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Article ; Online: Macrofibers with tunable mechanical performance and reversible rotational motion based on a bacterial cellulose hydrogel film

Fu, Feiya / Chen, Qinqin / Chen, Lihuan / Cai, Shaojie / Lan, Yuxin / Pan, Zijun / Li, Haidong / Yao, Juming / Liu, Xiangdong

Colloids and Surfaces A: Physicochemical and Engineering Aspects. 2023 Aug. 09, p.132195-

2023 , Page(s) 132195–

Abstract: Mechanically twisting a yarn is a useful and important method for creating internal stress, changing macromolecular orientation, and affording interesting fiber properties, including mechanical, structural, physical and chemical properties. Bacterial ... ...

Abstract	Mechanically twisting a yarn is a useful and important method for creating internal stress, changing macromolecular orientation, and affording interesting fiber properties, including mechanical, structural, physical and chemical properties. Bacterial cellulose (BC) nanofibers are a new type of highly crystalline bionanofibers exhibiting excellent intrinsic mechanical properties. Herein, BC macrofibers with a diameter of 0.35–0.53mm were prepared from BC hydrogel films using a two-step technique involving drying and twisting processes. Moreover, the effects of the drying method (oven- and freeze-drying) and those of the processing steps on the morphologies, structures, and physicochemical properties of the macrofibers were investigated. Results indicated that only the wet twisting–first process affords continuous macrofibers with a compact and uniform structure. The tensile strength and elongation at break of the macrofibers were 199MPa and 24%, respectively. Furthermore, by introducing graphene oxide (GO) to the macrofibers, a photothermal and moisture actuator was facilely constructed, which could produce a twisting motion of 0.39rpm and an untwisting motion of 0.6rpm. This study provides insights into methods to easily alter the properties of BC macrofibers, which is pivotal for the macrofiber’s potential application in intelligent devices.
Keywords	cellulose ; freeze drying ; graphene oxide ; hydrogels ; nanofibers ; tensile strength ; bacterial cellulose ; macrofibers ; processing methods ; mechanical properties ; photothermal responsiveness ; moisture responsiveness
Language	English
Dates of publication	2023-0809
Publishing place	Elsevier B.V.
Document type	Article ; Online
Note	Pre-press version
ZDB-ID	1500517-3
ISSN	0927-7757
ISSN	0927-7757
DOI	10.1016/j.colsurfa.2023.132195
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: PAG neuronal NMDARs activation mediated morphine-induced hyperalgesia by HMGB1-TLR4 dependent microglial inflammation.

Mo, Jingjing / Lu, Zijing / Peng, Jialing / Li, Xiang-Pen / Lan, Lihuan / Wang, Hongxuan / Peng, Ying

Journal of psychiatric research

2023 Volume 164, Page(s) 150–161

Abstract: Morphine is one of the most effective and widely used analgesic drugs. However, chronic morphine use caused opioid-induced hyperalgesia (OIH). The development of OIH limits the use of morphine. The mechanisms of OIH are not fully understood. Toll-like ... ...

