Traditional mammalian models present certain limitations in disease research. The tree shrew (Tupaia belangeri) has emerged as a  promising alternative to primate experimental animals due to its genetic, anatomical, and immunological similarities to humans, as well as advantages such as small body size and low breeding costs. In the field of infectious diseases, tree shrews  are capable of mimicking various viral infections, including influenza and hepatitis, thereby providing a platform for vaccine screening and  the investigation of immunological mechanism. In neuroscience, tree shrews are utilized to develop models of Alzheimer's disease and brain injury, thereby facilitating studies on neuroprotection and regeneration. In cancer research, tree shrew enable the models of liver cancer, breast cancer, and other malignancies, offering insights into tumor mechanisms and supporting drug screening. Nonetheless, challenges persist in tree shrew modeling, including the need for modification experimental techniques, shortages of antibodies, imperfect breeding systems, and ethical constraints. This review explores the applications of tree shrews in medical research from multiple perspectives, including genetics, immunology, infectious diseases, neuroscience, and oncology.  The aim is to provide references for promoting tree shrews as key models in precision medicine and novel drug discovery across broader fields.

The 2025 American Society of Clinical Oncology⁃Gastrointestinal Cancers Symposium (ASCO⁃GI) , convened in San Francisco, USA，　from January 23 to 25, 2025,  focused on pivotal topics within the fields of liver cancer, biliary tract cancer, and pancreatic cancer. Key areas of discussion included immunotherapy, targeted therapy, the integration of locoregional and systemic therapy, and precision medicine,  all underscoring numerous research findings of significant clinical relevance. These studies provide new evidence⁃based insights for the diagnosis and treatment of hepatobiliary and pancreatic tumors, offering valuable references for addressing unresolved clinical challenges and optimizing therapeutic strategies. This article systematically reviews the cutting⁃edge advancements in hepatobiliary and pancreatic tumors reported in ASCO⁃GI 2025, conducts an in⁃depth analysis of their clinical application value, and explores future research directions.

Tertiary lymphoid structures (TLS) are ectopic aggregates of lymphocytes that formed in the context of autoimmune diseases, chronic inflammation, or within the tumor microenvironment, where they play a crucial role in the anti⁃tumor immune response. In recent years, the positive promotional effects of TLS in hepatocellular carcinoma (HCC) and solid other malignancies have become increasingly apparent,  establishing TLS as a new research focus. This article aims to elaborate the characteristics, formation mechanism, distribution patterns in HCC, and prognostic implications of TLS. Additionally, it investigates the potential applications of TLS in the immunotherapy of HCC and conducts a comparative analysis of TLS effects across other solid tumors, providing novel insights and references for tumor immunotherapy, especially HCC immunotherapy.

Objective To evaluate the efficacy of transcatheter arterial chemoembolization (TACE) for intermediate to advanced hepatocellular carcinoma (HCC) patients with microvascular invasion (MVI) after radical resection. Methods A retrospective analysis was conducted on patients with intermediate to advanced HCC, who were postoperatively diagnosed with revealed MVI through pathological examination, across at five hospitals from January 14,2019 to June 20,2024. The study compared recurrence⁃free survival (RFS), overall survival (OS), and safety between patients who received postoperative TACE and underwent active surveillance. Results In a cohort of 335 included patients, 148 received postoperative TACE and 187 underwent active surveillance. During follow⁃up period, the postoperative TACE group demonstrated a significantly longer median RFS compared to the active surveillance group (15.2 months  vs 12.0 months; HR=0.69, 95%CI: 0.54-0.88, P=0.003). Although the median OS was not reached in the postoperative TACE group, there was a trend toward improved OS relative to the active surveillance group (not reached vs 33.1 months; HR=0.55, 95%CI: 0.40-0.77, P=0.001). Following propensity score matching, the postoperative TACE group demonstrated significantly superior RFS and OS compared to the active surveillance group (all P<0.05). Subgroup analysis based on tumor staging revealed comparable outcomes for patients with intermediate stage HCC in both groups, but significantly improved RFS and OS with advanced stage HCC patients in the postoperative TACE group (all P<0.05). Adverse events associated with postoperative TACE were primarily transient liver injury and nausea/vomiting, with no grade 4 or 5 events reported. Conclusions TACE following radical resection could improve the RFS and OS in some patients with intermediate to advanced HCC exhibiting MVI, particularly in those at advanced stages. However, further prospective randomized trials are crucial to validate these findings.

