Jingjing Yao

Ministry of Education of the People's Republic of China

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Linlin Lu

Guangzhou University of Chinese Medicine

Yaqiu Zheng

Guangzhou University of Chinese Medicine

Zhongqiu Liu

Guangzhou University of Chinese Medicine

Zibo Li

First Affiliated Hospital of Henan University

Yuefang Lin

Guangzhou University of Chinese Medicine

Jindong Fu

People’s Hospital of Rizhao

Wenxin Yan

Dalian Medical University

Jianghui Yang

Tsinghua University

Gangjun Du

Henan University

Chaoyue Ji

Beijing Tsinghua Chang Gung Hospital

Cooperative Institutions

Guangzhou University of Chinese Medicine

Tsinghua University

Ministry of Education of the People's Republic of China

Chinese Academy of Sciences

Beijing Tsinghua Chang Gung Hospital

Peking University

Chinese Academy of Medical Sciences & Peking Union Medical College

Sun Yat-sen University

Second Military Medical University

Zhejiang University

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First case report of a novel KIF13A-ALK fusion in a lung adenocarcinoma patient and response to alectinib with a 4-year follow-up

Frontiers in Genetics (2023)

Zheng Mo Cunliang Cai Jingjing Yao Jingquan Zhao Ming‐Qiang Zhang

The prevalence of Anaplastic Lymphoma Kinase gene ( ALK ) fusion is about 5% among patients with lung adenocarcinoma, underscoring the importance of pinpointing distinct fusion variants for optimizing treatment approaches. This is the first reported case of a 74-year-old female with stage IV lung adenocarcinoma, featuring a novel Kinesin Family Member 13A ( KIF13A ) -ALK fusion, identified via next-generation sequencing (NGS) and confirmed with fluorescence in situ hybridization (FISH). Initially undergoing chemotherapy and then crizotinib, she achieved a partial response (PR) before progressing with multiple bone metastases. However, subsequent treatment with alectinib as a third-line option yielded positive results. A stable disease state persisted for an impressive 31 months of progression-free survival (PFS), accompanied by minimal toxicity symptoms. Up until now, a remarkable near 4-year span of overall survival (OS) has been consistently observed and monitored. This report of a KIF13A-ALK fusion case benefit significantly from alectinib with extensive follow-up. The case diversifies the array of ALK fusion partners and holds clinical relevance in refining therapeutic choices for KIF13A-ALK fusion-associated lung cancer.

Alectinib

10.3389/fgene.2023.1289346

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Frontiers in Genetics (2022)

YANG Liuqing Jinling Yu Tao Lu Handan Huang Ying Gao

Background: Cuproptosis is a new type of cell death that induces protein toxic stress and eventually leads to cell death. Hence, regulating cuproptosis in tumor cells is a new therapeutic approach. However, studies on cuproptosis-related long noncoding RNA (lncRNA) in head and neck squamous cell carcinoma (HNSC) have not been found. This study aimed to explore the cuproptosis-related lncRNAs prognostic marker and their relationship to immune microenvironment in HNSC by using bioinformatics methods. Methods: RNA sequencing, genomic mutations, and clinical data of TCGA_HNSC were downloaded from The Cancer Genome Atlas. HNSC patients were randomly assigned to either a training group or a validation cohort. The least absolute shrinkage and selection operator Cox regression and multivariate Cox regression models were used to determine the prognostic model in the training cohort, and its independent prognostic effect was further confirmed in the validation and entire cohorts. Results: Based on previous literature, we collected 19 genes associated with cuproptosis. Afterward, 783 cuproptosis-related lncRNAs were obtained through coexpression. Cox model revealed and constructed eight cuproptosis-related lncRNAs prognostic marker (AL132800.1, AC090587.1, AC079160.1, AC011462.4, AL157888.1, GRHL3-AS1, SNHG16, and AC021148.2). Patients were divided into high- and low-risk groups based on the median risk score. The Kaplan-Meier survival curve revealed that the overall survival between the high- and low-risk groups was statistically significant. The receiver operating characteristic curve and principal component analysis demonstrated the accurate prognostic ability of the model. Univariate and multivariate Cox regression analysis showed that risk score was an independent prognostic factor. In addition, we used multivariate Cox regression to establish a nomogram of the predictive power of prognostic markers. The tumor mutation burden showed significant differences between the high- and low-risk groups. HNSC patients in the high-risk group responded better to immunotherapy than those in the low-risk group. We also found that risk scores were significantly associated with drug sensitivity in HNSC. Conclusion: In summary, our study identified eight cuprotosis-related lncRNAs signature of HNSC as the prognostic predictor, which may be promising biomarkers for predicting the benefit of HNSC immunotherapy as well as drug sensitivity.

