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Article ; Online: The key roles of cancer stem cell-derived extracellular vesicles

Chaoyue Su / Jianye Zhang / Yosef Yarden / Liwu Fu

Signal Transduction and Targeted Therapy, Vol 6, Iss 1, Pp 1-

2021 Volume 15

Abstract: Abstract Cancer stem cells (CSCs), the subpopulation of cancer cells, have the capability of proliferation, self-renewal, and differentiation. The presence of CSCs is a key factor leading to tumor progression and metastasis. Extracellular vesicles (EVs) ... ...

Abstract	Abstract Cancer stem cells (CSCs), the subpopulation of cancer cells, have the capability of proliferation, self-renewal, and differentiation. The presence of CSCs is a key factor leading to tumor progression and metastasis. Extracellular vesicles (EVs) are nano-sized particles released by different kinds of cells and have the capacity to deliver certain cargoes, such as nucleic acids, proteins, and lipids, which have been recognized as a vital mediator in cell-to-cell communication. Recently, more and more studies have reported that EVs shed by CSCs make a significant contribution to tumor progression. CSCs-derived EVs are involved in tumor resistance, metastasis, angiogenesis, as well as the maintenance of stemness phenotype and tumor immunosuppression microenvironment. Here, we summarized the molecular mechanism by which CSCs-derived EVs in tumor progression. We believed that the fully understanding of the roles of CSCs-derived EVs in tumor development will definitely provide new ideas for CSCs-based therapeutic strategies.
Keywords	Medicine ; R ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A Glossary for Chemical Approaches towards Unlocking the Trove of Metabolic Treasures in Actinomycetes

Jianye Zhang / Heba Ali Hassan / Usama Ramadan Abdelmohsen / Eman Maher Zahran

Molecules, Vol 27, Iss 142, p

2022 Volume 142

Abstract: Actinobacterial natural products showed a critical basis for the discovery of new antibiotics as well as other lead secondary metabolites. Varied environmental and physiological signals touch the antibiotic machinery that faced a serious decline in the ... ...

Abstract	Actinobacterial natural products showed a critical basis for the discovery of new antibiotics as well as other lead secondary metabolites. Varied environmental and physiological signals touch the antibiotic machinery that faced a serious decline in the last decades. The reason was exposed by genomic sequencing data, which revealed that Actinomycetes harbor a large portion of silent biosynthetic gene clusters in their genomes that encrypt for secondary metabolites. These gene clusters are linked with a great reservoir of yet unknown molecules, and arranging them is considered a major challenge for biotechnology approaches. In the present paper, we discuss the recent strategies that have been taken to augment the yield of secondary metabolites via awakening these cryptic genes in Actinomycetes with emphasis on chemical signaling molecules used to induce the antibiotics biosynthesis. The rationale, types, applications and mechanisms are discussed in detail, to reveal the productive path for the unearthing of new metabolites, covering the literature until the end of 2020.
Keywords	Actinomycetes ; antibiotics biosynthesis ; cryptic genes ; elicitors ; biological potential ; Organic chemistry ; QD241-441
Subject code	500 ; 540
Language	English
Publishing date	2022-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: M2‐like macrophage‐derived exosomes facilitate metastasis in non‐small‐cell lung cancer by delivering integrin αVβ3

Lamei Huang / Fang Wang / Xueping Wang / Chaoyue Su / Shaocong Wu / Chuan Yang / Min Luo / Jianye Zhang / Liwu Fu

MedComm, Vol 4, Iss 1, Pp n/a-n/a (2023)

2023

Abstract: Abstract Metastasis is the most prevalent cause of cancer deaths, and immunological components of the tumor microenvironment, especially tumor‐associated macrophages (TAMs), play a vital role in cancer metastasis. However, the underlying mechanisms of ... ...

