International Journal of Medical Sciences最新文献

{"title":"Application and research progress of artificial intelligence in allergic diseases.","authors":"Hong Tan, Xuehua Zhou, Huajie Wu, Min Wang, Han Zhou, Yue Qin, Yun Zhang, Qiuhong Li, Jianfeng Luo, Hui Su, Xin Sun","doi":"10.7150/ijms.105422","DOIUrl":"https://doi.org/10.7150/ijms.105422","url":null,"abstract":"<p><p>Artificial intelligence (AI), as a new technology that can assist or even replace some human functions, can collect and analyse large amounts of textual, visual and auditory data through techniques such as Reinforcement Learning, Machine Learning, Deep Learning and Natural Language Processing to establish complex, non-linear relationships and construct models. These can support doctors in disease prediction, diagnosis, treatment and management, and play a significant role in clinical risk prediction, improving the accuracy of disease diagnosis, assisting in the development of new drugs, and enabling precision treatment and personalised management. In recent years, AI has been used in the prediction, diagnosis, treatment and management of allergic diseases. Allergic diseases are a type of chronic non-communicable disease that have the potential to affect a number of different systems and organs, seriously impacting people's mental health and quality of life. In this paper, we focus on asthma and summarise the application and research progress of AI in asthma, atopic dermatitis, food allergies, allergic rhinitis and urticaria, from the perspectives of disease prediction, diagnosis, treatment and management. We also briefly analyse the advantages and limitations of various intelligent assistance methods, in order to provide a reference for research teams and medical staff.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2088-2102"},"PeriodicalIF":3.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144014492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced risk of diabetic retinopathy in osteoarthritis patients undergoing joint replacement surgery.","authors":"Chin-Te Huang, Yat-Yin Law, Kai Wang, Chia-Yi Lee, Jing-Yang Huang, Shun-Fa Yang, Hsiang-Wen Chien","doi":"10.7150/ijms.109689","DOIUrl":"https://doi.org/10.7150/ijms.109689","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a progressive joint disorder frequently associated with multiple comorbidities. Emerging research suggests a potential link between OA and diabetic retinopathy, a microvascular complication of diabetes mellitus. This study investigates whether joint replacement surgery influences the risk of developing diabetic retinopathy in individuals with OA. Using data from the TriNetX database, we conducted a retrospective cohort study, categorizing OA patients into two groups based on whether they had undergone joint replacement surgery, with each group comprising 164,653 individuals. The primary outcome was the incidence of diabetic retinopathy, analyzed using Cox proportional hazards regression. Among patients who underwent joint replacement surgery, 844 developed diabetic retinopathy, compared to 1,336 cases in the non-surgery group. The incidence of diabetic retinopathy was significantly lower in the surgery group (P < 0.001). Additionally, cumulative incidence analysis confirmed a reduced risk in the surgery group (P < 0.001). Subgroup analyses further demonstrated a consistently lower risk across most demographic subgroups. In conclusion, our findings suggest that joint replacement surgery in OA patients is associated with a reduced risk of developing diabetic retinopathy. Further research is warranted to explore the underlying mechanisms and potential clinical implications.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2132-2138"},"PeriodicalIF":3.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cordycepin ameliorates morphine tolerance by inhibiting spinal cord ferroptosis and inflammation via targeting SIRT1.","authors":"Zheng Li, Jie Liu, Jie Ju, Xiaoling Peng, Wei Zhao, Jihao Ren, Xiaoqian Jia, Jihong Wang, Feng Gao","doi":"10.7150/ijms.108518","DOIUrl":"https://doi.org/10.7150/ijms.108518","url":null,"abstract":"<p><p>Morphine tolerance caused by long-term use of morphine is a major medical problem. Neuroinflammation plays an important role in morphine tolerance, and currently no drugs have been found for clinical use to alleviate neuroinflammation during morphine tolerance. Cordycepin is the main active component of fungus cordycepin militaris, has been demonstrated to have anti-oxidative stress and anti-inflammatory properties in various diseases. In this study, we established a rat model of morphine tolerance, examined the effect of cordycepin on the development of morphine tolerance, and evaluated its potential regulatory mechanisms. We found that cordycepin treatment ameliorated the development of morphine tolerance, improved mitochondrial damage associated with ferroptosis, by reducing the levels of reactive oxygen species (ROS), malondialdehyde (MDA) and Fe²⁺, increasing superoxide dismutase (SOD) and glutathione (GSH) levels, and decreasing the secretion of pro-inflammatory factors (IL-1β, IL-6, and TNF-α). Besides, cordycepin upregulated the expression of SIRT1, SLC7A11 and GPX4. Further research found that the above effects of cordycepin on morphine-tolerant rats were abolished by SIRT1 selective inhibitor EX-527. Thus, these findings indicated that cordycepin could ameliorate the development of morphine tolerance by inhibiting spinal cord ferroptosis and inflammation via targeting SIRT1. Collectively, these results demonstrated the protective effects of cordycepin and highlighted its therapeutic potential as a drug component for morphine tolerance treatment and prevention.