Severe acute pancreatitis (SAP) is a life-threatening inflammatory disorder with an approximate mortality rate of 40

In recent years, magnetic hyperthermia therapy (MHT), recognized as a clinically promising anticancer treatment, has focused on enhancing therapeutic outcomes in tumor management, such as optimizing magnetic nanoparticle accumulation within tumor microenvironments and developing synergistic combination approaches with other therapies. Herein, we developed nanoengineered neutrophils (NE) by loading magnetic nanoparticles (FPP) onto healthy-derived NE, designated as FPPN. The combination of FPP's pronounced T2-weighted magnetic resonance imaging (MRI) and superior magnetothermal efficiency with the high tumor-targeting and cancer-killing activity of NE successfully achieved the synergistic implementation of MHT and NE. Under the guidance of T2-weighted MRI, the accumulation of FPPN within the tumor site demonstrated a significant enhancement compared with free FPP. Under exposure to alternating magnetic fields, the thermal energy produced by FPP and FPPN could ablate tumor cells directly. Intriguingly, mitochondria within NE exhibit significant reactive oxygen species (ROS) under magnetothermal activation, thereby enhancing therapeutic efficacy and enabling synergistic tumor treatment through the combination of MHT and NE-mediated ROS. This therapeutic strategy not only highlighted the significant potential of nanoengineered NE for highly efficient MHT but also established a novel therapeutic platform for precision-targeted treatment of deep-seated tumors.

Objective·To explore the mechanism at the atomic level by which the KRASG12D/R68G mutation induces tumor cell resistance to MRTX1133.Methods·The crystal structure data of the KRASG12D-MRTX1133 complex were obtained from the RCSB Protein Data Bank (PDB). PyMOL software was used to mutate arginine at position 68 of KRAS to glycine (R68G), constructing the initial conformations of the KRASG12D-MRTX1133 and KRASG12D/R68G-MRTX1133 complexes. The LEaP module was used to build simulation systems under periodic boundary conditions. The ff19SB force field was applied to standard amino acids in KRAS, GAFF (general AMBER force field) to MRTX1133, and TIP3P (intermolecular potential three point) to water molecules. Energy minimization was performed using the Amber software suite. The systems were then heated to 300 K, followed by NVT (constant volume and temperature) equilibration and NPT (constant pressure and temperature) production. Root mean square deviation (RMSD), root mean square fluctuation (RMSF), principal component analysis (PCA) and solvent-accessible surface area (SASA) of MRTX1133 and GDP were analyzed using cpptraj. The number of hydrogen bonds between regions and the dynamic cross-correlation matrix (DCCM) of amino acid movements were also calculated.Results·RMSD analysis showed greater structural variation in KRAS in the KRASG12D/R68G system compared to the KRASG12D system. RMSF analysis revealed significantly higher fluctuations in the Switch Ⅰ and Switch Ⅱ regions of the KRASG12D/R68G system. PCA indicated that Switch Ⅰ and Switch Ⅱ in the KRASG12D/R68G system were more frequently in an open conformation. The distances between Switch Ⅰ and the P-loop, and between Switch Ⅱ and the P-loop, were larger in the KRASG12D/R68G system, indicating an expanded binding pocket for GDP and MRTX1133 compared to the KRASG12D system. SASA analysis indicated that both GDP and MRTX1133 had increased solvent exposure in the KRASG12D/R68G system. DCCM analysis revealed more decoupled movements among the Switch Ⅰ, Switch Ⅱ and P-loop regions in the KRASG12D/R68G system.Conclusion·The KRASG12D/R68G mutation disrupts the interactions between the Switch Ⅰ and Switch Ⅱ regions, leading to their separation and the opening of the MRTX1133 binding pocket. This increases the solvent exposure of MRTX1133, accelerates its dissociation, and ultimately results in KRASG12D/R68G resistance to MRTX1133.

