المؤلفون: Gui, Xiao, Zhang, Haorui, Zhang, Rui, Li, Qing, Zhu, Weiye, Nie, Zheng, Zhao, Jiawei, Cui, Xiao, Hao, Weiju, Wen, Xudong, Shen, Wei, Song, Hongyuan

المصدر: Materials Today Bio ; volume 19, page 100602 ; ISSN 2590-0064

مصطلحات موضوعية: Cell Biology, Molecular Biology, Biomedical Engineering, Biomaterials, Bioengineering, Biotechnology

الإتاحة: https://doi.org/10.1016/j.mtbio.2023.100602Test
https://api.elsevier.com/content/article/PII:S2590006423000625?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S2590006423000625?httpAccept=text/plainTest

المؤلفون: Lin, Zhe-Tao, Ye, Run-Ze, Liu, Jin-Yue, Wang, Xiao-Yang, Zhu, Wen-Jie, Li, Yu-Yu, Cui, Xiao-Ming, Cao, Wu-Chun

المساهمون: National Natural Science Foundation of China

المصدر: Infection, Genetics and Evolution ; volume 115, page 105510 ; ISSN 1567-1348

مصطلحات موضوعية: Infectious Diseases, Microbiology (medical), Genetics, Molecular Biology, Ecology, Evolution, Behavior and Systematics, Microbiology

الإتاحة: https://doi.org/10.1016/j.meegid.2023.105510Test
https://api.elsevier.com/content/article/PII:S1567134823001089?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S1567134823001089?httpAccept=text/plainTest

المؤلفون: Zhang, Jianong, Wei, Jiangbo, Sun, Rui, Sheng, Haoyue, Yin, Kai, Pan, Yunqian, Jimenez, Rafael, Chen, Sujun, Cui, Xiao-long, Zou, Zhongyu, Yue, Zhiying, Emch, Michael J., Hawse, John R., Wang, Liguo, He, Housheng Hansen, Xia, Shujie, Han, Bangmin, He, Chuan, Huang, Haojie

المصدر: Molecular Cell ; volume 83, issue 15, page 2692-2708.e7 ; ISSN 1097-2765

مصطلحات موضوعية: Cell Biology, Molecular Biology

الإتاحة: https://doi.org/10.1016/j.molcel.2023.06.024Test
https://api.elsevier.com/content/article/PII:S1097276523004719?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S1097276523004719?httpAccept=text/plainTest

المؤلفون: Zhang, Teng, Gao, Shang, Zhang, Shao-wu, Cui, Xiao-dong

المساهمون: Natural Science Basic Research Program of Shaanxi Province, National Natural Science Foundation of China

المصدر: Methods ; volume 226, page 61-70 ; ISSN 1046-2023

مصطلحات موضوعية: General Biochemistry, Genetics and Molecular Biology, Molecular Biology

الإتاحة: https://doi.org/10.1016/j.ymeth.2024.04.011Test
https://api.elsevier.com/content/article/PII:S1046202324001014?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S1046202324001014?httpAccept=text/plainTest

المؤلفون: Cong, Si-Qi, Wang, Bo, Wang, Han, Zheng, Qiu-Cui, Yang, Qian-Ru, Yang, Ruo-Tong, Li, Qian-Li, Wang, Wen-Shu, Cui, Xiao-Jie, Luo, Fei-Xian

المساهمون: National Natural Science Foundation of China, Natural Science Foundation of Beijing Municipality, Minzu University of China

المصدر: International Journal of Biological Macromolecules ; volume 256, page 128233 ; ISSN 0141-8130

مصطلحات موضوعية: Molecular Biology, General Medicine, Biochemistry, Structural Biology

الإتاحة: https://doi.org/10.1016/j.ijbiomac.2023.128233Test
https://api.elsevier.com/content/article/PII:S0141813023051322?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0141813023051322?httpAccept=text/plainTest

