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Article: Mebendazole induces apoptosis and inhibits migration via the reactive oxygen species-mediated STAT3 signaling downregulation in non-small cell lung cancer.

Liang, Zhipan / Chen, Qiuyun / Pan, Liuying / She, Xiaowei / Chen, Tengfei

2024 Volume 16, Issue 2, Page(s) 1412–1423

Abstract: Background: The incidence and mortality of non-small cell lung cancer (NSCLC) are extremely high. Previous research has confirmed that the signal transducer and activator of the transcription 3 (STAT3) protein critically participate in the tumorigenesis ...

Abstract	Background: The incidence and mortality of non-small cell lung cancer (NSCLC) are extremely high. Previous research has confirmed that the signal transducer and activator of the transcription 3 (STAT3) protein critically participate in the tumorigenesis of NSCLC. Mebendazole (MBZ) has exerts a larger number of pharmacological activities and has anticancer effects in lung cancer, but its mechanism of action remains unclear. This study thus aimed to clarify the impacts of MBZ on NSCLC cell. Methods: Cell proliferation, migration, and apoptosis were investigated via cell counting kit 8 (CCK-8) assay, Transwell assay, colony formation assay, wound-healing assay, and flow cytometry. Reactive oxygen species (ROS) were detected with a multifunctional microplate reader. Markers of cell migration and apoptosis were detected with Western blotting. The transcriptional activity of STAT3 was detected via luciferase assay. ROS scavenger N-acetylcysteine (NAC) was used to determine the effect of MBZ on NSCLC via ROS-regulated STAT3 inactivation and apoptosis. A xenograft model was constructed Results: The findings demonstrated that MBZ inhibited NSCLC cell proliferation and migration while promoting apoptosis through triggering ROS generation. In addition, the Janus kinase 2 (JAK2)-STAT3 signaling pathway was abrogated with the treatment of MBZ. NAC could distinctly weaken MBZ-induced apoptosis and STAT3 inactivation. Moreover, MBZ inhibited the tumor growth of NSCLC Conclusions: In summary, MBZ inhibited NSCLC cell viability and migration by inducing cell apoptosis via the ROS-JAK2-STAT3 signaling pathway. These data provide a theoretical basis for the use of MBZ in treating NSCLC.
Language	English
Publishing date	2024-02-27
Publishing country	China
Document type	Journal Article
ZDB-ID	2573571-8
ISSN	2077-6624 ; 2072-1439
ISSN (online)	2077-6624
ISSN	2072-1439
DOI	10.21037/jtd-23-1978
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Promotion of non-small cell lung cancer tumor growth by

Chen, Tengfei / Chen, Jun / Chen, Qiuyun / Liang, Zhipan / Pan, Liuying / Zhao, Jun / She, Xiaowei

Journal of thoracic disease

2024 Volume 16, Issue 2, Page(s) 1424–1437

Abstract: Background: Antiangiogenetic therapy is one of the effective strategies for non-small cell lung cancer (NSCLC) treatment. Four-and-a-half LIM-domain protein 2 (: Methods: FHL2: Results: We demonstrated that : Conclusions: Our study revealed the ...

Abstract	Background: Antiangiogenetic therapy is one of the effective strategies for non-small cell lung cancer (NSCLC) treatment. Four-and-a-half LIM-domain protein 2 ( Methods: FHL2 Results: We demonstrated that Conclusions: Our study revealed the role of
Language	English
Publishing date	2024-02-23
Publishing country	China
Document type	Journal Article
ZDB-ID	2573571-8
ISSN	2077-6624 ; 2072-1439
ISSN (online)	2077-6624
ISSN	2072-1439
DOI	10.21037/jtd-23-1975
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Article: Modified surgical incision suturing technique in uniportal video-assisted thoracoscopic pulmonary resection.

Pan, Liuying / Chen, Tengfei / Liang, Zhipan / Solli, Piergiorgio / Bedetti, Benedetta / Kim, Kyung Soo / She, Xiaowei

Journal of thoracic disease

2024 Volume 16, Issue 2, Page(s) 1388–1396

Abstract: Background: In recent years, single-hole thoracoscopic surgery technology is widely used in major medical centers and chest-specialized hospitals for the treatment of lung diseases. However, the single-hole minimally invasive surgery method focuses on ... ...