10.3389/fgene.2022.947551

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Expressions of PAX-2 and PTEN in endometrial lesions and their correlation with endometrial intraepithelial neoplasia

Zhongliu yanjiu yu linchuang (2017)

Yiting Meng Donglin Ma Li Li Jingjing Yao Meiling Mao

Objective To observe the expression of PAX-2 and PTEN in different types of endometrial lesions, and to study their relationship with endometrial intraepithelial neoplasia (EIN). Methods 60 cases of endometrial hyperplasic lesions and 70 cases of endometrial carcinoma were enrolled. All cases were reclassified by using the diagnostic criteria of EIN, and PAX-2 and PTEN were stained to compare the difference among them. Results The deletion rates of PAX-2 in benign hyperplasia, EIN and endometrial carcinoma were 39.5% (15/38), 72.7% (16/22) and 78.6% (55/70), respectively, and there was a statistical difference (χ 2= 21.664, P= 0.000). The deletion rates of PTEN in benign hyperplasia, EIN and endometrial carcinoma were 47.4% (18/38), 54.5% (12/22) and 75.7% (53/70), respectively, and there was no statistical difference (χ 2= 2.878, P= 0.411). Conclusion The staining of PAX-2 could be considered as a reliable adjuvant diagnostic method in the diagnostic criteria of EIN, however, the loss of PTEN just should be regarded as a suggestion of EIN, not a confirmed diagnostic basis. Key words: Endometrial hyperplasia; Endometrial intraepithelial neoplasia; Endometrial neoplasms; PAX-2; PTEN

Endometrial hyperplasia

Atypical Hyperplasia

10.3760/cma.j.issn.1006-9801.2017.01.007

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Metformin inhibits cell proliferation and migration in gastric cancer cell line AGS

Shijie huaren xiaohua zazhi (2010)

Zhixin Xue Jie Zhong Danyu Zhao Ci Xu Ping-Hu Sun

Cancer cell lines

10.11569/wcjd.v18.i19.1974

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Stratification of Grade of Spinal Cord Non-Ependymal Gliomas by Magnetic Resonance Imaging

World Neurosurgery (2019)

Benqi Zhao Chen Zhang Xihai Zhao Jingjing Yao Jie Li

Ependymal Cell

Spinal Cord Neoplasm

10.1016/j.wneu.2019.01.205

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The optimal dose of arsenic trioxide induced opposite efficacy in autophagy between K562 cells and their initiating cells to eradicate human myelogenous leukemia

Journal of Ethnopharmacology (2016)

Zhenzhen Guo Mingjing Meng Shengnan Geng Zhenhua Du Yaqiu Zheng

Arsenic Trioxide

K562 cells

Acridine orange

10.1016/j.jep.2016.12.010

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Retraction: Berberine and cinnamaldehyde together prevent lung carcinogenesis

Oncotarget (2024)

Mingjing Meng Shengnan Geng Zhenhua Du Jingjing Yao Yaqiu Zheng

// Mingjing Meng 1 , * , Shengnan Geng 1 , * , Zhenhua Du 1 , Jingjing Yao 1 , Yaqiu Zheng 1 , Zibo Li 1 , Zhenzhen Zhang 2 , Jiahuan Li 1 , Yongjian Duan 2 and Gangjun Du 1 , 2 1 Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China 2 Department of Oncology, The First Hospital Affiliated to Henan University, Kaifeng, Henan Province 475001, China * These authors contributed equally to this work Correspondence to: Gangjun Du, email: 724200@henu.edu.cn Jiahuan Li, email: jiahuan1020@126.com Keywords: Received: RECEIVED_DATE Accepted: ACCEPTED_DATE Published: August 05, 2024 Copyright: © 2024 Meng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

10.18632/oncotarget.28577

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Discovery Potential Therapeutic Drugs for Oral Tongue Squamous Cell Carcinoma Based on Text Mining and Data Analysis

Research Square (Research Square) (2021)

Liuqing Yang Jue Wang Jinling Yu Handan Huang Ying Gao

Abstract Background : Oral tongue squamous cell carcinoma (OTSCC) is the most common malignant tumor of the oral cavity. The aim of this study was to use text mining and data analysis to discover some existing drugs that target genes and to explore potential therapeutic drugs for OTSCC. Methods : We used the text mining tool pubmed2ensembl to extract genes associated with OTSCC, and two datasets (GSE30784, GSE23558) from Gene Expression Omnibus (GEO) were used for the data analysis. Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed for the intersection of the three gene sets. Protein-protein interaction (PPI) network was constructed by STRING, gene module analysis was performed using the Molecular Complex Detection (MCODE), a plug-in in Cytoscape. Lastly, a database of drug-gene interactions was used to identify significant genes to explore potential drugs for the treatment of OTSCC. Results : We produced 403 unique genes associated with oral tongue squamous cell carcinoma through text mining. GSE23558 and GSE 30784 obtained 1637 and 1159 differentially expressed genes (DEGs) through data analysis, respectively. A total of 28 genes were obtained from the intersection gene sets, including 20 up-regulated genes and 8 down-regulated genes. We screened the most significant modules by using MCODE, among which 8 genes were associated with oral tongue squamous cell carcinoma as core genes. Eventually, nine drugs were found to target eight genes. Conclusions : In this study, PLAU, SERPINE1, MMP1, MMP3, MMP10, CXCL10, CXCL12, and SPP1 were potentially key genes involved in the treatment of OTSCC. Furthermore, 12 drugs were identified as potential therapeutic agents for oral tongue squamous cell carcinoma treatment and management