المؤلفون: Wu, Jianqi, Shen, Shuai, Liu, Tianqi, Ren, Xiufang, Zhu, Chen, Liang, Qingyu, Cui, Xiao, Chen, Ling, Cheng, Peng, Cheng, Wen, Wu, Anhua

المصدر: Oncogene ; volume 41, issue 21, page 3024-3036 ; ISSN 0950-9232 1476-5594

مصطلحات موضوعية: Cancer Research, Genetics, Molecular Biology

الوصف: Glioblastoma multiforme (GBM) with mesenchymal features exhibits enhanced chemotherapeutic resistance and results in reduced overall survival. Recent studies have suggested that there is a positive correlation between the GBM mesenchymal status and immune cell infiltration. However, the mechanisms by which GBM acquires its mesenchymal features in a tumor immune microenvironment-dependent manner remains unknown. Here, we uncovered a chemerin-mediated autocrine and paracrine network by which the mesenchymal phenotype of GBM cells is strengthened. We identified chemerin as a prognostic secretory protein mediating the mesenchymal phenotype-promoting network between tumor-associated macrophages (TAMs) and tumor cells in GBM. Mechanistically, chemerin promoted the mesenchymal features of GBM by suppressing the ubiquitin-proteasomal degradation of CMKLR1, a chemerin receptor predominantly expressed on TAMs and partially expressed on GBM cells, thereby enhancing NF-κB pathway activation. Moreover, chemerin was found to be involved in the recruitment of TAMs in the GBM tumor microenvironment. We revealed that chemerin also enhances the mesenchymal phenotype-promoting ability of TAMs and promotes their M2 polarization via a CMKLR1/NF-κB axis, which further exacerbates the mesenchymal features of GBM. Blocking the chemerin/CMKLR1 axis with 2-(α-naphthoyl) ethyltrimethylammonium iodide disrupted the mesenchymal network and suppressed tumor growth in GBM. These results suggest the therapeutic potential of targeting the chemerin/CMKLR1 axis to block the mesenchymal network in GBM.

الإتاحة: https://doi.org/10.1038/s41388-022-02295-wTest
https://www.nature.com/articles/s41388-022-02295-w.pdfTest
https://www.nature.com/articles/s41388-022-02295-wTest

المؤلفون: Zhang, Chengming, Zhang, Hong, Ge, Jing, Mi, Tingyan, Cui, Xiao, Tu, Fengjuan, Gu, Xuelan, Zeng, Tao, Chen, Luonan

المصدر: Journal of Molecular Cell Biology ; volume 14, issue 3 ; ISSN 1674-2788 1759-4685

مصطلحات موضوعية: Cell Biology, Genetics, Molecular Biology, General Medicine

الإتاحة: https://doi.org/10.1093/jmcb/mjac013Test
https://academic.oup.com/jmcb/article-pdf/14/3/mjac013/44408898/mjac013.pdfTest

المؤلفون: Liu, Xiaoyan, Chen, Zhenzhen, Li, Shuangyue, Jin, Ling, Cui, Xiao, Cui, Changting, Deng, Yue, Gao, Qiannan, Fan, Luyun, Niu, Yaping, Wang, Wenjie, Cui, Chunmei, Zhong, Jiuchang, Cui, Qinghua, Geng, Bin, Cai, Jun

المصدر: International Journal of Biological Sciences ; volume 18, issue 8, page 3237-3250 ; ISSN 1449-2288

مصطلحات موضوعية: Cell Biology, Developmental Biology, Molecular Biology, Applied Microbiology and Biotechnology, Ecology, Evolution, Behavior and Systematics

الإتاحة: https://doi.org/10.7150/ijbs.70455Test
https://www.ijbs.com/v18p3237.htmTest

المؤلفون: Zhang, Chengming, Zhang, Hong, Ge, Jing, Mi, Tingyan, Cui, Xiao, Tu, Fengjuan, Gu, Xuelan, Zeng, Tao, Chen, Luonan

