Xiangqing Ren’s research while affiliated with Lanzhou University and other places

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Publications (7)


The mechanism diagram of CD39-CD73-eAdo/A2aR axis in tumor microenvironment.
Annual publications from 2015 to 2024.
Paper publication status in various countries. (A) Number of publications from the top 20 countries. (B) Patterns of international collaboration in paper publication: Single Country Publications (SCP); Multi-country Collaboration Publications (MCP). (C) Average article citations of each country.
The visualization of cooperation between countries by VOSviewer. (A) International cooperation network diagram. The same-colored logo indicates the cluster group of countries, the thickness of the line reflects the closeness of cooperation, and the node’s size corresponds to the number of papers published by each country. (B) Heat map of cooperation analysis between countries. Each label represents a country, and the color on the heat map changes gradually from cool to warm, indicating low to high cooperation.
Annual publication growth trend chart of institutions.

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Current perspectives and trends of CD39-CD73-eAdo/A2aR research in tumor microenvironment: a bibliometric analysis
  • Literature Review
  • Full-text available

August 2024

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37 Reads

Tian Huang

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Xiangqing Ren

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[...]

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Yongning Zhou

Background and objective Extracellular adenosine (eAdo) bridges tumor metabolism and immune regulation. CD39-CD73-eAdo/A2aR axis regulates tumor microenvironment (TME) and immunotherapy response. In the era of immunotherapy, exploring the impact of the CD39-CD73-eAdo/A2aR axis on TME and developing targeted therapeutic drugs to enhance the efficacy of immunotherapy are the current research hotspots. This study summarizes and explores the research trends and hotspots of the adenosine axis in the field of TME to provide ideas for further in-depth research. Methods Literature information was obtained from the Web of Science core collection database. The VOS viewer and the bibliometric tool based on R were used to quantify and identify cooperation information and individual influence by analyzing the detailed information of the global annual publication volume, country/region and institution distribution, article authors and co-cited authors, and journal distribution of these articles. At the same time, the distribution of author keywords and the co-occurrence of author keywords, highly cited articles, and highly co-cited references of CD39-CD73-eAdo/A2aR in the field of TME were analyzed to determine research hotspots and trends. Result 1,721 articles published in the past ten years were included in this study. Through bibliometric analysis, we found that (1) 69 countries and regions explored the effect of the CD39-CD73-eAdo/A2aR on TME, and the research was generally on the rise. Researchers in the United States dominated research in this area, with the highest total citation rate. China had the most significant number of publications. (2) Harvard University has published the most articles in this field. (3) 12,065 authors contributed to the publication of papers in this field, of which 23 published at least eight papers. STAGG J had significant academic influence, with 24 published articles and 2,776 citations. Co-cited authors can be clustered into three categories. Stagg J, Allard B, Ohta A, and Antonioli, L occupied a central position in the network. (4) 579 scholarly journals have published articles in this field. The journal FRONTIERS IN IMMUNOLOGY published the most significant number of papers, with 97 articles and a total of 2,317 citations, and the number of publications increased year by year. (5) “The ectonucleotidases CD39 and CD73: Novel checkpoint inhibitor targets” was the most frequently local cited article (163 times). The “A2A adenosine receptor protects tumors from antitumor T cells” was the most co-cited reference (224 times). (6) Through the analysis of author keywords, we found that the relationship between adenosine and immunotherapy was a core concept for many researchers in this field. Breast cancer, melanoma, colorectal cancer, ovarian cancer, glioblastoma, pancreatic cancer, hepatocellular carcinoma, and lung cancer were the most frequent cancer types in adenosine-related tumor studies. Immunotherapy, immunosuppression, immune checkpoint, and immune checkpoint inhibitors were the hot keywords in the research, reflecting the importance of the adenosine metabolic pathway in tumor immunotherapy. The keywords such as Immunogenic cell death, T cells, Sting, regulatory T cells, innate immunity, and immune infiltration demonstrated the pathways by which adenosine affected the TME. The famous author keywords in recent years have been immunotherapy, immunogenic cell death, inflammation, lung cancer, and gastric cancer. Conclusion The effect of CD39-CD73-eAdo/A2aR on the infiltration and function of various immune cells in TME, tumor immunotherapy response, and patient prognosis has attracted the attention of researchers from many countries/regions. American scholars still dominate the research in this field, but Chinese scholars produce the most research results. The journal FRONTIERS IN IMMUNOLOGY has published the wealthiest research in the field. Stagg J was a highly influential researcher in this field. Further exploration of targeted inhibition of CD39-CD73-eAdo/A2aR alone or in combination with other immunotherapy, radiotherapy, and chemotherapy in treating various cancer types and developing effective clinical therapeutic drugs are continuous research hotspots in this field.