Objective To construct a nomogram that integraties imaging features and biomarkers to predict pathologic complete response (pCR) in patients with hepatocellular carcinoma (HCC) undergoing conversion therapy.  Methods The study cohort comprised HCC patients who received the transcatheter arterial chemoembolization (TACE) and/or hepatic arterial infusion chemotherapy (HAIC) in conjunction with targeted therapy and immunotherapy at Guangxi Medical University Cancer Hospital from November 2019 to October 2024. Independent predictors of pCR were identified through univariable and multivariable logistic regression analyses, and these predictors were utilized to develop the nomogram. The performance of the nomogram was evaluated using the area under the receiver operating characteristic curve (AUC), calibration curves, and decision curve analysis (DCA).  Results Among the 135 patients with HCC, 27.4% (37/135) achieved pCR following treatment. The systemic inflammatory response index (SIRI), tumor biomarker response, tumor number, and tumor complete response as assessed by the modified Response Evaluation Criteria in Solid Tumors (mRECIST) were identified as independent predictors of pCR (all P<0.05). A nomogram model was developed with AUC of  0.925 (95%CI: 0.882-0.967), demonstrating significantly superior predictive performance compared to the alpha⁃fetoprotein  (AFP) response (AUC=0.655) or mRECIST complete response (AUC=0.785)  (both  P<0.001). Internal validation using 1,000 times bootstrap resamples resulted in an AUC of 0.918 (95%CI: 0.873-0.963) for the nomogram model. The calibration curve confirmed excellent model calibration， and DCA demonstrated significant clinical utility. Conclusions The nomogram model,  incorporating SIRI, tumor biomarker response, tumor number, and mRECIST complete response,  provides an accurate pCR prediction following HCC conversion therapy in HCC patients and may serve as a foundation for individualized surgical decision⁃making.

Objective To investigate the role of glutamate⁃cysteine ligase catalytic subunit (GCLC) promoter methylation in the malignant transformation of hepatocyte induced by microcystin⁃LR (MCLR), as well as to assess the intervention effects of the DNA methylation inhibitor 5⁃aza⁃2'⁃deoxycytidine (5⁃aza). Methods A malignant transformation model was established by subjecting WRL68 cells to chronic exposure to 10 nmol/L MCLR until passage 25. Four experimental groups were constituted: the control group, the MCLR⁃exposed group, the 5⁃aza intervention group, and the MCLR plus 5⁃aza intervention group. The methylation status of the  GCLC gene promoter was assessed using Agena MassArray mass spectrometry⁃based nucleic acid analysis technology. Protein expression levels of GCLC and DNA methyltransferases (DNMTs) were determined via Western blot. Cellular proliferation, invasion, and migration capabilities were detected via Colony formation assay, soft agar assay, and Transwell assays, respectively. Additionally, glutamate⁃cysteine ligase (GCL) activity, glutathione (GSH) content, and 8⁃hydroxydeoxyguanosine (8⁃OHdG) levels were quantified using corresponding reagent kits. Results During the MCLR⁃induced malignant transformation of WRL68 cells, there was a progressive increase in the methylation level of the GCLC promoter, accompanied by a gradual decrease in both mRNA and protein expression levels (all  P<0.05). At passage 25 in the MCLR⁃exposed group, there was a significant elevation in the protein levels of DNMT⁃1, DNMT⁃3a, and DNMT⁃3b, while GCL activity and GSH content were markedly reduced, and 8⁃OHdG levels were significantly elevated (all P<0.05). Intervention with 5⁃aza at passage 25 in the MCLR⁃exposed group resulted in a reduction of GCLC promoter methylation levels, significantly upregulating GCLC mRNA and protein expression, enhanced GCL activity and GSH content, and reduced 8⁃OHdG levels (all P<0.05). Furthermore, 5⁃aza attenuated the migration, invasion, and cell colony formation capabilities of the MCLR⁃exposed group (all P<0.05). Conclusions GCLC promoter methylation contributes to the MCLR⁃induced malignant transformation of WRL68 cells. 5⁃aza may inhibit this malignant transformation by downregulating DNMTs expression, suppressing hypermethylation of the GCLC promoter, reactivating the expression of the silenced GCLC gene, and restoring its tumor⁃suppressive function.