Abstract	Abstract Metastasis is the most prevalent cause of cancer deaths, and immunological components of the tumor microenvironment, especially tumor‐associated macrophages (TAMs), play a vital role in cancer metastasis. However, the underlying mechanisms of TAMs on non‐small‐cell lung cancer (NSCLC) metastasis remain largely unexplored. Herein, we demonstrated that M2‐like TAMs facilitate the migration and invasion of cancer cells in vitro and in vivo through intercellular delivery of M2‐like macrophage‐derived exosomes (M2‐exos). Importantly, we found that M2‐exos had considerably higher levels of integrin (ITG) αV and β3. The impact of M2‐like macrophage‐mediated invasion and migration of NSCLC cells was clearly decreased when ITG αVβ3 was blocked. Mechanistically, exosomal ITG αVβ3 produced from M2‐like macrophages successfully triggered the focal adhesion kinase signaling pathway in recipient cells, boosting the migratory and invasive abilities of NSCLC cells. Clinically, we found that metastatic NSCLC patients had greater ITG αV and β3 expression, which was associated with a worse prognosis. This study reveals a novel mechanism by which M2‐exos significantly increased NSCLC cell migration and invasion by delivering integrin αVβ3. Exosomal ITG αVβ3 can be used as a potential prognostic marker, and blocking ITG αVβ3 could be a viable treatment option for preventing tumor metastasis.
Keywords	exosomes ; integrin αVβ3 ; M2‐like macrophage ; metastasis ; NSCLC ; Medicine ; R
Subject code	610
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: UCseek

Ping Wang / Yue Shi / Jianye Zhang / Jianzhong Shou / Mingxin Zhang / Daojia Zou / Yuan Liang / Juan Li / Yezhen Tan / Mei Zhang / Xingang Bi / Liqun Zhou / Weimin Ci / Xuesong Li

EBioMedicine, Vol 89, Iss , Pp 104437- (2023)

ultrasensitive early detection and recurrence monitoring of urothelial carcinoma by shallow-depth genome-wide bisulfite sequencing of urinary sediment DNAResearch in context

2023

Abstract: Summary: Background: Current methods for the detection and surveillance of urothelial carcinomas (UCs) are often invasive, costly, and not effective for low-grade, early-stage, and minimal residual disease (MRD) tumors. We aimed to develop and validate a ...

Abstract	Summary: Background: Current methods for the detection and surveillance of urothelial carcinomas (UCs) are often invasive, costly, and not effective for low-grade, early-stage, and minimal residual disease (MRD) tumors. We aimed to develop and validate a model from urine sediments to predict different grade and stage UCs with low cost and high accuracy. Methods: We collected 167 samples, including 90 tumors and 77 individuals without tumors, as a discovery cohort. We assessed copy number variations and methylation values for them and constructed a diagnostic classifier to detect UC, UCseek, by using an individual read-based method and support vector machine. The performance of UCseek was validated in an independent cohort derived from three hospitals (n = 206) and a relapse cohort (n = 42) for monitoring recurrence. Findings: We constructed UCseek, which could predict UCs with high sensitivity (92.7%), high specificity (90.7%), and high accuracy (91.7%) in the independent validation set. The accuracy of UCseek in low-grade and early-stage patients reached 91.8% and 94.3%, respectively. Notably, UCseek retained great performance at ultralow sequencing depths (0.3X-0.5X). It also demonstrated a powerful ability to monitor recurrence in a surveillance cohort compared with cystoscopy (90.91% vs. 59.09%). Interpretation: We optimized an improved approach named UCseek for the noninvasive diagnosis and monitoring of UCs in both low- and high-grade tumors and in early- and advanced-stage tumors, even at ultralow sequencing depths, which may reduce the burden of cystoscopy and blind second surgery. Funding: A full list of funding bodies that contributed to this study can be found in the Acknowledgments section.
Keywords	Urothelial carcinoma ; Molecular diagnostics ; Tumor markers ; Diagnosis ; Relapse monitoring ; Machine learning ; Medicine ; R ; Medicine (General) ; R5-920
Subject code	616
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The RNA N6-Methyladenosine Methyltransferase METTL3 Promotes the Progression of Kidney Cancer via N6-Methyladenosine-Dependent Translational Enhancement of ABCD1

Yue Shi / Yanliang Dou / Jianye Zhang / Jie Qi / Zijuan Xin / Mingxin Zhang / Yu Xiao / Weimin Ci

Frontiers in Cell and Developmental Biology, Vol

2021 Volume 9

Abstract: The role of N6-methyladenosine (m6A)-modifying proteins in cancer progression depends on the cell type and mRNA affected. However, the biological role and underlying mechanism of m6A in kidney cancer is limited. Here, we discovered the variability in m6A ...