KEGG

MMP1

10.21203/rs.3.rs-970755/v1

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Sp1 upregulates expression of TRF2 and TRF2 inhibition reduces tumorigenesis in human colorectal carcinoma cells

Cancer Biology & Therapy (2009)

Wenjie Dong Ruizhe Shen Qi Wang Yabo Gao Xiaoguang Qi

Telomeres are essential for the maintenance of genomic integrality, they enablecomplete DNA replication, organize subnuclear domains, and protect chromosome endsagainst fusion. Loss of telomere function in human cells results in the formation ofdicentric chromosomes and other abnormalities such as end-to-end fusions.TRF2 is aubiquitously expressed protein which binds directly to the tandem array of duplextelomeric repeats and is involved in the telomere structure and chromosome endprotection. Inhibition of TRF2 induces end-to-end chromosome fusions and growth arrestor apoptosis in human melanoma cells.Lack of TRF2 in ALT cells also caused PMLdependentp53 activation and loss of telomeric DNA.TRF2 over-expression is found inseveral human tumors such as breast carcinomas, liver hepatocarcinomas, lungcarcinomas and gastric carcinomas. This suggests that TRF2 may have a role intumorigenisis.Cancers of the gastrointestinal tract share numerous common geneticfeatures despite differing widely in incidence and outcome.However, the role andmechanisms that lead to over-expressed TRF2 in colorectal carcinoma are not wellknown. Sp1 is a member of the multigene family with sequence-specific DNA-bindingC-terminal zinc-finger motifs, which plays a critical role in the regulation of expressionof mammalian genes lacking a TATA box, by binding to GC/GT boxes to activatetranscription.Cancer-related Sp1 targets include PDEGF, p21, VEGF, TGF-β, cyclinD1, E2F1, c-fos, transforming growth factor α and osteopontin (OPN).The promoterof TRF2 is GC-rich sequence (70-75%), which lacks an obvious TATA box. It is unclearwhether or not TRF2 is regulated via Sp1, which may in turn be regulated to genomicstability. We tested the expression of TRF2 in colorectal carcinoma tissues and coloncarcinoma SW480 cell line, and studied the role of Sp1 in regulating TRF2 expression incolon carcinoma. Results showed that TRF2 was over-expressed in colorectal carcinomatissues and SW480 cell line. It was also shown that Sp1 transcription factor is involved inthe up-regulation of TRF2 expression.

Shelterin

10.4161/cbt.8.22.9880

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Bile acids promote the development of HCC by activating the inflammasome

Hepatology Communications (2023)

Wenbo Chen Ming Ding Liyan Ji Jingjing Yao Yajuan Guo

Background: Hepatocellular carcinoma (HCC) is associated with chronic inflammation caused by different factors; especially, the interaction of inflammatory pathways and bile acids (BAs) can affect hepatocyte proliferation, death, and regeneration, but whether BAs promote HCC progression through inflammatory pathways and the mechanisms is still unclear. Methods and results: By examining cancer and tumor-adjacent tissue BA levels and genes associated with BA homeostasis in 37 HCC patients, we found that total bile acids (TBAs) were decreased by 36% and varying degrees of changes in factors regulating BA homeostasis ( p < 0.05). In addition, we found that BA homeostasis was disturbed in diethylnitrosamine-induced HCC mouse models, and TBA was correlated with inflammasome activation during HCC progression (6–24 W) ( p < 0.05). Similarly, the inflammasome and chenodeoxycholic acid (CDCA) content were suppressed in cholestasis model mice (Mrp2-deficient mice) ( p < 0.05). In vitro, CDCA significantly promoted the malignant transformation of hepatocytes ( p < 0.001), activated the inflammasome by triggering the release of mitochondrial reactive oxygen species and mitochondrial DNA, and ultimately induced pyroptosis. Furthermore, we found that CDCA has a targeted binding effect with HO-1 through molecular docking and Cellular Thermal Shift Assay experiments. Conclusions: In conclusion, we found that CDCA can trigger the excessive accumulation of mitochondrial reactive oxygen species by targeting HO-1 to promote the activation of the inflammasome and ultimately promote the progression of HCC. Our study provides a novel mechanism by which BAs promote HCC by activating the inflammasome and establishes the important role of BA homeostasis imbalance in the progression of HCC from the aspect of inflammation.

Chenodeoxycholic acid

Pyroptosis

Liver Regeneration

Homeostasis

10.1097/hc9.0000000000000217

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Citations (13)