Colorectal cancer (CRC), identified as the third most prevalent malignant tumor worldwide, has achieved substantial progress in its prevention and treatment paradigms. In the field of early detection, the implementation of artificial intelligence technology has markedly enhanced screening efficiency, addressing the limitations inherent in traditional invasive diagnostic methods. On the therapeutic front, transanal total mesorectal excision has facilitated the preservation of organ function, while total neoadjuvant therapy strategies have notably improved tumor regression and pathological downstaging in locally advanced CRC. Immunotherapy has conferred long⁃term survival benefits for CRC patients exhibiting deficient mismatch repair or high microsatellite instability. Additionally, novel targeted therapies  have significantly elevated both  the objective response rate and clinical benefit rate for patients with advanced CRC. The current landscape of CRC prevention has entered a new phase, characterized by the integration of precision surgery with multidimensional diagnostic and therapeutic approaches. This article provides a systematic review of recent significant research advance ments in CRC, with an emphasis on innovations in early screening and diagnosis, precise prevention strategies, advancements in minimally invasive surgical techniques, optimization of neoadjuvant treatment regimens, and breakthroughs in personalized treatment for metastatic CRC prevention and treatment. The aimis to offer decision⁃making references for clinical practice and establish theoretical foundations for future research directions.

Gastric cancer is a significant global public health challenge, causing a substantial disease burden. RNA alternative splicing（AS） is a critical gene expression regulation mechanism prevalent in higher eukaryotes. Through differential splicing patterns during the conversion of precursor mRNA to mature mRNA, a single gene can produce multiple splicing isoforms, thereby increasing the diversity and complexity of both transcriptomes and proteomes to meet the diverse physiological needs of an organism. RNA⁃AS dysregulation has been found to be associated with nearly all tumor types, contributing directly or indirectly to gastric cancer initiation, progression, drug resistance, and prognosis. Additionally, RNA⁃AS⁃related genetic variations play a crucial role in gastric cancer. This article systematically reviews research advances in the regulatory mechanisms of RNA⁃AS, as well as the impact of its dysregulation and related genetic variantions on gastric cancer, aiming to provide novel theoretical foundation and research perspectives for both RNA⁃AS⁃related further investigations and precision medicine strategies of gastric cancer.

Preoperative neoadjuvant chemoradiotherapy (nCRT) followed by total mesorectal excision (TME) has become the standard treatment protocol for patients with locally advanced rectal cancer (LARC). nCRT significantly reduces tumor volume and decreases the likelihood of recurrence. Accurate prediction of  treatment efficacy, prognosis, and toxicity in LARC patients undergoing nCRT is crucial for optimizing individualized diagnostic and therapeutic strategies. With the  advancement of radiomics and the rapid development of artificial intelligence technology, both fields have demonstrated substantial potential in medical image analysis. This article reviews the progress and limitations of radiomics and artificial intelligence in LARC patients undergoing nCRT, with the aim of providing a reference for development of individualized diagnostic and treatment strategies and exploring future research endeavors.