Pancreatic cancer, characterized by its insidious onset, high invasiveness, resistance to chemotherapy, and a grim prognosis, with a five-year survival rate hovering below 10 %. The identification of novel therapeutic targets addressing tumor progression is therefore critically important. While perineural invasion (PNI) is recognized as a pathological hallmark and key driver of pancreatic cancer progression, its role in metabolic reprogramming of malignant cells has not been fully elucidated. Using integrated metabolomics approaches, we found perineural invasion in pancreatic cancer significantly enhancing glycolytic flux of pancreatic cancer. Our data delineate a neuroendocrine-paracrine signaling axis in which neurturin secreted by neuronal cells binds to the GFRA2 receptor on pancreatic cancer cells, inducing RET kinase recruitment and subsequent heterodimer assembly. This receptor tyrosine kinase complex phosphorylates hexokinase 2 (HK2) at the evolutionarily conserved Ser122 residue, augmenting its hexokinase activity, ultimately driving aerobic glycolysis flux and fueling pancreatic cancer growth. In vivo experiments corroborate our findings, revealing that neurturin blockade effectively halts pancreatic cancer progression and synergizes with RET inhibitors. Our research underscores neurturin as a promising therapeutic target for the treatment of pancreatic cancer.

Disulfidptosis is a newly discovered formation of programmed cell death. However, the significance of disulfidptosis in pancreatic adenocarcinoma remains unclear. Our investigation aims to elucidate the significance of disulfidptosis in pancreatic ductal adenocarcinoma by integrating diverse datasets, including bulk RNA sequencing data, microarray profiles, single-cell transcriptome profiles, spatial transcriptome data, and biospecimens. Utilizing various bioinformatics tools, we screened disulfidptosis-related genes based on single-cell RNA sequencing profiles, subsequently validating them through enrichment analysis. An 8-gene disulfidptosis-related prognostic signature was established by constructing massive LASSO-Cox regression models and validated by multiple external PDAC cohorts. Evaluation methods, such as Kaplan-Meier curves, ROC curves, time-dependent ROC curves, and decision curve analysis, were employed to assess the prognostic signature’s reliability. High disulfidptosis-related scores were associated with a poorer prognosis and diminished sensitivity to immune checkpoint blockade. Further investigation uncovered that the potential components of elevated DPS involve malignant tumor hallmarks, extensive interactions between myCAFs and tumor cells, and the exclusion of immune cells. Cell-cell communication analysis highlighted myCAFs’ role in signaling, potentially influencing tumor cells towards increased malignancy through collagen, laminin, and FN1 signaling networks. Spatial transcriptome analysis confirmed the crosstalk between myCAFs and tumor cells. Biospecimens including 20 pairs of PDAC samples and adjacent normal tissues further demonstrated the robustness of DPS and its correlation with CAF markers. In conclusion, our study introduces a novel disulfidptosis-related signature with high efficacy in patient risk stratification, which has the ability to predict the sensitivity to immune checkpoint blockade.