Abstract	The role of N6-methyladenosine (m6A)-modifying proteins in cancer progression depends on the cell type and mRNA affected. However, the biological role and underlying mechanism of m6A in kidney cancer is limited. Here, we discovered the variability in m6A methyltransferase METTL3 expression was significantly increased in clear cell renal cell carcinoma (ccRCC) the most common subtype of renal cell carcinoma (RCC), and high METTL3 expression predicts poor prognosis in ccRCC patients using a dataset from The Cancer Genome Atlas (TCGA). Importantly, knockdown of METTL3 in ccRCC cell line impaired both cell migration capacity and tumor spheroid formation in soft fibrin gel, a mechanical method for selecting stem-cell-like tumorigenic cells. Consistently, overexpression of METTL3 but not methyltransferase activity mutant METTL3 can promote cell migration, spheroid formation in cell line and tumor growth in xenograft model. Transcriptional profiling of m6A in ccRCC tissues identified the aberrant m6A transcripts were enriched in cancer-related pathways. Further m6A-sequencing of METTL3 knockdown cells and functional studies confirmed that translation of ABCD1, an ATP-binding cassette (ABC) transporter of fatty acids, was inhibited by METTL3 in m6A-dependent manner. Moreover, knockdown of ABCD1 in ccRCC cells decreased cancer cell migration and spheroid formation, and upregulation of ABCD1 acts as an adverse prognosis factor of kidney cancer patients. In summary, our study identifies that METTL3 promotes ccRCC progression through m6A modification-mediated translation of ABCD1, providing an epitranscriptional insight into the molecular mechanism in kidney cancer.
Keywords	METTL3 ; kidney cancer ; m6A ; ABCD1 ; cancer progression ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Transcriptomics and enzymology combined five gene expressions to reveal the responses of earthworms (Eisenia fetida) to the long-term exposure of cyantraniliprole in soil

Zhihua Qiao / Xiangfeng Yao / Xiang Liu / Jianye Zhang / Qingzhi Du / Fengwen Zhang / Xiangdong Li / Xingyin Jiang

Ecotoxicology and Environmental Safety, Vol 209, Iss , Pp 111824- (2021)

2021

Abstract: Cyantraniliprole is a novel diamide insecticide that acts upon the ryanodine receptor (RyR) and has broad application prospects. Accordingly, it is very important to evaluate the toxicity of cyantraniliprole to earthworms (Eisenia fetida) because of ... ...

Abstract	Cyantraniliprole is a novel diamide insecticide that acts upon the ryanodine receptor (RyR) and has broad application prospects. Accordingly, it is very important to evaluate the toxicity of cyantraniliprole to earthworms (Eisenia fetida) because of their vital role in maintaining a healthy soil ecosystem. In this study, an experiment was set up, using four concentrations (0.1, 1, 5, and 10 mg/kg) and solvent control group (0 mg/kg), to investigate the ecotoxicity of cyantraniliprole to earthworms. Our results showed that, after 28 days of exposure to cyantraniliprole, both cocoon production and the number of juvenile earthworms had decreased significantly at concentrations of either 5 or 10 mg/kg. On day 14, we measured the activities of digestive enzymes and ion pumps in the intestinal tissues of earthworms. These results revealed that cyantraniliprole exposure caused intestinal damage in earthworm, specifically changes to its intestinal enzyme activity and calcium ion content. Cyantraniliprole could lead to proteins’ carbonylation under the high-dose treatments (i.e., 5 mg/kg, 10 mg/kg). At the same time, we also found that cyantraniliprole can cause the abnormal expression of key functional genes (including HSP70, CAT, RYR, ANN, and CAM genes). Moreover, the transcriptomics data showed that exposure to cyantraniliprole would affect the synthesis of carbohydrates, proteins and lipids, as well as their absorption and transformation, while cyantraniliprole would also affect signal transduction. In general, high-dose exposure to cyantraniliprole causes reproductive toxicity, genotoxicity, and intestinal damage to earthworms.
Keywords	Cyantraniliprole ; Earthworms ; Reproductive toxicity ; Genotoxicity ; Transcriptomics ; Environmental pollution ; TD172-193.5 ; Environmental sciences ; GE1-350
Subject code	333 ; 610
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Extracellular Vesicles in Cancer Drug Resistance