المساهمون: Wu, Jiarui, National Natural Science Foundation of China, Strategic Priority Project of CAS, National Key R&D Program of China, JST Moonshot R&D program

المصدر: Journal of Molecular Cell Biology ; volume 13, issue 11, page 822-833 ; ISSN 1759-4685

مصطلحات موضوعية: Cell Biology, Genetics, Molecular Biology, General Medicine

الوصف: Skin, as the outmost layer of human body, is frequently exposed to environmental stressors including pollutants and ultraviolet (UV), which could lead to skin disorders. Generally, skin response process to ultraviolet B (UVB) irradiation is a nonlinear dynamic process, with unknown underlying molecular mechanism of critical transition. Here, the landscape dynamic network biomarker (l-DNB) analysis of time series transcriptome data on 3D skin model was conducted to reveal the complicated process of skin response to UV irradiation at both molecular and network levels. The advanced l-DNB analysis approach showed that: (i) there was a tipping point before critical transition state during pigmentation process, validated by 3D skin model; (ii) 13 core DNB genes were identified to detect the tipping point as a network biomarker, supported by computational assessment; (iii) core DNB genes such as COL7A1 and CTNNB1 can effectively predict skin lightening, validated by independent human skin data. Overall, this study provides new insights for skin response to repetitive UVB irradiation, including dynamic pathway pattern, biphasic response, and DNBs for skin lightening change, and enables us to further understand the skin resilience process after external stress.

الإتاحة: https://doi.org/10.1093/jmcb/mjab060Test
https://academic.oup.com/jmcb/article-pdf/13/11/822/42256827/mjab060.pdfTest

المؤلفون: Chen, Zhiwei, Cai, Aimin, Zheng, Hailun, Huang, Huirong, Sun, Rui, Cui, Xiao, Ye, Weijian, Yao, Qing, Chen, Ruijie, Kou, Longfa

المصدر: Oncogenesis ; volume 9, issue 5 ; ISSN 2157-9024

مصطلحات موضوعية: Cancer Research, Molecular Biology

الوصف: Carbidopa, a peripheral decarboxylase inhibitor used with L-DOPA to treat Parkinson’s disease, has attracted significant interest in recent years for its anticancer effect. Increasing evidence reveals that Carbidopa can inhibit cancer cell growth and induce apoptosis through aryl hydrocarbon receptor (AHR) in some cancers. However, the antitumor effect of Carbidopa in prostate cancer (PCa) is not fully understood. Androgen receptor (AR) plays a central role in PCa, even in advanced “castrate-resistant” disease. In the present study, we report that Carbidopa suppresses the growth of PCa by downregulating the protein expression of AR. Carbidopa inhibits proliferation and migration of LNCaP cells and promotes apoptosis, but has no effect on the AR-independent prostate cell line DU145. Carbidopa increases ubiquitination of AR in LNCaP cells. Several studies have shown that AHR can act as an E3 ubiquitin ligase and promote the proteasomal degradation of AR. Quantitative RT-PCR, immunofluorescence staining and immunoblotting assay demonstrate that AHR is induced and activated by Carbidopa, and the co-immunoprecipitation assay shows that AR interacts with AHR, firmly confirming that Carbidopa decreases AR protein level though AHR-induced proteasomal degradation. In addition, Carbidopa suppresses PCa growth in vivo when xenografted into immunocompromised mice. Carbidopa treatment increases AHR protein level and decreases AR protein level in tumor tissues. Taken together, our study implicates Carbidopa for the first time in effective suppression of prostate cancer via a mechanism, involving AHR-mediated proteasomal degradation of AR.

الإتاحة: https://doi.org/10.1038/s41389-020-0236-xTest
https://www.nature.com/articles/s41389-020-0236-x.pdfTest
https://www.nature.com/articles/s41389-020-0236-xTest