Abstract	Background: In recent years, single-hole thoracoscopic surgery technology is widely used in major medical centers and chest-specialized hospitals for the treatment of lung diseases. However, the single-hole minimally invasive surgery method focuses on one incision, and all surgical instruments need to pass through the same hole, resulting in repeated extrusion and tissue damage of the surgical incision. Therefore, we have improved the suture method of conventional surgical incision in order to reduce the probability of wound infection and dehiscence, promote early healing, and reduce the severity of postoperative wound scar, thereby enhancing the postoperative rapid recovery of patients. The purpose of this study is to explore the clinical efficacy of a modified surgical incision suture technique applied to uniportal thoracoscopic pulmonary resection. Methods: This study retrospectively analyzed 151 patients who were admitted to the Department of Thoracic Surgery and underwent pulmonary resection from January 2019 to October 2021 in the North District of Suzhou Municipal Hospital. The patients were divided into two groups according to the different surgical incision suture methods: a modified group and a conventional group. The postoperative general clinical indexes, incision infection rate, secondary suture rate, postoperative incision pain score, and the severity of postoperative incision scar were compared and analyzed between the two groups. Results: There were no statistically significant differences between the two groups in terms of chest tube duration or postoperative drainage and postoperative incision pain scores; the incision infection rate (1.3% Conclusions: Our modified suture method reduces the chance of infection and splitting and the severity of postoperative incision scar formation, promoting early healing. It can be safely and effectively applied to the incision suture of uniportal thoracoscopic pulmonary resection, enhancing the rapid postoperative recovery of patients.
Language	English
Publishing date	2024-02-26
Publishing country	China
Document type	Journal Article
ZDB-ID	2573571-8
ISSN	2077-6624 ; 2072-1439
ISSN (online)	2077-6624
ISSN	2072-1439
DOI	10.21037/jtd-23-1968
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Article ; Online: Association of Interleukin-1

She, Xiaowei / Xiao, Hua / Lu, Shuang / Guo, Lijun

Genetics research

2021 Volume 2021, Page(s) 6614835

Abstract: Chronic periodontitis (CP) is a common inflammatory illness affecting a large proportion of humans. Genetic factors are thought to play important roles in its onset and development. A functional polymorphism (rs1800587) in the promoter of the interleukin- ...

Abstract	Chronic periodontitis (CP) is a common inflammatory illness affecting a large proportion of humans. Genetic factors are thought to play important roles in its onset and development. A functional polymorphism (rs1800587) in the promoter of the interleukin-1
MeSH term(s)	Case-Control Studies ; China ; Chronic Periodontitis/genetics ; Gene Frequency ; Genetic Predisposition to Disease/genetics ; Genotype ; Humans ; Interleukin-1alpha/genetics ; Polymorphism, Single Nucleotide/genetics
Chemical Substances	Interleukin-1alpha
Language	English
Publishing date	2021-03-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2412681-0
ISSN	1469-5073 ; 0016-6723
ISSN (online)	1469-5073
ISSN	0016-6723
DOI	10.1155/2021/6614835
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Article ; Online: USP26 promotes colorectal cancer tumorigenesis by restraining PRKN-mediated mitophagy.

Wu, Qi / Wang, Zhihong / Chen, Siqi / She, Xiaowei / Zhu, Shengyu / Li, Pengcheng / Liu, Lang / Zhao, Chongchong / Li, Kangdi / Liu, Anyi / Huang, Changsheng / Chen, Yaqi / Hu, Fuqing / Wang, Guihua / Hu, Junbo

Oncogene

2024

Abstract: Deubiquitinating enzymes (DUBs) are promising targets for cancer therapy because of their pivotal roles in various physiological and pathological processes. Among these, ubiquitin-specific peptidase 26 (USP26) is a protease with crucial regulatory ... ...