Objective To evaluate the health economic benefits of various screening strategies for upper gastrointestinal cancer in Fujian Province and to determine the most effective approach. Methods A Markov model was developed from the perspective of the healthcare system, utilizing both survey and literature data. Four distinct screening strategies were proposed⁃screening every 2 years, 3 years, 5 years, and 10 years with no screening serving as the control. The life years (LY), quality⁃adjusted life years (QALY) and net present value (NPV) were served as the cost⁃effectiveness, cost⁃utility, cost⁃benefit evaluation indicators, respectively. The incremental cost⁃effectiveness ratio (ICER), incremental cost⁃utility ratio (ICUR), and NPV were calculated for each screening strategy. The economic viability of each strategy was assessed using the 2023 per capita GDP of Fujian Province (¥129,865) as the willingness⁃to⁃pay (WTP) threshold. One⁃way sensitivity analysis and probability sensitivity analysis were performed to assess the robustness of the results. Results Compared with no⁃screening strategy, the ICERs for screening strategies conducted every 10, 5, 3, and 2 years were ¥4,215.47/LY, ¥5,208.17/LY, ¥5,566.44/LY, and ¥5,940.07/LY, respectively. Similarly, the ICURs were ¥4,316.71/QALY, ¥5,397.35/QALY, ¥5,788.25/QALY, and ¥6,183.54/QALY, respectively, all of which were significantly below the WTP threshold.The NPVs of  four screening strategies were positive, with biennial screening emerging as the most cost⁃effective option. Sensitivity analysis showed that the biennial screening remained highly cost⁃effective across all reasonable parameter variations, achieving a cost⁃effectiveness probability of 90% and stabilizing when the WTP threshold exceeded ¥20,000 per QALY. Conclusions Upper gastrointestinal cancer screening in Fujian Province offers favorable economic benefits, with biennial screening identified as the optimal strategy.

Objective To develop a discrimination model for differentiating between pancreatic cancer and benign pancreatic lesions using machine learning methods. Methods The study population consisted of 251 patients diagnosed with pancreatic diseases and treated at the Second Affiliated Hospital of Nanchang University between January 2018 and December 2023. Six machine learning models were developed, including logistic regression, random forest, eXtreme gradient boosting (XGBoost), support vector machine, multilayer perceptron, and Gaussian Naive Bayes, to distinguish pancreatic cancer from benign pancreatic lesions. The models' discriminatory capabilities were assessed using the receiver operating characteristic (ROC) curve. Model consistency was evaluated using a calibration curve, clinical applicability was assessed through a decision curve, and model interpretation was facilitated by the  SHapley Additive exPlanations (SHAP) method. Results Out of the  251 patients with pancreatic diseases, 100 were diagnosed with pancreatic cancer, while 151 were diagnosed with benign pancreatic lesions. Six machine learning models were successfully developed, with the area under the ROC curve (AUC) for the random forest, XGBoost, support vector machine, and multilayer perceptron models demonstrated superior performance compared to the carbohydrate antigen 19⁃9 (CA19⁃9) marker (all P<0.05). Notably, the XGBoost model exhibited the highest AUC （AUC=0.886）, and analyses using decision and calibration curves further confirmed its substantial clinical net benefit and consistency. SHAP analysis identified CA19⁃9 as the most significant contributor to the XGBoost model. Conclusions　XGBoost model developed using tumor markers and clinical test data, significantly enhances the ability to discriminate  between pancreatic cancer from benign pancreatic lesions, indicating potential for clinical application.