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The Role of FTO in EC (A-C) and GC (D-H). A: Mechanically, FTO reduced the stability of SIM2 mRNA by reducing the m6A methylation level of SIM2; Phenotypically, FTO promoted proliferation and inhibited apoptosis. B: Mechanically, FTO positively regulated mRNA and protein expression levels of MMP13; Phenotypically, FTO promoted proliferation and migration. (C): Mechanically, FTO increased LINC00022 mRNA stability; Phenotypically, FTO promoted proliferation. (D): Mechanically, FTO promoted ITGB1 mRNA expression, and enhanced the phosphorylation of FAK. Phenotypically, FTO promoted proliferation and invasion. (E): Mechanically, FTO enhanced the degradation of Caveolin-1 mRNA. Phenotypically, FTO promoted proliferation, migration, and invasion. (F): Mechanically, FTO negatively regulated DDIT3 in an m6A-dependent manner. Phenotypically, FTO inhibited apoptosis. (G): Mechanically, FTO activated Wnt and PI3K/Akt signaling pathways. Phenotypically, FTO promoted proliferation, migration, and invasion. (H): Mechanically, FTO stabilized MYC mRNA by removing the m6A modification. Phenotypically, FTO promoted proliferation, migration, and invasion.
The Role of FTO in CRC (A-C), PLC (D-F), and PAAD (G, H). (A): Mechanically, FTO regulated the expression level of G6PD/PARP1 through m6A; Phenotypically, FTO promoted proliferation. (B): Mechanically, FTO promoted MZF1 expression in an m6A-dependent manner; Phenotypically, FTO promoted proliferation/migration and inhibited apoptosis. (C): Mechanically, FTO-induced ATF4 promoted pro-survival autophagy. (D): Mechanically, FTO led to the demethylation of PKM2 mRNA, promoting its mRNA production and accelerating its translation process. Phenotypically, FTO promotes proliferation and inhibits apoptosis. (E): Mechanically, FTO significantly promoted the expression of NANOG, SOX2 and KLF4 in HCC cells by mRNA demethylation. Phenotypically, FTO promoted HCC cell stemness. (F): Mechanically, reduced FTO can increase the m6A level of estrogen receptor alpha (ERa) mRNA, thereby reducing the protein translation of ERa. Phenotypically, FTO promoted proliferation. (G): Mechanically, FTO improved the stability of c-MYC expression. Phenotypically, FTO promoted proliferation. (H): Mechanically, FTO inhibited the stability of TFPI-2 mRNA through the m6A reader YTHDF1. Phenotypically, FTO promoted proliferation, migration, and invasion.
FTO regulated the tumor immune microenvironment in m6A-dependent manner and gene mutation in CRC. FTO increased PD-L1 mRNA expression levels in an IFN-γ independent manner. The HLA-A0201-restricted peptide FSP11 was derived from a (−1) mutation of U79260(FTO) gene. The peptide FSP11 sensitized peripheral CD8+ T cells for specific release of IFN-γ.
FTO regulated the tumor immune microenvironment in OC and HCC. FTO improved the stability of PD-L1 mRNA in an m6A-dependent manner, and MYC promoted PD-L1 transcription. TAAs and FB23-2 co-delivered to TIDCs were expected to help ICBs inhibit HCC progression by increasing m6A methylation, enhancing T-cell infiltration, and generating immune memory.
FTO promoted M1 and M2 macrophage activation. FTO promoted the polarization of M1 macrophages by improving STAT1 mRNA stability and enhancing the phosphorylation of IKKα/β, IκBα and P65. FTO promoted the polarization of M2 macrophages by enhancing the stability of PPAR-γ mRNA and increasing the expression of STAT6. FTO KO macrophages can reduce inflammatory responses by increasing m6A levels in Socs1 mRNA. YTHDF1 was identified as an m6A reader that recognizes Socs1 mRNA and enhances its stability, thus facilitating its translation.
FTO plays a crucial role in gastrointestinal cancer and may be a target for immunotherapy: an updated review

October 2023

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57 Reads

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4 Citations

Gastrointestinal cancer is a common malignancy with high mortality and poor prognosis. Therefore, developing novel effective markers and therapeutic targets for gastrointestinal cancer is currently a challenging and popular topic in oncology research. Accumulating studies have reported that N6-methyladenosine is the most abundant epigenetic modification in eukaryotes. N6-methyladenosine plays an essential role in regulating RNA expression and metabolism, including splicing, translation, stability, decay, and transport. FTO, the earliest demethylase discovered to maintain the balance of N6-adenosine methylation, is abnormally expressed in many tumors. In this review, we discuss the molecular structure and substrate selectivity of FTO. we focus on the role of FTO in gastrointestinal tumor proliferation, migration, invasion, apoptosis, autophagy, immune microenvironment, and its molecular mechanisms. We also discuss its potential in the treatment of gastrointestinal cancers.