Abstract	Morphine is one of the most effective and widely used analgesic drugs. However, chronic morphine use caused opioid-induced hyperalgesia (OIH). The development of OIH limits the use of morphine. The mechanisms of OIH are not fully understood. Toll-like receptor4 (TLR4) and glutamate receptors in the periaqueductal gray (PAG) are critical in OIH, however, the association between TLR4 and N-methyl-D-aspartate Receptors (NMDARs) activation in PAG remains unclear. Microglia activation, increased TLR4/p65 nuclear factor-kappa B (p65 NF-κB) and proinflammatory cytokines in microglia, and phosphorylation of NMDAR1 subunit (NR1) and NMDAR2B subunit (NR2B) in neurons were observed in PAG of OIH mice. Up-regulations of TLR4/p65 NF-κB and proinflammatory cytokines (IL-1β, IL-6, TNF-α) in BV2 cells were prevented by inhibiting and knocking down TLR4. By inhibiting myeloid differentiation factor 2 (MD2) and knocking down the High-mobility group box 1 (HMGB1), we found that morphine activated TLR4 by HMGB1 but not MD2. We co-cultured Neuro-2a (N2A) with BV2 microglial cell line and found that instead of directly phosphorylating NMDAR subunits, morphine increased the phosphorylation of NR1 and NR2B by inducing TLR4-mediated microglia inflammation. Knocking TLR4 out of PAG by Lentivirus-GFP-TLR4 shRNA reversed these changes and relieved OIH. Our findings suggested that the secretion of HMGB1 induced by morphine-activated TLR4 in microglia, and the proinflammatory factors released by activated microglia phosphorylated NR1 and NR2B of adjacent neurons, induced increased neuronal excitability. In conclusion, TLR4/NMDARs in PAG were involved in the development and maintenance of OIH and supported novel strategies for OIH treatment.
MeSH term(s)	Mice ; Animals ; Morphine/adverse effects ; Morphine/metabolism ; Hyperalgesia/chemically induced ; Hyperalgesia/metabolism ; NF-kappa B/metabolism ; Microglia/metabolism ; Toll-Like Receptor 4/metabolism ; Periaqueductal Gray/metabolism ; Signal Transduction ; HMGB1 Protein/adverse effects ; HMGB1 Protein/metabolism ; Inflammation/chemically induced ; Inflammation/metabolism ; Analgesics, Opioid/adverse effects ; Cytokines/metabolism ; Neurons
Chemical Substances	Morphine (76I7G6D29C) ; NF-kappa B ; Toll-Like Receptor 4 ; HMGB1 Protein ; Analgesics, Opioid ; Cytokines
Language	English
Publishing date	2023-06-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3148-3
ISSN	1879-1379 ; 0022-3956
ISSN (online)	1879-1379
ISSN	0022-3956
DOI	10.1016/j.jpsychires.2023.05.082
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Article ; Online: Morphine-induced microglial immunosuppression via activation of insufficient mitophagy regulated by NLRX1.

Peng, Jialing / Pan, Jingrui / Wang, Hongxuan / Mo, Jingjing / Lan, Lihuan / Peng, Ying

Journal of neuroinflammation

2022 Volume 19, Issue 1, Page(s) 87

Abstract: Background: Chronic morphine exposure induces immunosuppression in the peripheral and central nervous system, resulting in susceptibility of patients to invading pathogens. Mitophagy is a crucial regulator of inflammation, and dysregulated mitophagy may ...

Abstract	Background: Chronic morphine exposure induces immunosuppression in the peripheral and central nervous system, resulting in susceptibility of patients to invading pathogens. Mitophagy is a crucial regulator of inflammation, and dysregulated mitophagy may cause immunosuppression, but whether mitophagy is linked with morphine-induced immunosuppression in the brain remains unknown. NLRX1 is the only mitochondrially localized NOD family receptor protein which serves as a critical regulator in immunity and mitophagy activation, but it remains an enigma how NLRX1 functions in the crosstalk between microglial inflammatory defense and mitophagy in the presence of morphine. Methods: Primary microglia and astrocytes, BV2 and MA cell lines were utilized. Mice were stimulated with repeated morphine treatment to mimic chronic morphine exposure, and activation of mitophagy, lysosomal functions, and inflammation were assayed in specific brain regions and immune organs with or without NLRX1-silencing. Results: Morphine induced microglial mitophagy in a LC3 (microtubule-associated proteins light chain 3)-dependent manner, which was mediated by NLRX1. Contrastingly, morphine impaired lysosomal functions, including generation, acidification and mitophagosome-lysosome fusion, thus leading to insufficient mitophagy activation in microglia. NLRX1-silencing inhibited mitophagy activity and rescued lysosomal functions including generation and acidification in microglia. The NLRX1-mediated incomplete mitophagy in microglial cells contributed to immunosuppression and vulnerability towards pathogenic challenge after morphine treatment. In vivo, NLRX1-mediated microglial mitophagy activation by morphine was mainly located in the murine brain cortex, striatum, and cerebellum, where NLRX1 functioned as a negative immune regulator and facilitated septic shock. Collectively, microglial immune responses to septic shock were amenable to NLRX1 silencing in the brain with morphine treatment. Conclusion: Morphine activated insufficient mitophagy in microglia which was regulated by NLRX1, ultimately leading to host immunosuppression and susceptible conditions in the brain.
MeSH term(s)	Animals ; Humans ; Immunosuppression Therapy ; Mice ; Mice, Inbred NOD ; Microglia/metabolism ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; Mitophagy ; Morphine/toxicity ; Shock, Septic/metabolism ; Shock, Septic/pathology
Chemical Substances	Mitochondrial Proteins ; NLRX1 protein, human ; NLRX1 protein, mouse ; Morphine (76I7G6D29C)
Language	English
Publishing date	2022-04-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-022-02453-7
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Article: Ototoxicity of polystyrene nanoplastics in mice, HEI-OC1 cells and zebrafish.