Objective To investigate the impact of Egl⁃9 family hypoxia⁃inducible factor 1 (EGLN1) deficiency on the proliferation, migration, invasion, and autophagic pathway of colorectal cancer (CRC) cells, and to provide potential targets for precision therapy in CRC. Methods EGLN1⁃knockout LoVo and RKO cell lines were generated using CRISPR⁃Cas9 technology. Cell proliferation, invasion, and migration were assessed through CCK⁃8 assay, colony formation assay, Transwell assay, and scratch wound⁃healing assay, respectively. Western blot analysis was performed to determine the LC3B⁃Ⅱ/LC3B⁃Ⅰratio and p62 protein expression levels, thereby assessing the activation of the autophagy pathway. A subcutaneous xenograft model in nude mice was developed to evaluate the effects of the autophagy activator Rapamycin on tumor growth in EGLN1 knockout xenografts. The cell proliferation of xenograft tissues was detected by hematoxylin and eosin (HE) staining and Ki⁃67 immunohistochemical staining. Results Stable EGLN1 knockout cell lines were successfully developed. The deletion of EGLN1 significantly enhanced proliferation, migration, and invasion in both LoVo and RKO cell lines (all P<0.05). The analysis results of autophagy⁃related proteins revealed a decreased LC3B⁃Ⅱ/LC3B⁃Ⅰratio and significant accumulation of p62 following EGLN1 knockout.  Treatment with the late⁃stage autophagy inhibitor chloroquine or the early⁃stage inhibitor 3⁃methyladenine  further exacerbated the inhibition of autophagy. In vivo experiments demonstrated that the EGLN1 knockout group developed significantly larger tumor volumes compared to the EGLN1 wild⁃type group (P<0.05), whlie treatment with Rapamycin effectively suppressed tumor growth. HE staining and Ki⁃67 immunohistochemistry confirmed that EGLN1 knockout promoted cell proliferation in xenografts, an effect that was reversible with rapamycin treatment. Conclusions EGLN1 appears to suppress the malignant phenotype of CRC cells by activating the autophagic pathway. Its deficiency may lead to  autophagy inhibition, thereby promoting tumor cell proliferation, migration, and invasion. Targeting the EGLN1/autophagy axis may represent an effective therapeutic strategy for CRC.

Nasopharyngeal carcinoma (NPC) is a highly prevalent head and neck malignancy in China, presenting significant challenges in early diagnosis. In 2019, the Expert Committee of Nasopharyngeal Cancer Biomarker, under the Tumor Biomarker Committee of China Anti⁃Cancer Association, convened a panel of multidisciplinary experts to publish the inaugural edition of the Expert consensus on the clinical application of nasopharyngeal carcinoma biomarkers, providing standardized guidance for clinical practice. With rapid advancements in novel biomarker research, this consensus has been comprehensively revised from the first edition, incorporating the latest research developments in NPC biomarkers and expert recommendations. The updates focus on supplementing clinical application evidence for novel serum biomarkers (P85⁃Ab), microbiome biomarkers, and immune microenvironment biomarkers, as well as optimizing the dynamic monitoring pathway of epstein⁃barr virus DNA and strategies for multi⁃biomarker application. This consensus aims to further enhance the precision of NPC screening, efficacy evaluation, and prognosis prediction through the systematic integration of cutting⁃edge research findings.

Objective To systematically evaluate and compare the efficacy and safety profiles of proton therapy (PT)  and X⁃ray radiation therapy (XRT)  in head and neck cancer. Methods  A systematic review and meta⁃analysis were conducted, incorporating thirteen studies published between 2015 and 2024, comprising 863 cases in the PT group and 2，443 cases in the XRT group. The analysis evaluated local control (LC) rate at 1 and 2 years, disease⁃free survival/progression⁃free survival (DFS/PFS) rate at 1, 2, and 3 years,  as well as overall survival (OS) rate. Additionally, it examined the incidence of acute toxicities of grade 2 or higher. Results No statistically significant differences were observed between the PT group and the XRT group in terms of 1⁃year LC rate  OR=1.16, 95%CI: 0.19-7.25) or 2⁃year LC rate (RR=0.74, 95%CI: 0.54-1.02). Furthermore , there were no statistically significant differences in DFS/PFS rate between the two groups at 1⁃year (RR=0.93, 95%CI: 0.67-1.29), 2⁃year (RR=0.91, 95%CI: 0.67-1.22), and 3⁃year (RR=0.99, 95%CI: 0.75-1.29). However, the PT group demonstrated superior OS at 1⁃year (CI=0.47, 95%CI: 0.35-0.65), 2⁃year (RR=0.52, 95%CI: 0.40-0.67), and 3⁃year (RR=0.56, 95%CI: 0.45-0.69) compared to the XRT group. Additionally, the incidence of  ≥grade 2 dysphagia (OR=0.35, 95%CI: 0.18-0.69) and fatigue (OR=0.46, 95%CI: 0.24-0.90) was lower in the PT group than in the XRT group. Conclusions The PT group demonstrates superior survival benefits and reduced acute toxicity risks compared to the XRT group in the treatment of head and neck cancer. Further prospective studies are warranted to validate the efficacy and safety of PT.