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2059-2074"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of Chemotherapy Sensitivity of Breast Cancer Cells through Transforming Growth Factor-beta Pathway-mediated Alterations in DNA Damage Response.","authors":"Abdullah S Alhamed, Mohammad S El-Wetidy, Mervat M Abdelwahed, Sabry M Attia, Abdulrahman M Alabkka, Saleh A Alaraj, Khalid Alhazzani, Ahmed Z Alanazi, Faris Almutairi, Ibrahem A Alotibi, Mohammed Alqinyah","doi":"10.7150/ijms.111217","DOIUrl":"https://doi.org/10.7150/ijms.111217","url":null,"abstract":"<p><p>Chemotherapeutic drugs, like cisplatin, function by damaging genomic DNA, thus inducing cell apoptosis. Cancer cells can enhance their DNA repair capacity, leading to chemotherapeutic resistance. Nucleotide excision repair (NER) involves repairing DNA adducts and crosslinks caused by chemotherapeutic agents. Transforming growth factor-beta (TGF-β) pathway contributes to carcinogenesis, DNA repair alteration, and chemoresistance. However, the connection between TGF-β pathway, NER function alteration, and resistance to cisplatin therapy remains elusive. Therefore, the objective of current study was to fill this gap by assessing the impact of TGF-β inhibition and activation on cisplatin-induced antiproliferation, apoptosis, and DNA damage using the MTT assay, flow cytometry analysis, and COMET assay, respectively. Four NER genes, XPA, XPB, XPC, and XPF, were measured using Real-time Polymerase Chain Reaction (qPCR). MDA-MB-231 cell line was utilized as a model of breast cancer. Blockade of the TGF-β pathway strengthened cisplatin cytotoxicity, whereas induction of the TGF-β pathway suppressed cisplatin cytotoxicity. In cisplatin-treated breast cancer cells, DNA damage significantly increased upon the TGF-β pathway inhibition. Conversely, cisplatin-induced DNA damage decreased significantly upon TGF-β pathway stimulation. Finally, cisplatin caused an overexpression of the four NER genes which was curtailed and augmented by TGF-β inhibition and stimulation, respectively. Overall, this study presented evidence of the impact exerted by TGF-β pathway on NER and cisplatin sensitivity of breast cancer cells.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2031-2039"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emodin: an alveolar macrophage protector in acute pancreatitis induced lung injury.","authors":"Zhe Chen, Xuanchi Dong, Yongwei Song, Bowen Lan, Yalan Luo, Haiyun Wen, Hailong Chen","doi":"10.7150/ijms.105965","DOIUrl":"https://doi.org/10.7150/ijms.105965","url":null,"abstract":"<p><p><b>Background:</b> Emodin (EMO), an anthraquinone derivative from roots and leaves of various plants, has been widely used in many inflammatory diseases. Alveolar macrophages (AMs) play a critical role in maintaining alveolar homeostasis in the lung. However, the comprehensive mechanisms of EMO therapy on AMs during acute pancreatitis-associated lung injury (AP-ALI) have not been reported. <b>Methods:</b> Both in vivo [caerulein/ lipopolysaccharides (LPS)-induced AP-ALI in mice] and in vitro MH-S models were generated to assess the protective features of EMO on mitochondrial damage and mitophagy dysfunction of AMs during AP-ALI progression. <b>Results:</b> First, in vivo, the relative quantity of AMs was significantly decreased with time in AP-ALI mice; however, the mitochondrial flux presented earlier changes than the relative quantity of AMs in our experimental system. EMO pretreatment significantly alleviated the severity of lung injury and improved the damaged alveolar structure, reversing mitochondrial impairment in AMs. Secondly, in vitro, EMO significantly enhanced mitophagy and alleviated mitochondrial damage. Furthermore, the results following mitophagy inhibition by 3-methyladenine (3-MA) demonstrated that the protective effects of EMO were partially achieved by manipulating the mitophagy-mitochondria-alveolar macrophage axis. <b>Conclusion:</b> These data enabled a more comprehensive understanding of the therapeutic effects of EMO in AP-ALI.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2075-2087"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144011435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Malignant features related PRDX1 associated with osimertinib sensitivity of EGFR-mutant lung adenocarcinoma.","authors":"Wenying Jiang, Maonan Wang, Xiaoqian Yu, Guoqian Liu, Xiaoyun He, Cheng Mei, Chunlin Ou","doi":"10.7150/ijms.107255","DOIUrl":"https://doi.org/10.7150/ijms.107255","url":null,"abstract":"<p><p>The peroxiredoxin (PRDX) family, also known as the peroxidase family, consists of six members that participate in a variety of essential bio-processes in carcinogenesis. However, their molecular role in lung adenocarcinoma (LUAD) has not been systematically explored. Using bioinformatic tools, we systematically analyzed the expression, prognostic value and drug sensitivity of the PRDX gene family members in LUAD. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to verify the expression of PRDX1 in both LUAD tissues and cells. Cell Counting Kit-8 (CCK-8) assay was applied to detect the half-maximal inhibitory concentration (IC₅₀) of osimertinib in LUAD. A series of cellular drug assays, including 5-Ethynyl-2'-deoxyuridine (EdU), colony formation, and apoptosis assays, were performed to explore the correlation of PRDX1 with epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) sensitivity by using EGFR-mutant and wild-type LUAD cell lines. Among all the PRDX family members, PRDX1 has a promising prognostic value and is associated with EGFR mutations, as verified by experiments conducted on collected LUAD specimens. In addition, pathway enrichment analysis suggested that PRDX1 expression positively correlated with DNA repair, which is often considered to be inextricably linked to drug resistance in tumor cells. Thus, we validated the correlation between PRDX1 and EGFR-TKI sensitivity through a series of <i>in vitro</i> experiments and found that PRDX1 inhibition along with osimertinib treatment resulted in synergistic inhibition of tumor growth. Moreover, we found that PRDX1 was negatively correlated with the immune infiltration of dendritic cells (DCs) in the tumor microenvironment (TME) of LUAD, further suggesting an oncogenic role of PRDX1. This study demonstrates that high PRDX1 expression could be a potential diagnostic and prognostic marker of LUAD, and the strategy of PRDX1 knockdown provides new insights into improving the therapeutic sensitivity of EGFR-TKI in patients with LUAD.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2040-2058"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144011438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Transcription factor 7-like 2</i> rs77961654 polymorphism is related to stable angina and acute coronary syndrome in a Chinese population.","authors":"Teng-Hung Yu, Wei-Hua Tang, Thung-Lip Lee, Chin-Feng Hsuan, Chia-Chang Hsu, Chao-Ping Wang, Ching-Ting Wei, Min-Chih Cheng, Fu-Mei Chung, Yau-Jiunn Lee, I-Ting Tsai","doi":"10.7150/ijms.108111","DOIUrl":"https://doi.org/10.7150/ijms.108111","url":null,"abstract":"<p><p><b>Background:</b> Transcription factor 7-like 2 (TCF7L2) is a key member of the T-cell factor/lymphoid enhancer factor family, and it plays a pivotal role in human physiological processes and has been implicated in various pathological conditions. TCF7L2 has been associated with inflammation, metabolic regulation, and the development of atherosclerosis. Notably, TCF7L2 exerts an anti-atherosclerotic effect by activating specific molecular pathways. Furthermore, <i>TCF7L2</i> polymorphisms have been associated with the severity of coronary artery disease (CAD) and related mortality. This study aimed to investigate whether the <i>TCF7L2</i> gene polymorphism rs77961654 A/C influences the risk of CAD. <b>Methods:</b> A total of 262 patients with acute coronary syndrome (ACS), 313 patients with stable angina, and 488 healthy individuals were enrolled. The rs77961654 variant of <i>TCF7L2</i> was genotyped. <b>Results:</b> The frequency of the CC genotype of <i>TCF7L2</i> was higher in the stable angina and ACS groups compared to the healthy controls. After adjusting for confounding factors including age, sex, systolic blood pressure, body mass index, fasting blood glucose, total cholesterol, triglycerides, and smoking status, the CC genotype was associated with 10.46-fold and 8.00-fold higher risks of ACS and stable angina, respectively, than the AA genotype. In addition, the CC genotype was positively correlated with both stable angina and ACS, while the AA genotype was negatively correlated with ACS. Furthermore, the patients with stable angina or ACS carrying the CC genotype had significantly elevated levels of HbA1C, total white blood cell count, and lymphocyte count, and lower levels of adiponectin and secreted frizzled-related protein 5 compared to those with the AA genotype. A significant association was also identified between <i>TCF7L2</i> gene polymorphisms and type 2 diabetes mellitus (p for trend < 0.039). <b>Conclusion:</b> Polymorphisms in the <i>TCF7L2</i> gene may be associated with a higher risk of stable angina and ACS.