Wu, Yuancheng / Li, Lianzhen / Tang, Lihuan / Peijnenburg, Willie / Zhang, Huangruici / Xie, Daoli / Geng, Ruishuang / Zheng, Tihua / Bi, Liyan / Wei, Xiaodan / Chae, Han-Jung / Wang, Lan / Zhao, Li / Li, Bo / Zheng, Qingyin

Frontiers in molecular neuroscience

2024 Volume 17, Page(s) 1345536

Abstract: Polystyrene nanoplastics are a novel class of pollutants. They are easily absorbed by living organisms, and their potential toxicity has raised concerns. However, the impact of polystyrene nanoplastics on auditory organs remains unknown. Here, our ... ...

Abstract	Polystyrene nanoplastics are a novel class of pollutants. They are easily absorbed by living organisms, and their potential toxicity has raised concerns. However, the impact of polystyrene nanoplastics on auditory organs remains unknown. Here, our results showed that polystyrene nanoplastics entered the cochlea of mice, HEI-OC1 cells, and lateral line hair cells of zebrafish, causing cellular injury and increasing apoptosis. Additionally, we found that exposure to polystyrene nanoplastics resulted in a significant elevation in the auditory brainstem response thresholds, a loss of auditory sensory hair cells, stereocilia degeneration and a decrease in expression of Claudin-5 and Occludin proteins at the blood-lymphatic barrier in mice. We also observed a significant decrease in the acoustic alarm response of zebrafish after exposure to polystyrene nanoplastics. Mechanistic analysis revealed that polystyrene nanoplastics induced up-regulation of the Nrf2/HO-1 pathway, increased levels of malondialdehyde, and decreased superoxide dismutase and catalase levels in cochlea and HEI-OC1 cells. Furthermore, we observed that the expression of ferroptosis-related indicators GPX4 and SLC7A11 decreased as well as increased expression of ACLS4 in cochlea and HEI-OC1 cells. This study also revealed that polystyrene nanoplastics exposure led to increased expression of the inflammatory factors TNF-α, IL-1β and COX2 in cochlea and HEI-OC1 cells. Further research found that the cell apoptosis, ferroptosis and inflammatory reactions induced by polystyrene nanoplastics in HEI-OC1 cells was reversed through the pretreatment with N-acetylcysteine, a reactive oxygen species inhibitor. Overall, our study first discovered and systematically revealed the ototoxicity of polystyrene nanoplastics and its underlying mechanism.
Language	English
Publishing date	2024-02-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2024.1345536
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Article ; Online: Chronic exposure of alcohol triggers microglia-mediated synaptic elimination inducing cognitive impairment.

Lan, Lihuan / Wang, Hongxuan / Zhang, Xiaoni / Shen, Qingyu / Li, Xiangpen / He, Lei / Rong, Xiaoming / Peng, Jialing / Mo, Jingjing / Peng, Ying

Experimental neurology

2022 Volume 353, Page(s) 114061

Abstract: Background and aims: Long-term alcohol intake leads to cognitive impairment and dementia. The impairment of the cerebral cortex and limbic structures in alcoholics is associated with the loss of synapses instead of neurons. Synapse loss is considered to ...