Objective To systematically evaluate and compare the efficacy and safety profiles of proton therapy (PT)  and X⁃ray radiation therapy (XRT)  in head and neck cancer. Methods  A systematic review and meta⁃analysis were conducted, incorporating thirteen studies published between 2015 and 2024, comprising 863 cases in the PT group and 2，443 cases in the XRT group. The analysis evaluated local control (LC) rate at 1 and 2 years, disease⁃free survival/progression⁃free survival (DFS/PFS) rate at 1, 2, and 3 years,  as well as overall survival (OS) rate. Additionally, it examined the incidence of acute toxicities of grade 2 or higher. Results No statistically significant differences were observed between the PT group and the XRT group in terms of 1⁃year LC rate  (RR=1.16, 95%CI: 0.19-7.25) or 2⁃year LC rate (RR=0.74, 95%CI: 0.54-1.02). Furthermore , there were no statistically significant differences in DFS/PFS rate between the two groups at 1⁃year (RR=0.93, 95%CI: 0.67-1.29), 2⁃year (RR=0.91, 95%CI: 0.67-1.22), and 3⁃year (RR=0.99, 95%CI: 0.75-1.29). However, the PT group demonstrated superior OS at 1⁃year (RR=0.47, 95%CI: 0.35-0.65), 2⁃year (RR=0.52, 95%CI: 0.40-0.67), and 3⁃year (RR=0.56, 95%CI: 0.45-0.69) compared to the XRT group. Additionally, the incidence of  ≥grade 2 dysphagia (OR=0.35, 95%CI: 0.18-0.69) and fatigue (OR=0.46, 95%CI: 0.24-0.90) was lower in the PT group than in the XRT group. Conclusions The PT group demonstrates superior survival benefits and reduced acute toxicity risks compared to the XRT group in the treatment of head and neck cancer. Further prospective studies are warranted to validate the efficacy and safety of PT.

Objective To identify potential key genes associated with radiotherapy response in head and neck squamous cell carcinoma (HNSCC) and validate their functional. Methods Differentially expressed genes (DEGs) between the radiotherapy response group and the non⁃response group were screened using the GSE39366 dataset. Prognostically relevant genes were selected through Cox proportional hazards regression analysis within the cancer genome atlas (TCGA). The key genes were identified through a Venn diagram analysis, followed by functional enrichment analysis. The immune microenvironment, including the ESTIMATE score and immune cell infiltration analysis, as well as interactions with immune⁃related genes, were performed on these key genes. A prognostic prediction model was developed by integrating these key genes with the clinical characteristics of patients. The prognostic impact of the key genes was validated using the external dataset GSE41613. Differences in radiosensitivity among cells with varying levels of gene expression were assessed via CCK⁃8 assays and flow cytometry. Changes in the expression of key genes under different radiotherapy doses were detected by RT⁃qPCR. Results A total of 519 DEGs and 81 prognostic⁃related genes were identified, with CCR7, MS4A1, TBC1D10C and CTTN being determined as key genes influencing radiosensitivity in HNSCC. These genes exhibited significant correlations with tumor immune infiltration, and the nomogram model constructed based on them demonstrated good predictive performance. External dataset validation indicated that CCR7 and CTTN were significantly associated with patient prognosis (all P<0.05), whereas MS4A1 and TBC1D10C did not show significant prognostic value (all P>0.05). In vitro experiments further confirmed that HNSCC cells with elevated CCR7 expression and reduced CTTN expression exhibited increased sensitive to radiotherapy. The expression levels of CCR7 and CTTN were observed to change dynamically with varying radiotherapy doses.  Conclusions The expression levels of CCR7 and CTTN are closely related to radiosensitivity and prognosis in HNSCC, potentially throungh mechanisms involving the regulation of immune microenvironment. CRRT and CTTN may serve as predictive biomarkers for HNSCC radiosensitivity and potential therapeutic targets.