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2020-2030"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143994562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacterial exotoxins in medicine: potential value and perspectives.","authors":"Yuming Xiao, Zhou Yan, Fangyuan Ren, Yurong Tan","doi":"10.7150/ijms.110104","DOIUrl":"https://doi.org/10.7150/ijms.110104","url":null,"abstract":"<p><p>Bacterial exotoxins are protein- or peptide-based substances secreted by bacteria with high toxicity and specificity. They have diverse mechanisms of action on host cells, leading to host injury by destroying the cellular structure or interfering with physiological functions. With the continuous progress in biotechnology, bacterial exotoxins have broad application prospects in immunotherapy, vaccine development, drug design, and other fields. Appropriate modification of exotoxins can lead to the preparation of highly efficient immune agents and targeted drugs, which brings new hope for overcoming difficult diseases. This study provides a comprehensive and in-depth introduction to the application of bacterial exotoxins in the field of medicine and further explores the potential value of bacterial exotoxins, which is expected to make greater contributions to human health in the future.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"2010-2019"},"PeriodicalIF":3.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA-binding proteins as a molecular link between COPD and pulmonary hypertension.","authors":"Yi Liu, Ran Wang, Tao Jiang","doi":"10.7150/ijms.108587","DOIUrl":"https://doi.org/10.7150/ijms.108587","url":null,"abstract":"<p><p>Pulmonary hypertension (PH) is a vascular disease characterized by remodeling of the pulmonary arteries and right heart failure. Chronic obstructive pulmonary disease (COPD) patients often have PH, which can worsen symptoms and raise morbidity and mortality. There are several reasons for increased pulmonary vascular resistance, pulmonary vascular remodeling, and ultimately the development of PH in COPD. These factors include genetics, inflammation caused by chemicals breathed, and changes in the alveoli seen in COPD and its physiology. Genes involved in mRNA conversion, subcellular localization, splicing, and translation are all finely tuned by RBPs in their post-transcriptional regulation. Erythropoietin regulates cytokines, chemokines, proteins, growth factors, and other pro-inflammatory mediators that change the lung microenvironment. Over the past few years, we have learned more about how RBPs act in PH and COPD. Here, we discuss the existing understanding of RBPs' location in the same pathogenic pathways shared by PH and COPD in order to emphasize their potential relevance as disease determinant/biomarker and, consequently, for possible therapeutic targeting.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 8","pages":"1979-1991"},"PeriodicalIF":3.2,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11983306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Solute Carrier Family 35 A2 (SLC35A2) Promotes Tumor Progression through MYC-Mediated Pathways in Colorectal Cancer.","authors":"Kuei-Yen Tsai, Po-Li Wei, Cheng-Chin Lee, Crystal Ngofi Zumbi, G M Shazzad Hossain Prince, Uyanga Batzorig, Chien-Yu Huang, Yu-Jia Chang","doi":"10.7150/ijms.109767","DOIUrl":"https://doi.org/10.7150/ijms.109767","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most prevalent cancers, posing a significant threat to human life. Although therapeutic approaches for advanced-stage patients have improved in recent years, there is still room for enhancing treatment response. Recent evidence suggests that dysregulation of nucleotide sugar transporters (NSTs) is associated with the development and progression of tumors. Therefore, this study aims to explore the potential therapeutic and prognostic implications of the solute carrier family 35 A (SLC35A) members in CRC. To achieve this, we performed integrative bioinformatics analysis using various publicly available databases, including GENT2, TCGA, UALCAN, cBioPortal, Kaplan-Meier plotter, The ROC plotter, GDSC, TISIDB, and TIMER. We compared gene expression profiles between CRC tumors and adjacent normal tissues, revealing that only SLC35A2 exhibited significant upregulation in tumors, while the other family members were downregulated. Additionally, higher SLC35A2 expression was found in microsatellite stable (MSS) colorectal tumors. Further analysis of TCGA and GEO datasets showed that patients with high SLC35A2 expression experienced poorer relapse-free survival. Next, we conducted gene set enrichment analysis (GSEA), and the results indicated that the upregulation of SLC35A2 is linked to cellular metabolism pathways, such as MYC Targets V2, Steroid Biosynthesis, Pentose Phosphate Pathway, and TCA Cycle. Furthermore, our CRC cell models revealed the tumor-promoting role of SLC35A2 and discovered that the upregulation of SLC35A2 is associated with chemoresistance against irinotecan. Additionally, we observed a negative correlation between SLC35A2 expression and the infiltration of immune cells, particularly cytotoxic CD8+ T cells and B cells. This suggests the immunomodulatory role of SLC35A2. In summary, SLC35A2 is abnormally upregulated in CRC, and patients with high SLC35A2 expression tend to have poor relapse-free survival. This may be due to its involvement in regulating cancer cell metabolic reprogramming, promoting tumor progression, modulating the immune landscape, and influencing treatment response. Consequently, SLC35A2 could serve as a significant prognostic factor and a potential therapeutic target in CRC.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 9","pages":"1992-2009"},"PeriodicalIF":3.2,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}