration, as indicated by an approximately 50% reduction in the number of colonies and an approximately 70% reduction in the number of migrated cells. Loss of ZBTB7A inhibited tumor growth in vivo, resulting in a 75% decrease in tumor volume and an 80% decrease in tumor weight. Further mechanistic studies revealed that ZBTB7A bound to the hypermethylated in cancer 1 (HIC1) promoter and downregulated HIC1 expression, accelerating the malignant behavior of BC. Increased expression of ZBTB7A in BC tissues was negatively corrected with the expression of HIC1. Moreover, ZBTB7A was a target of miR-144-3p, which decreased ZBTB7A expression in BC. CONCLUSION: Our data demonstrate that ZBTB7A, a targeted gene of miR-144-3p, promoted tumorigenesis of BC through downregulating HIC1 expression.