Abstract	Deubiquitinating enzymes (DUBs) are promising targets for cancer therapy because of their pivotal roles in various physiological and pathological processes. Among these, ubiquitin-specific peptidase 26 (USP26) is a protease with crucial regulatory functions. Our study sheds light on the upregulation of USP26 in colorectal cancer (CRC), in which its increased expression correlates with an unfavorable prognosis. Herein, we evidenced the role of USP26 in promoting CRC tumorigenesis in a parkin RBR E3 ubiquitin-protein ligase (PRKN) protein-dependent manner. Our investigation revealed that USP26 directly interacted with PRKN protein, facilitating its deubiquitination, and subsequently reducing its activity. Additionally, we identified the K129 site on PRKN as a specific target for USP26-mediated deubiquitination. Our research highlights that a K-to-R mutation at the site on PRKN diminishes its potential for activation and ability to mediate mitophagy. In summary, our findings underscore the significance of USP26-mediated deubiquitination in restraining the activation of the PRKN-mediated mitophagy pathway, ultimately driving CRC tumorigenesis. This study not only elucidated the multifaceted role of USP26 in CRC but also introduced a promising avenue for therapeutic exploration through the development of small molecule inhibitors targeting USP26. This strategy holds promise as a novel therapeutic approach for CRC.
Language	English
Publishing date	2024-04-02
Publishing country	England
Document type	Journal Article
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-024-03009-0
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Zs.A 2218: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
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Article ; Online: SOD1-high fibroblasts derived exosomal miR-3960 promotes cisplatin resistance in triple-negative breast cancer by suppressing BRSK2-mediated phosphorylation of PIMREG.

Li, Kangdi / Lin, Han / Liu, Anyi / Qiu, Cheng / Rao, Zejun / Wang, Zhihong / Chen, Siqi / She, Xiaowei / Zhu, Shengyu / Li, Pengcheng / Liu, Lang / Wu, Qi / Wang, Guihua / Xu, Feng / Li, Shaotang

Cancer letters

2024 Volume 590, Page(s) 216842

Abstract: Platinum-based neoadjuvant therapy represented by cisplatin is widely employed in treating Triple-Negative Breast Cancer (TNBC), a particularly aggressive subtype of breast cancer. Nevertheless, the emergence of cisplatin resistance presents a formidable ...

Abstract	Platinum-based neoadjuvant therapy represented by cisplatin is widely employed in treating Triple-Negative Breast Cancer (TNBC), a particularly aggressive subtype of breast cancer. Nevertheless, the emergence of cisplatin resistance presents a formidable challenge to clinical chemotherapy efficacy. Herein, we revealed the critical role of tumor microenvironment (TME) derived exosomal miR-3960 and phosphorylation at the S16 site of PIMREG in activating NF-κB signaling pathway and promoting cisplatin resistance of TNBC. Detailed regulatory mechanisms revealed that SOD1-upregulated fibroblasts secrete miR-3960 and are then transported into TNBC cells via exosomes. Within TNBC cells, miR-3960 targets and inhibits the expression of BRSK2, an AMPK protein kinase family member. Furthermore, we emphasized that BRSK2 contributes to ubiquitination degradation of PIMREG and modulates subsequent activation of the NF-κB signaling pathway by mediating PIMREG phosphorylation at the S16 site, ultimately affects the cisplatin resistance of TNBC. In conclusion, our research demonstrated the crucial role of SOD1
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cisplatin/pharmacology ; Drug Resistance, Neoplasm ; Exosomes/metabolism ; Exosomes/genetics ; Fibroblasts/metabolism ; Fibroblasts/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; MicroRNAs/genetics ; MicroRNAs/metabolism ; NF-kappa B/metabolism ; NF-kappa B/genetics ; Phosphorylation ; Signal Transduction/drug effects ; Superoxide Dismutase-1/genetics ; Superoxide Dismutase-1/metabolism ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/pathology ; Triple Negative Breast Neoplasms/metabolism ; Tumor Microenvironment
Chemical Substances	SOD1 protein, human
Language	English
Publishing date	2024-04-04
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2024.216842
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Zs.A 1177: Show issues

Location:
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Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: NSD2 methylates AROS to promote SIRT1 activation and regulates fatty acid metabolism-mediated cancer radiotherapy.