Background: With the rising demand for minimally invasive and cosmetically appealing surgeries, transumbilical single-incision laparoscopic cholecystectomy (SILC) has been increasingly adopted, albeit in a limited number of medical centers. Our team has successfully executed transumbilical SILC for benign gallbladder diseases. This study retrospectively analyzed and compared the efficacy of transumbilical SILC with that of conventional laparoscopic cholecystectomy (CLC). Methods: We analyzed data from 358 cases of laparoscopic cholecystectomy performed at Shanghai East Hospital of Tongji University between January 2021 and October 2023. Of these, 186 cases underwent SILC (observation group), while 172 cases underwent CLC (control group). We compared patient demographics, perioperative outcomes, and satisfaction with incision scars. Primary outcomes included surgical efficacy and safety, whereas secondary outcomes encompassed postoperative hospitalization duration, pain levels, hospital costs, and scar satisfaction. Results: No significant differences were observed in patient demographics between the two groups. Both the SILC and CLC groups exhibited similar operative times (39.56 ± 14.55 minutes versus 41.82 ± 16.13 minutes, P = .164) and intraoperative blood loss (11.34 ± 3.90 mL versus 11.28 ± 3.87 mL, P = .885). The single-incision approach led to earlier postoperative bowel function recovery (22.03 ± 3.60 hours versus 24.17 ± 3.22 hours, P < .01), lower 24-hour postoperative pain scores (2.06 ± 0.84 versus 2.35 ± 0.72, P < .01), shorter postoperative hospital stays (2.88 ± 0.86 days versus 3.33 ± 0.96 days, P < .01), comparable hospitalization costs (3411.67 ± 790.86$ versus 3494.50 ± 558.76$, P = .257), and better Scar Cosmesis Assessment and Rating scores (1.78 ± 0.70 versus 2.17 ± 0.89, P < .01). Patient satisfaction was higher with the single-incision technique (8.52 ± 0.79 versus 7.80 ± 0.75, P < .01). Both groups experienced one case of incision infection (SILC 0.54%, CLC 0.58%), and there was one case of postoperative bile leakage in the CLC group (0.58%). However, the difference in complications was not statistically significant (P > .05). Conclusion: Transumbilical SILC demonstrates safe and effective near-term efficacy, offering benefits such as reduced postoperative pain and improved cosmetic outcomes, which support its clinical adoption.

Background: Minimally invasive treatments for cholelithiasis have gained popularity. The complexity of diagnosing and treating choledocholithiasis offers multiple surgical options, including laparoscopic common bile duct exploration plus laparoscopic cholecystectomy (LCBDE+LC) and endoscopic retrograde cholangiopancreatography and/or endoscopic sphincterotomy plus laparoscopic cholecystectomy (ERCP/EST+LC). Objective: To compare outcomes in patients with typical signs, symptoms, laboratory, and imaging features of cholelithiasis combined with common bile duct stones, we retrospectively analyzed the short-term outcomes of LCBDE+LC and ERCP/EST+LC. Methods: We analyzed 318 patients with gallbladder stones treated between January 2022 and May 2024. Of these, 152 underwent LCBDE+LC, and 166 underwent ERCP/EST+LC. We compared patients' baseline characteristics, perioperative outcomes, and short-term complications between the two groups. The primary outcome was the effectiveness of choledochal stone removal, while secondary outcomes included length of stay, hospitalization costs, and patient satisfaction. Results: Patients' baseline characteristics were similar between the LCBDE+LC and ERCP/EST+LC groups. Stone clearance rates were comparable (97.37% versus 95.18%, P = .306), with a slight advantage in the LCBDE+LC group. The length of hospitalization was significantly shorter in the LCBDE+LC group (6.49 +/- 1.18 days versus 6.77 +/- 1.11 days, P < .05). The LCBDE+LC group also had lower total hospitalization costs ($5188.78 +/- 861.26 versus $6498.76 +/- 1190.58 P < .01). Additionally, the incidence of pancreatitis was lower in the LCBDE+LC group (0.66% versus 6.02%, P < .01). There were no significant differences between the groups in other short-term complications such as abdominal infection, cholangitis, biliary bleeding, or bile leakage. Postoperative follow-up indicated higher patient satisfaction and acceptance in the LCBDE+LC group (SSQ-8, 85.84 +/- 4.31 points versus 81.20 +/- 4.54 points, P < .01). Conclusion: Our findings suggest that the LCBDE+LC holds promise as a safe and efficacious approach for the management of cholelithiasis combined with common bile duct stones. However, further prospective clinical trials are essential to corroborate these results and confirm their broader applicability.