Development and validation of nomogram models to predict radiotherapy or chemotherapy benefit in stage III/IV gastric adenocarcinoma with surgery

August 2023

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31 Reads

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4 Citations

Objectives The advanced gastric adenocarcinoma (GAC) patients (stage III/IV) with surgery may have inconsistent prognoses due to different demographic and clinicopathological factors. In this retrospective study, we developed clinical prediction models for estimating the overall survival (OS) and cancer-specific survival (CSS) in advanced GAC patients with surgery Methods A retrospective analysis was conducted using the Surveillance, Epidemiology, and End Results (SEER) database. The total population from 2004 to 2015 was divided into four levels according to age, of which 179 were younger than 45 years old, 695 were 45-59 years old, 1064 were 60-74 years old, and 708 were older than 75 years old. There were 1,712 men and 934 women. Univariate and multivariate Cox regression analyses were performed to identify prognostic factors for OS and CSS. Nomograms were constructed to predict the 1-, 3-, and 5-year OS and CSS. The models’ calibration and discrimination efficiency were validated. Discrimination and accuracy were evaluated using the consistency index, area under the receiver operating characteristic curve, and calibration plots; and clinical usefulness was assessed using decision curve analysis. Cross-validation was also conducted to evaluate the accuracy and stability of the models. Prognostic factors identified by Cox regression were analyzed using Kaplan-Meier survival analysis. Results A total of 2,646 patients were included in our OS study. Age, primary site, differentiation grade, AJCC 6th_TNM stage, chemotherapy, radiotherapy, and number of regional nodes examined were identified as prognostic factors for OS in advanced GAC patients with surgery (P < 0.05). A total of 2,369 patients were included in our CSS study. Age, primary site, differentiation grade, AJCC 6th_TNM stage, chemotherapy, radiotherapy, and number of regional nodes examined were identified as risk factors for CSS in these patients (P < 0.05). These factors were used to construct the nomogram to predict the 1-, 3-, and 5-year OS and CSS of advanced GAC patients with surgery. The consistency index and area under the receiver operating characteristic curve demonstrated that the models effectively differentiated between events and nonevents. The calibration plots for 1-, 3-, and 5-year OS and CSS probability showed good consistence between the predicted and the actual events. The decision curve analysis indicated that the nomogram had higher clinical predictive value and more significant net gain than AJCC 6th_TNM stage in predicting OS and CSS of advanced GAC patients with surgery. Cross-validation also revealed good accuracy and stability of the models. Conclusion The developed predictive models provided available prognostic estimates for advanced GAC patients with surgery. Our findings suggested that both OS and CSS can benefit from chemotherapy or radiotherapy in these patients.


Prognostic and Immunological Significance of the Molecular Subtypes and Risk Signatures Based on Cuproptosis in Hepatocellular Carcinoma

April 2023

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54 Reads

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8 Citations

Background: Hepatocellular carcinoma (HCC) remains a challenging medical problem. Cuproptosis is a novel form of cell death that plays a crucial role in tumorigenesis, angiogenesis, and metastasis. However, it remains unclear whether cuproptosis-related genes (CRGs) influence the outcomes and immune microenvironment of HCC patients. Method: From The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) databases, we obtained the mRNA expression file and related clinical information of HCC patients. We selected 19 CRGs as candidate genes for this study according to previous literature. We performed a differential expression analysis of the 19 CRGs between malignant and precancerous tissue. Based on the 19 CRGs, we enrolled cluster analysis to identify cuproptosis-related subtypes of HCC patients. A prognostic risk signature was created utilizing univariate Cox regression and least absolute shrinkage and selection operator (LASSO) regression analyses. We employed independent and stratification survival analyses to investigate the predictive value of this model. The functional enrichment features, mutation signatures, immune profile, and response to immunotherapy of HCC patients were also investigated according to the two molecular subtypes and the prognostic signature. Results: We found that 17 CRGs significantly differed in HCC versus normal samples. Cluster analysis showed two distinct molecular subtypes of cuproptosis. Cluster 1 is preferentially related to poor prognosis, high activity of immune response signaling, high mutant frequency of TP53, and distinct immune cell infiltration versus cluster 2. Through univariate and LASSO Cox regression analyses, we created a cuproptosis-related prognostic risk signature containing LIPT1, DLAT, MTF1, GLS, and CDKN2A. High-risk HCC patients were shown to have a worse prognosis. The risk signature was proved to be an independent predictor of prognosis in both the TCGA and ICGC datasets, according to multivariate analysis. The signature also performed well in different stratification of clinical features. The immune cells, which included regulatory T cells (Treg), B cells, macrophages, mast cells, NK cells, and aDCs, as well as immune functions containing cytolytic activity, MHC class I, and type II IFN response, were remarkably distinct between the high-risk and low-risk groups. The tumor immune dysfunction and exclusion (TIDE) score suggested that high-risk patients had a higher response rate to immune checkpoint inhibitors than low-risk patients. Conclusion: This research discovered the potential prognostic and immunological significance of cuproptosis in HCC, improved the understanding of cuproptosis, and may deliver new directions for developing more efficacious therapeutic techniques for HCC patients.