Qiurong Yang / Jing Xu / Jianmei Gu / Hui Shi / Jiayin Zhang / Jianye Zhang / Zhe‐Sheng Chen / Xinjian Fang / Taofeng Zhu / Xu Zhang

Advanced Science, Vol 9, Iss 34, Pp n/a-n/a (2022)

Roles, Mechanisms, and Implications

2022

Abstract: Abstract Extracellular vesicles (EVs) are cell‐derived nanosized vesicles that mediate cell‐to‐cell communication via transporting bioactive molecules and thus are critically involved in various physiological and pathological conditions. EVs contribute ... ...

Abstract	Abstract Extracellular vesicles (EVs) are cell‐derived nanosized vesicles that mediate cell‐to‐cell communication via transporting bioactive molecules and thus are critically involved in various physiological and pathological conditions. EVs contribute to different aspects of cancer progression, such as cancer growth, angiogenesis, metastasis, immune evasion, and drug resistance. EVs induce the resistance of cancer cells to chemotherapy, radiotherapy, targeted therapy, antiangiogenesis therapy, and immunotherapy by transferring specific cargos that affect drug efflux and regulate signaling pathways associated with epithelial‐mesenchymal transition, autophagy, metabolism, and cancer stemness. In addition, EVs modulate the reciprocal interaction between cancer cells and noncancer cells in the tumor microenvironment (TME) to develop therapy resistance. EVs are detectable in many biofluids of cancer patients, and thus are regarded as novel biomarkers for monitoring therapy response and predicting prognosis. Moreover, EVs are suggested as promising targets and engineered as nanovehicles to deliver drugs for overcoming drug resistance in cancer therapy. In this review, the biological roles of EVs and their mechanisms of action in cancer drug resistance are summarized. The preclinical studies on using EVs in monitoring and overcoming cancer drug resistance are also discussed.
Keywords	cancer therapy ; drug delivery ; drug resistance ; extracellular vesicles ; nanomedicine ; Science ; Q
Subject code	610
Language	English
Publishing date	2022-12-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Metabolism-Related Signature Analysis Uncovers the Prognostic and Immunotherapeutic Characteristics of Renal Cell Carcinoma

Jianye Zhang / Qi Zhang / Yue Shi / Ping Wang / Yanqing Gong / Shiming He / Zhihua Li / Ninghan Feng / Yang Wang / Peng Jiang / Weimin Ci / Xuesong Li / Liqun Zhou

Frontiers in Molecular Biosciences, Vol

2022 Volume 9

Abstract: Renal cell carcinoma (RCC) is one of the most common urological cancers. RCC has a poor prognosis and is considered a metabolic disease. It has been reported that many metabolic pathways are associated with the development of RCC. However, the prognostic ...

Abstract	Renal cell carcinoma (RCC) is one of the most common urological cancers. RCC has a poor prognosis and is considered a metabolic disease. It has been reported that many metabolic pathways are associated with the development of RCC. However, the prognostic value of metabolism-related genes in RCC is unclear. We herein aimed to establish a scoring system based on the gene expression profile of metabolic genes to evaluate the response to immunotherapy and predict the prognosis of RCC. In this study, we collected multicentre RCC data and performed integrated analysis to characterize the role of tumour metabolism in RCC and explore the relationship between metabolism and prognosis and immune therapy. Based on transcriptomic data, metabolism-related genes were used for nonnegative matrix factorization clustering. We obtained three subclasses of RCC (M1, M2, and M3), and they are associated with different prognoses and immune infiltrate levels. Then, based on the pathway activity of 113 metabolism-related gene signatures, we classified patients into three distinct metabolism-related signatures. Finally, we provide a metabolism-related pathway score (MRPScore) that is significantly associated with RCC prognosis and the response to immunotherapy. Taken together, in this study, we established an RCC classification system based on metabolic gene expression profiles that could further the understanding of the diversity of RCC. We also present the MRPScore, which may be used as an indicator to predict the response to clinical immune therapy.
Keywords	renal cell carcinoma ; metabolism ; MRPScore ; prognosis ; immunotherapy ; Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Single‐Cell RNA‐seq Reveals a Developmental Hierarchy Super‐Imposed Over Subclonal Evolution in the Cellular Ecosystem of Prostate Cancer