Objective To elucidate the molecular mechanisms through which ubiquitin⁃specific peptidase 41 (USP41) modulates the malignant biological behavior of head and neck squamous cell carcinoma (HNSCC). Methods The Gene Expression Profiling Interactive Analysis (GEPIA) database was used to examine expression profiling of USP41 across various tumors, including HNSCC. HNSCC cells lines (UM2, UM1, and HN31), along with normal oral keratinocyte (HOK) cells were cultured in vitro. Plasmid transfections were conducted to achieve knockdown of USP41 utilizing shRNA constructs (shRNA#1 and shRNA#2) and to facilitate the overexpression of signal transducer and activator of transcription 1 (STAT1). and USP41. Corresponding empty vector controls were included concurrently. Reverse transcription quantitative polymerase chain reaction (RT⁃qPCR) was used to quantify the mRNA expression levels of USP41, epithelial⁃mesenchymal transition (EMT) markers (E⁃cadherin, vimentin, and N⁃cadherin), and STAT1. Western blot analysis was used to determine the protein expression and ubiquitination levels of USP41and STAT1. Cell Counting Kit⁃8 (CCK⁃8), colony formation, and Transwell assays were conducted to assess the cells proliferation, migration, and invasion capabilities. Co⁃immunoprecipitation combined with Western blot analysis was used to validate the interaction between USP41 and STAT1 in UM1 cells. Results USP41 expression was upregulated in various tumor types, including HNSCC (P<0.05). Both mRNA and protein levels of USP41 were elevated in UM1 and HN31 cell lines (all P<0.05). Knockdown of USP41 resulted in the inhibition of cell proliferation, migration and invasion, accompanied by an increase in E⁃cadherin expression and a decrease Vimentin and N⁃cadherin expression (all P<0.01). These effects were reversed upon overexpression of STAT1. USP41 overexpression led to a reduction in  ubiquitinated protein levels while enhancing the expression of STAT1 and USP41 protein in UM1 cell lines. Co⁃immunoprecipitation and Western blot confirmed the interaction between USP41 and STAT1 in UM1 cell lines. Conclusions USP41 is markedly overexpressed in HNSCC cell lines and facilitates cell proliferation, migration, invasion, and EMT progression through STAT1 deubiquitination, suggesting its potential as a therapeutic target for HNSCC.

Perioperative lung injury (PLI) represents a prevalent clinical complication. Although significant advancements have been made in elucidating its pathogenesis in recent years, the development of effective early diagnostic and intervention strategies remains limited in clinical practice. This limitation is primarily attributed to the complexity of the factors inducing PLI and the heterogeneity of its pathological processes. Current research underscores the pivotal roles of immune⁃inflammatory responses and cellular stress states in the initiation and progression of PLI. This article provides a comprehensive review of  the latest advancements in PLI⁃related immune recognition, organelle dysfunction, programmed cell death, and regulatory mechanisms of repair. The aim is to furnish theoretical support for the exploration of perioperative lung protection strategies and the development of novel intervention approaches.