NcRNA-mediated upregulation of CAMK2N1 is associated with poor prognosis and tumor immune infiltration of gastric cancer

August 2022

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50 Reads

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3 Citations

Gastric cancer (GC) is still notorious for its poor prognosis and aggressive characteristics. Though great developments have been made in diagnosis and therapy for GC, the prognosis of patient is still perishing. In this study, differentially expressed genes (DEGs) in GC were first screened using three Gene Expression Omnibus (GEO) datasets (GSE13911, GSE29998, and GSE26899). Second, The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data were used to validate expression of these DEGs and perform survival analysis. We selected seven candidate genes (CAMK2N1, OLFML2B, AKR7A3, CYP4X1, FMO5, MT1H, and MT1X) to carry out the next analysis. To construct the ceRNA network, we screened the most potential upstream ncRNAs of the candidate genes. A series of bioinformatics analyses, including expression analysis, correlation analysis, and survival analysis, revealed that the SNHG10–hsa-miR-378a-3p might be the most potential regulatory axis in GC. Then, the expression of CAMK2N1, miR-378a-3p, and SNHG10 was verified in GC cell lines (GES-1, MGC-803, BGC-823, HGC-27, MKN-45, and AGS) by qRT-PCR and Western blotting. We found that SNHG10 and CAMK2N1 were highly expressed in gastric cancer lines, and the miR-378a-3p was lowly expressed in BGC-823, HGC-27, and MKN-45. Furthermore, CAMK2N1 levels were significantly negatively associated with tumor immune cell infiltration, biomarkers of immune cells, and immune checkpoint expression. In summary, our results suggest that the ncRNA-mediated high expression of CAMK2N1 is associated with poor prognosis and tumor immune infiltration of GC.


Integrated pan-cancer analysis of CSMD2 as a potential prognostic, diagnostic, and immune biomarker

August 2022

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37 Reads

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7 Citations

The protein encoded by CUB and Sushi Multiple Domains 2 (CSMD2) is likely involved in regulating the complement cascade reaction of the immune system. However, current scientific evidence on the comprehensive roles of CSMD2 in pan-cancer is relatively scarce. Therefore, in this study, we explored the transcriptional level of CSMD2 in pan-caner using TCGA, GEO, and International Cancer Genome Consortium databases. Receiver operating characteristic curve analysis was used to investigate the diagnostic efficacy of CSMD2. The Kaplan-Meier Plotter and Oncolnc were used to investigate the correlation between CSMD2 expression and prognosis. Additionally, we analyzed the correlation between epigenetic methylation and CSMD2 expression in various cancers based on UALCAN, as well as, the correlation between CSMD2 and tumor mutational burden (TMB), microsatellite instability (MSI), and tumor neoantigen burden (TNB) in tumors. TIMER2.0 database was employed to investigate the correlation between CSMD2 and immune cells in the tumor microenvironment and immune checkpoints. Based on TISIDB, the correlation between CSMD2 and MHC molecules and immunostimulators was analyzed. Ultimately, we observed with a pan-cancer analysis that CSMD2 was upregulated in most tumors and had moderate to high diagnostic efficiency, and that high expression was closely associated with poor prognosis in patients with tumors. Moreover, hypermethylation of CSMD2 promoter and high levels of m6A methylation regulators were also observed in most cancers. CSMD2 expression was negatively correlated with TMB and MSI in stomach adenocarcinoma (STAD) and stomach and esophageal carcinoma (STES), as well as with tumor mutational burden, microsatellite instability, and TNB in head-neck squamous cell carcinoma (HNSC). In most cancers, CSMD2 might be associated with immune evasion or immunosuppression, as deficient anti-tumor immunity and upregulation of immune checkpoints were also observed in this study. In conclusion, CSMD2 could serve as a promising prognostic, diagnostic and immune biomarker in pan-cancer.