Guangzhe Ge / Yang Han / Jianye Zhang / Xinxin Li / Xiaodan Liu / Yanqing Gong / Zhentao Lei / Jie Wang / Weijie Zhu / Yangyang Xu / Yiji Peng / Jianhua Deng / Bao Zhang / Xuesong Li / Liqun Zhou / Huiying He / Weimin Ci

Advanced Science, Vol 9, Iss 15, Pp n/a-n/a (2022)

2022

Abstract: Abstract Prostate cancer (PCa) is a complex disease. An ongoing accumulation of mutations results in increased genetic diversity, with the tumor acquiring distinct subclones. However, non‐genetic intra‐tumoral heterogeneity, the cellular differentiation ... ...

Abstract	Abstract Prostate cancer (PCa) is a complex disease. An ongoing accumulation of mutations results in increased genetic diversity, with the tumor acquiring distinct subclones. However, non‐genetic intra‐tumoral heterogeneity, the cellular differentiation state and the interplay between subclonal evolution and transcriptional heterogeneity are poorly understood. Here, the authors perform single‐cell RNA sequencing from 14 untreated PCa patients. They create an extensive cell atlas of the PCa patients and mapped developmental states onto tumor subclonal evolution. They identify distinct subclones across PCa patients and then stratify tumor cells into four transcriptional subtypes, EMT‐like (subtype 0), luminal A‐like (subtype 1), luminal B/C‐like (subtype 2), and basal‐like (subtype 3). These subtypes are hierarchically organized into stem cell‐like and differentiated status. Strikingly, multiple subclones within a single primary tumor present with distinct combinations of preferential subtypes. In addition, subclones show different communication strengths with other cell types within the tumor ecosystem, which may modulate the distinct transcriptional subtypes of the subclones. Notably, by integrating TCGA data, they discover that both tumor cell transcriptional heterogeneity and cellular ecosystem diversity correlate with features of a poor prognosis. Collectively, their study provides the analysis of subclonal and transcriptional heterogeneity and its implication for patient prognosis.
Keywords	cellular ecosystem ; epithelial‐to‐mesenchymal transition ; prostate cancer ; subtype ; transcriptional heterogeneity ; tumor subclone ; Science ; Q
Subject code	610
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Euphorbia factor L2 induces apoptosis in A549 cells through the mitochondrial pathway

Minting Lin / Sili Tang / Chao Zhang / Hubiao Chen / Wenjing Huang / Yun Liu / Jianye Zhang

Acta Pharmaceutica Sinica B, Vol 7, Iss 1, Pp 59-

2017 Volume 64

Abstract: Euphorbia factor L2, a lathyrane diterpenoid isolated from caper euphorbia seed (the seeds of Euphorbia lathyris L.), has been traditionally applied to treat cancer. This article focuses on the cytotoxic activity of Euphorbia factor L2 against lung ... ...

Abstract	Euphorbia factor L2, a lathyrane diterpenoid isolated from caper euphorbia seed (the seeds of Euphorbia lathyris L.), has been traditionally applied to treat cancer. This article focuses on the cytotoxic activity of Euphorbia factor L2 against lung carcinoma A549 cells and the mechanism by which apoptosis is induced. We analyzed the cytotoxicity and related mechanism of Euphorbia factor L2 with an MTT assay, an annexin V-FITC/PI test, a colorimetric assay, and immunoblotting. Euphorbia factor L2 showed potent cytotoxicity to A549 cells. Euphorbia factor L2 led to an increase in reactive oxygen species (ROS) generation, a loss of mitochondrial electrochemical potential, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase, suggesting that Euphorbia factor L2 induced apoptosis through a mitochondrial pathway. The cytotoxic activity of Euphorbia factor L2 in A549 cells and the related mechanisms of apoptotic induction provide support for the further investigation of caper euphorbia seeds.
Keywords	Euphorbia Factor L2 ; Caper euphorbia seed ; Euphorbia lathyris L. ; Anticancer agent ; Apoptosis ; Mitochondrial pathway ; Medicine ; R ; Therapeutics. Pharmacology ; RM1-950
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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