Abstract	Background and aims: Long-term alcohol intake leads to cognitive impairment and dementia. The impairment of the cerebral cortex and limbic structures in alcoholics is associated with the loss of synapses instead of neurons. Synapse loss is considered to be an early and key feature of many neurodegenerative diseases, in which microglia-mediated synapse elimination is vital. However, the underlying mechanisms of synapse loss and cognitive impairment caused by long-term alcohol intake are still largely unknown. Methods: We investigated the relationship of synapse impairment, the microglial innate immune receptor-TREM2, and microglia-mediated synaptic elimination in long-term alcohol exposure. Results: We found that long-term alcohol exposure increased expression of TREM2, decreased expression of synaptic proteins and glutamate receptor subunits, reduced dendrite spine density, and impaired long-term potentiation (LTP) in the hippocampus. Minocycline reduced the amount of the postsynaptic marker PSD95 in microglia, attenuated dendrite spine density loss, and slow down the forgetting process of already-formed memory. Furthermore, we found that TREM2 participated in microglia-mediated synapse elimination in chronic alcohol exposure in vivo. Significantly fewer PSD95 were detectable in microglial phagolysosomes in TREM2 knockdown mice. Besides, TREM2 gene silencing ameliorated synapse loss, LTP impairment, and forgetting of remote memories. Conclusions: Our data suggests that TREM2 is associated with synaptic plasticity impairment and memory deficits, indicating microglia-mediated synaptic pruning might be the underlying mechanism involved in synapse loss and memory impairment induced by long-term alcohol intake. These findings provide new evidence for the receptor's participation in neurodegeneration diseases.
MeSH term(s)	Animals ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/metabolism ; Hippocampus/metabolism ; Membrane Glycoproteins/metabolism ; Memory Disorders/metabolism ; Mice ; Mice, Knockout ; Microglia/metabolism ; Neuronal Plasticity/physiology ; Receptors, Immunologic/metabolism ; Synapses/metabolism
Chemical Substances	Membrane Glycoproteins ; Receptors, Immunologic ; Trem2 protein, mouse
Language	English
Publishing date	2022-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2022.114061
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Article ; Online: Effect of alteplase versus aspirin plus clopidogrel in acute minor stroke.

Lan, Lihuan / Rong, Xiaoming / Shen, Qingyu / Gong, Hanxian / Li, Xiangpen / Wang, Hongxuan / Li, Mei / Pan, Jingrui / Zhang, Xiaoni / Peng, Ying

The International journal of neuroscience

2020 Volume 130, Issue 9, Page(s) 857–864

Abstract: Background and purpose: ...

Abstract	Background and purpose:
MeSH term(s)	Aged ; Aspirin/adverse effects ; Aspirin/pharmacology ; Clopidogrel/adverse effects ; Clopidogrel/pharmacology ; Drug Therapy, Combination ; Female ; Fibrinolytic Agents/adverse effects ; Fibrinolytic Agents/pharmacology ; Humans ; Intracranial Hemorrhages/chemically induced ; Ischemic Stroke/drug therapy ; Male ; Middle Aged ; Outcome Assessment, Health Care ; Platelet Aggregation Inhibitors/adverse effects ; Platelet Aggregation Inhibitors/pharmacology ; Retrospective Studies ; Severity of Illness Index ; Tissue Plasminogen Activator/adverse effects ; Tissue Plasminogen Activator/pharmacology
Chemical Substances	Fibrinolytic Agents ; Platelet Aggregation Inhibitors ; Clopidogrel (A74586SNO7) ; Tissue Plasminogen Activator (EC 3.4.21.68) ; Aspirin (R16CO5Y76E)
Language	English
Publishing date	2020-01-12
Publishing country	England
Document type	Comparative Study ; Journal Article
ZDB-ID	3061-2
ISSN	1563-5279 ; 1543-5245 ; 0020-7454
ISSN (online)	1563-5279 ; 1543-5245
ISSN	0020-7454
DOI	10.1080/00207454.2019.1707822
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Article: Validation and Factor Analysis of the Obsessive Compulsive Drinking Scale (OCDS) in the Chinese Population.

Wang, Hongxuan / Lan, Lihuan / Lan, Xiaochang / Chen, Peiyun / Liu, Gaoxin / Rong, Xiaoming / Liu, Lei / Kang, Chuan-Yi / Yang, Jianzhong / Guan, Yan-Zhong / Zhu, Xiao-Feng / Hu, Jian / Yang, Mei / Zheng, Dong / Peng, Ying

Frontiers in psychiatry

2021 Volume 12, Page(s) 770860

Abstract: Obsessive Compulsive Drinking Scale (OCDS) was established and introduced to measure the craving for alcohol and the severity of alcohol dependence. However, the Chinese version of OCDS is still unavailable and has not been validated in the Chinese ... ...