Prognostic biomarker HAMP and associates with immune infiltration in gastric cancer

July 2022

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27 Reads

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6 Citations

International Immunopharmacology

Background Gastric cancer remains one of the most common malignant tumors and has high morbidity and mortality rates. Hepcidin, as a peptide hormone, plays a vital role in regulating systemic iron homeostasis. Nevertheless, the clinical predictive value of HAMP, especially its correlation with immune cell infiltration in gastric cancer, has not yet been elucidated. Methods HAMP expression in gastric cancer cells and tissues was assessed using experiments and bioinformatics platforms. Clinical and pathologic information was collected to stratify patients with gastric cancer for comparison. We used Kaplan-Meier and Cox regression methods to explore the association between HAMP expression levels and overall survival. Based on “The Cancer Genome Atlas” datasets, we analyzed whether HAMP expression is associated with immune cell infiltration levels and evaluated the prognostic impact of HAMP on survival of patients with gastric cancer partially through immune cell infiltration. Results HAMP mRNA was more highly expressed in gastric cancer cells and tumor tissues than in normal tissues. Moreover, elevated HAMP expression was correlated with poor overall survival. In addition, HAMP expression was related to sex, tumor stage, node stage, metastasis stage, Lauren classification, and differentiation in stratified patients. Notably, HAMP gene expression was found to be significantly related to the infiltration levels of immune cells, and that HAMP affects the survival rate in gastric cancer through the immune pathway. Conclusion High HAMP expression may serve as an independent prognostic biomarker through the immune pathway in patients with gastric cancer.

Citations (5)


... Data spanning 2004 to 2020 were extracted from the SEER database comprising 18 population-based registries (SEER* Stat 8.3.6), which cover approximately half of the United States population [11]. The International Classification of Diseases for Oncology, third edition (site code: C21.0-9) was used. ...

Reference:

Comparative evaluation of TNM staging systems (eighth vs. ninth edition) for the non-surgical treatment of localized and locally advanced anal squamous cell carcinoma: Prognostic significance of T classification and lymph node status
Development and validation of nomogram models to predict radiotherapy or chemotherapy benefit in stage III/IV gastric adenocarcinoma with surgery

... An enzyme of the lipoic acid pathway, LIAS generates antioxidants in mitochondria [68]. LIPT1 and DLD also represent enzymes of the lipoic acid pathway and participate in protein lipoylation, required for activation of cuproptosis [69]. CTR1/SLC31A1 and ATP7A/B, the copper transporter, are required for intracellular transport of the element, the trigger of cytotoxicity [70]. ...

Prognostic and Immunological Significance of the Molecular Subtypes and Risk Signatures Based on Cuproptosis in Hepatocellular Carcinoma

... This is the first time it has been reported in lung cancer prognosis research. Calcium/Calmodulin Dependent Protein Kinase II Inhibitor 1 (CAMK2N1), in lung cancer, its high expression has been linked to unfavorable outcomes [61]. RAB27B belongs to the RAB family of small GTPases, which are pivotal in vesicle trafficking processes. ...

NcRNA-mediated upregulation of CAMK2N1 is associated with poor prognosis and tumor immune infiltration of gastric cancer

... www.nature.com/scientificreports/ Some of the eight deletion-affected genes we found have human orthologs with variants documented in various cancer types [47][48][49][50][51] . Examples include SMIM30 in hepatocellular carcinoma 47 and CDV3, in breast 49,51 and colorectal adenosarcoma cancers 48,49 In a recent pan-cancer study, CSMD2 was identified in 25 of 33 cancer types, with the highest expression found in gastric, lung, colorectal, and prostate cancer 50 . ...

Integrated pan-cancer analysis of CSMD2 as a potential prognostic, diagnostic, and immune biomarker

... A group of researchers has also suggested that modulating iron physiology, especially in the tumor microenvironment by iron deprivation and iron overload toxicity, with exercise, can be used to treat cancer patients (67). Furthermore, research evidence suggest the successful use of iron biomarkers as prognostics for certain types of cancer (68). All this warrants further research to better employ iron physiology in cancer therapies. ...

Prognostic biomarker HAMP and associates with immune infiltration in gastric cancer
  • Citing Article
  • July 2022

International Immunopharmacology