Li, Xun / Song, Da / Chen, Yaqi / Huang, Changsheng / Liu, Anyi / Wu, Qi / She, Xiaowei / Li, Kangdi / Wan, Kairui / Yu, Chengxin / Qiu, Cheng / Liu, Lang / Wang, Guihua / Xu, Feng / Wang, Jing / Hu, Junbo

Cell reports

2023 Volume 42, Issue 10, Page(s) 113126

Abstract: Fatty acid metabolism plays a critical role in both tumorigenesis and cancer radiotherapy. However, the regulatory mechanism of fatty acid metabolism has not been fully elucidated. NSD2, a histone methyltransferase that catalyzes di-methylation of ... ...

Abstract	Fatty acid metabolism plays a critical role in both tumorigenesis and cancer radiotherapy. However, the regulatory mechanism of fatty acid metabolism has not been fully elucidated. NSD2, a histone methyltransferase that catalyzes di-methylation of histone H3 at lysine 36, has been shown to play an essential role in tumorigenesis and cancer progression. Here, we show that NSD2 promotes fatty acid oxidation (FAO) by methylating AROS (active regulator of SIRT1) at lysine 27, facilitating the physical interaction between AROS and SIRT1. The mutation of lysine 27 to arginine weakens the interaction between AROS and SIRT1 and impairs AROS-SIRT1-mediated FAO. Additionally, we examine the effect of NSD2 inhibition on radiotherapy efficacy and find an enhanced effectiveness of radiotherapy. Together, our findings identify a NSD2-dependent methylation regulation pattern of the AROS-SIRT1 axis, suggesting that NSD2 inhibition may be a potential adjunct for tumor radiotherapy.
MeSH term(s)	Humans ; Sirtuin 1/genetics ; Repressor Proteins/metabolism ; Lysine/metabolism ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Neoplasms/genetics ; Neoplasms/radiotherapy ; Carcinogenesis ; Fatty Acids
Chemical Substances	Sirtuin 1 (EC 3.5.1.-) ; Repressor Proteins ; Lysine (K3Z4F929H6) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Fatty Acids ; SIRT1 protein, human (EC 3.5.1.-)
Language	English
Publishing date	2023-09-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113126
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Article ; Online: Tiam1 methylation by NSD2 promotes Rac1 signaling activation and colon cancer metastasis.

Song, Da / Hu, Fuqing / Huang, Changsheng / Lan, Jingqin / She, Xiaowei / Zhao, Chongchong / Wu, Hong / Liu, Anyi / Wu, Qi / Chen, Yaqi / Luo, Xuelai / Feng, Yongdong / Yang, Xiangping / Xu, Chuan / Hu, Junbo / Wang, Guihua

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 52, Page(s) e2305684120

Abstract: Metastasis is a major cause of cancer therapy failure and mortality. However, targeting metastatic seeding and colonization remains a significant challenge. In this study, we identified NSD2, a histone methyltransferase responsible for dimethylating ... ...

Abstract	Metastasis is a major cause of cancer therapy failure and mortality. However, targeting metastatic seeding and colonization remains a significant challenge. In this study, we identified NSD2, a histone methyltransferase responsible for dimethylating histone 3 at lysine 36, as being overexpressed in metastatic tumors. Our findings suggest that NSD2 overexpression enhances tumor metastasis both in vitro and in vivo. Further analysis revealed that NSD2 promotes tumor metastasis by activating Rac1 signaling. Mechanistically, NSD2 combines with and activates Tiam1 (T lymphoma invasion and metastasis 1) and promotes Rac1 signaling by methylating Tiam1 at K724. In vivo and in vitro studies revealed that Tiam1 K724 methylation could be a predictive factor for cancer prognosis and a potential target for metastasis inhibition. Furthermore, we have developed inhibitory peptide which was proved to inhibit tumor metastasis through blocking the interaction between NSD2 and Tiam1. Our results demonstrate that NSD2-methylated Tiam1 promotes Rac1 signaling and cancer metastasis. These results provide insights into the inhibition of tumor metastasis.
MeSH term(s)	Humans ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/metabolism ; Signal Transduction/physiology ; Colonic Neoplasms ; Neoplasm Invasiveness/pathology ; Methylation ; rac1 GTP-Binding Protein/genetics ; rac1 GTP-Binding Protein/metabolism
Chemical Substances	Guanine Nucleotide Exchange Factors ; rac1 GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2023-12-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2305684120
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Zs.A 1148: Show issues

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Article ; Online: Inhibition of CARM1-Mediated Methylation of ACSL4 Promotes Ferroptosis in Colorectal Cancer.