Abstract	Obsessive Compulsive Drinking Scale (OCDS) was established and introduced to measure the craving for alcohol and the severity of alcohol dependence. However, the Chinese version of OCDS is still unavailable and has not been validated in the Chinese population. We tended to translate and validate the OCDS in Chinese. We translated original OCDS into Chinese through bi-direction translations and tested the reliability and validity. We found that Chinese OCDS had high internal consistency and good test-retest reliability. The Chinese OCDS also presented good internal structure to reflect the severity of alcohol dependence. The Chinese OCDS could be used in clinical studies and research among the Chinese population.
Language	English
Publishing date	2021-12-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564218-2
ISSN	1664-0640
ISSN	1664-0640
DOI	10.3389/fpsyt.2021.770860
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Article ; Online: Peptidase inhibitor (PI16) impairs bladder cancer metastasis by inhibiting NF-κB activation via disrupting multiple-site ubiquitination of NEMO.

Kuang, Xiangqin / Zhang, Zhuojun / Li, Difeng / Bao, Wenhao / Pan, Jinyuan / Zhou, Ping / Chen, Han / Gao, Zhiqing / Xie, Xiaoyi / Yang, Chunxiao / Zhu, Ge / Zhou, Zhongqiu / Tang, Ruiming / Feng, Zhengfu / Zhou, Lihuan / Feng, Xiaoli / Wang, Lan / Yang, Jianan / Jiang, Lili

Cellular & molecular biology letters

2023 Volume 28, Issue 1, Page(s) 62

Abstract: Background: Bladder cancer (BLCA) is a malignancy that frequently metastasizes and leads to poor patient prognosis. It is essential to understand the molecular mechanisms underlying the progression and metastasis of BLCA and identify potential ... ...

Abstract	Background: Bladder cancer (BLCA) is a malignancy that frequently metastasizes and leads to poor patient prognosis. It is essential to understand the molecular mechanisms underlying the progression and metastasis of BLCA and identify potential biomarkers. Methods: The expression of peptidase inhibitor 16 (PI16) was analysed using quantitative PCR, immunoblotting and immunohistochemistry assays. The functional roles of PI16 were evaluated using wound healing, transwell, and human umbilical vein endothelial cell tube formation assays, as well as in vivo tumour models. The effects of PI16 on nuclear factor κB (NF-κB) signalling activation were examined using luciferase reporter gene systems, immunoblotting and immunofluorescence assays. Co-immunoprecipitation was used to investigate the interaction of PI16 with annexin-A1 (ANXA1) and NEMO. Results: PI16 expression was downregulated in bladder cancer tissues, and lower PI16 levels correlated with disease progression and poor survival in patients with BLCA. Overexpressing PI16 inhibited BLCA cell growth, motility, invasion and angiogenesis in vitro and in vivo, while silencing PI16 had the opposite effects. Mechanistically, PI16 inhibited the activation of the NF-κB pathway by interacting with ANXA1, which inhibited K63 and M1 ubiquitination of NEMO. Conclusions: These results indicate that PI16 functions as a tumour suppressor in BLCA by inhibiting tumour growth and metastasis. Additionally, PI16 may serve as a potential biomarker for metastatic BLCA.
MeSH term(s)	Humans ; NF-kappa B/metabolism ; Protease Inhibitors ; Signal Transduction ; Ubiquitination ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/metabolism ; Cell Line, Tumor ; Carrier Proteins/genetics ; Glycoproteins/genetics ; Glycoproteins/metabolism
Chemical Substances	NF-kappa B ; Protease Inhibitors ; PI16 protein, human ; Carrier Proteins ; Glycoproteins
Language	English
Publishing date	2023-07-31
Publishing country	England
Document type	Journal Article
ZDB-ID	2108724-6
ISSN	1689-1392 ; 1689-1392
ISSN (online)	1689-1392
ISSN	1689-1392
DOI	10.1186/s11658-023-00465-6
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Article ; Online: The efficacy of transcranial magnetic stimulation on migraine: a meta-analysis of randomized controlled trails.

Lan, Lihuan / Zhang, Xiaoni / Li, Xiangpen / Rong, Xiaoming / Peng, Ying

The journal of headache and pain

2017 Volume 18, Issue 1, Page(s) 86

Abstract: Objectives: As a non-invasive therapy, whether transcranial magnetic stimulation (TMS) is effective on migraine. This article was aimed to assess the efficacy of TMS on migraine based on randomized controlled trails (RCTs).: Methods: We searched ... ...

Abstract	Objectives: As a non-invasive therapy, whether transcranial magnetic stimulation (TMS) is effective on migraine. This article was aimed to assess the efficacy of TMS on migraine based on randomized controlled trails (RCTs). Methods: We searched PubMed, Embase and Cochrane Library electronic databases for published studies which compared TMS group with sham group, conducted a meta-analysis of all RCTs. Results: Five studies, consisting of 313 migraine patients, were identified. Single-pulse transcranial magnetic stimulation is effective for the acute treatment of migraine with aura after the first attack (p = 0.02). And, the efficacy of TMS on chronic migraine was not significant (OR 2.93; 95% CI 0.71-12.15; p = 0.14). Conclusions: TMS is effective for migraine based on the studies included in the article.
MeSH term(s)	Databases, Factual ; Humans ; Migraine Disorders/therapy ; Pain Management/methods ; Randomized Controlled Trials as Topic ; Transcranial Magnetic Stimulation/methods
Language	English
Publishing date	2017-08-22
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Review
ZDB-ID	2036768-5
ISSN	1129-2377 ; 1129-2369
ISSN (online)	1129-2377
ISSN	1129-2369
DOI	10.1186/s10194-017-0792-4
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Article ; Online: SBSN drives bladder cancer metastasis via EGFR/SRC/STAT3 signalling.

Zhou, Zhongqiu / Zhang, Zhuojun / Chen, Han / Bao, Wenhao / Kuang, Xiangqin / Zhou, Ping / Gao, Zhiqing / Li, Difeng / Xie, Xiaoyi / Yang, Chunxiao / Chen, Xuhong / Pan, Jinyuan / Tang, Ruiming / Feng, Zhengfu / Zhou, Lihuan / Wang, Lan / Yang, Jianan / Jiang, Lili

British journal of cancer

2022 Volume 127, Issue 2, Page(s) 211–222

Abstract: Background: Patients with metastatic bladder cancer have very poor prognosis and predictive biomarkers are urgently needed for early clinical detection and intervention. In this study, we evaluate the effect and mechanism of Suprabasin (SBSN) on bladder ...

Abstract	Background: Patients with metastatic bladder cancer have very poor prognosis and predictive biomarkers are urgently needed for early clinical detection and intervention. In this study, we evaluate the effect and mechanism of Suprabasin (SBSN) on bladder cancer metastasis. Methods: A tissue array was used to detect SBSN expression by immunohistochemistry. A tumour-bearing mouse model was used for metastasis evaluation in vivo. Transwell and wound-healing assays were used for in vitro evaluation of migration and invasion. Comprehensive molecular screening was achieved by western blotting, immunofluorescence, luciferase reporter assay, and ELISA. Results: SBSN was found markedly overexpressed in bladder cancer, and indicated poor prognosis of patients. SBSN promoted invasion and metastasis of bladder cancer cells both in vivo and in vitro. The secreted SBSN exhibited identical biological function and regulation in bladder cancer metastasis, and the interaction of secreted SBSN and EGFR could play an essential role in activating the signalling in which SBSN enhanced the phosphorylation of EGFR and SRC kinase, followed with phosphorylation and nuclear location of STAT3. Conclusions: Our findings highlight that SBSN, and secreted SBSN, promote bladder cancer metastasis through activation of EGFR/SRC/STAT3 pathway and identify SBSN as a potential diagnostic and therapeutic target for bladder cancer.
MeSH term(s)	Animals ; Antigens, Differentiation/metabolism ; Cell Line, Tumor ; Cell Movement ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Gene Expression Regulation, Neoplastic ; Mice ; Neoplasm Metastasis ; Prognosis ; Proto-Oncogene Proteins pp60(c-src)/metabolism ; Signal Transduction ; Urinary Bladder Neoplasms/pathology ; src-Family Kinases/metabolism
Chemical Substances	Antigens, Differentiation ; suprabasin protein, mouse ; ErbB Receptors (EC 2.7.10.1) ; Proto-Oncogene Proteins pp60(c-src) (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2022-04-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/s41416-022-01794-7
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