Feng, Shengjie / Rao, Zejun / Zhang, Jiakun / She, Xiaowei / Chen, Yaqi / Wan, Kairui / Li, Haijie / Zhao, Chongchong / Feng, Yongdong / Wang, Guihua / Hu, Junbo / Luo, Xuelai

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2023 Volume 10, Issue 36, Page(s) e2303484

Abstract: Ferroptosis, which is caused by iron-dependent accumulation of lipid peroxides, is an emerging form of regulated cell death and is considered a potential target for cancer therapy. However, the regulatory mechanisms underlying ferroptosis remain unclear. ...

Abstract	Ferroptosis, which is caused by iron-dependent accumulation of lipid peroxides, is an emerging form of regulated cell death and is considered a potential target for cancer therapy. However, the regulatory mechanisms underlying ferroptosis remain unclear. This study defines a distinctive role of ferroptosis. Inhibition of CARM1 can increase the sensitivity of tumor cells to ferroptosis inducers in vitro and in vivo. Mechanistically, it is found that ACSL4 is methylated by CARM1 at arginine 339 (R339). Furthermore, ACSL4 R339 methylation promotes RNF25 binding to ACSL4, which contributes to the ubiquitylation of ACSL4. The blockade of CARM1 facilitates ferroptosis and effectively enhances ferroptosis-associated cancer immunotherapy. Overall, this study demonstrates that CARM1 is a critical contributor to ferroptosis resistance and highlights CARM1 as a candidate therapeutic target for improving the effects of ferroptosis-based antitumor therapy.
MeSH term(s)	Humans ; Ferroptosis ; Methylation ; Protein-Arginine N-Methyltransferases/genetics ; Colorectal Neoplasms/genetics
Chemical Substances	coactivator-associated arginine methyltransferase 1 (EC 2.1.1.319) ; Protein-Arginine N-Methyltransferases (EC 2.1.1.319)
Language	English
Publishing date	2023-11-09
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202303484
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Article ; Online: SETDB1 Methylates MCT1 Promoting Tumor Progression by Enhancing the Lactate Shuttle.

She, Xiaowei / Wu, Qi / Rao, Zejun / Song, Da / Huang, Changsheng / Feng, Shengjie / Liu, Anyi / Liu, Lang / Wan, Kairui / Li, Xun / Yu, Chengxin / Qiu, Cheng / Luo, Xuelai / Hu, Junbo / Wang, Guihua / Xu, Feng / Sun, Li

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2023 Volume 10, Issue 28, Page(s) e2301871

Abstract: MCT1 is a critical protein found in monocarboxylate transporters that plays a significant role in regulating the lactate shuttle. However, the post-transcriptional modifications that regulate MCT1 are not clearly identified. In this study, it is reported ...

Abstract	MCT1 is a critical protein found in monocarboxylate transporters that plays a significant role in regulating the lactate shuttle. However, the post-transcriptional modifications that regulate MCT1 are not clearly identified. In this study, it is reported that SETDB1 interacts with MCT1, leading to its stabilization. These findings reveal a novel post-translational modification of MCT1, in which SETDB1 methylation occurs at K473 in vitro and in vivo. This methylation inhibits the interaction between MCT1 and Tollip, which blocks Tollip-mediated autophagic degradation of MCT1. Furthermore, MCT1 K473 tri-methylation promotes tumor glycolysis and M2-like polarization of tumor-associated macrophages in colorectal cancer (CRC), which enhances the lactate shuttle. In clinical studies, MCT1 K473 tri-methylation is found to be upregulated and positively correlated with tumor progression and overall survival in CRC. This discovery suggests that SETDB1-mediated tri-methylation at K473 is a vital regulatory mechanism for lactate shuttle and tumor progression. Additionally, MCT1 K473 methylation may be a potential prognostic biomarker and promising therapeutic target for CRC.
MeSH term(s)	Humans ; Lactic Acid/metabolism ; Symporters ; Neoplasms ; Histone-Lysine N-Methyltransferase/metabolism
Chemical Substances	Lactic Acid (33X04XA5AT) ; Symporters ; SETDB1 protein, human (EC 2.1.1.43) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
Language	English
Publishing date	2023-08-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202301871
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