Ocular melanoma, including uveal melanoma (UM) and conjunctival melanoma (CM), is the most common ocular cancer among adults with a high rate of recurrence and poor prognosis. Loss of epigenetic homeostasis disturbed gene expression patterns, resulting in oncogenesis. Herein, we comprehensively analyzed the DNA methylation, transcriptome profiles, and corresponding clinical information of UM patients through multiple machine-learning algorithms, finding that a methylation-driven gene RBMS1 was correlated with poor clinical outcomes of UM patients. RNA-seq and single-cell RNA-seq analyses revealed that RBMS1 reflected diverse tumor microenvironments, where high RBMS1 expression marked an immune active TME. Furthermore, we found that tumor cells were identified to have the higher communication probability in RBMS1+ state. The functional enrichment analysis revealed that RBMS1 was associated with pigment granule and melanosome, participating in cell proliferation as well as apoptotic signaling pathway. Biological experiments were performed and demonstrated that the silencing of RBMS1 inhibited ocular melanoma proliferation and promoted apoptosis. Our study highlighted that RBMS1 reflects a distinct microenvironment and promotes tumor progression in ocular melanoma, contributing to the therapeutic customization and clinical decision-making.

Pancreatic cancer is one of the most lethal tumors due to its rapid proliferation and aggressiveness. RAD51AP1 is a protein-coding gene with critical functions in many cancers but few studies have assessed RAD51AP1 in pancreatic cancer. Bioinformatics methods and cell function experiments were performed to reveal the functions of RAD51AP1 in vitro. Gene Expression Profiling Interactive Analysis (GEPIA) was used to explore key proteins and their relationships with RAD51AP1 in the PI3K/AKT/NF-κB signaling pathways. Western blotting (WB) was conducted to detect the expression of key proteins after the downregulation of RAD51AP1. Co-Immunoprecipitation (Co-IP) was applied to confirm the binding of RAD51AP1 and PI3K. In addition, the lentivirus was used to construct subcutaneous tumors in nude mice to verify the function of RAD51AP1 in vivo. The Kaplan-Meier curves illustrated that elevated expression levels of RAD51AP1 were significantly correlated with reduced overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI) in pancreatic cancer patients. The results of WB showed that several key proteins in the PI3K/AKT/NF-κB signaling pathway (including PI3K, AKT, IKK1, IKK2, P65, P50, C-FLIP, and XIAP) exhibited a significant knockdown upon reducing the expression of RAD51AP1. Co-IP suggested that RAD51AP1 could directly bind to PI3K. In vitro, CCK-8, wound healing, and Transwell assays revealed that high RAD51AP1 expression was significantly correlated with increased cell proliferation, migration, and invasion. In vivo, mouse tumor formation experiments showed that RAD51AP1 inhibition significantly inhibited tumor growth. RAD51AP1 plays an important role in fostering cellular proliferation, invasion, metastasis, and tumor enlargement via the PI3K/AKT/NF-κB signaling pathway.

BackgroundOcular melanoma is an aggressive malignancy with a high rate of metastasis and poor prognosis. Increasing evidence indicated that DNA methylation plays an important role in the occurrence and development of ocular melanoma. Hence, exploring new diagnostic and prognostic biomarkers at the genetic level may be beneficial to the prognosis of patients with ocular melanoma.MethodsWe collected DNA methylation and gene expression profiles of human UM (uveal melanoma) and CM (conjunctival melanoma) samples from various datasets. We conducted differential methylation and expression analyses to screen the potential biomarkers. Correlation analysis was performed to investigate the relationships between the expression level of DLL3 (delta-like protein 3) and the methylation level of its corresponding CpGs. We explored the prognostic and diagnostic value of DLL3 in UM and CM. Functional annotation and GSEA (gene set enrichment analysis) were applied to get insight into the possible biological roles of DLL3. A cohort of 60 ocular melanoma patients as well as UM and CM cell lines were used to validate our findings in bioinformatic analyses.ResultsWe found that DLL3 was a methylation-driven gene correlating with UM metastasis. The CpGs of DLL3 are mainly located in the gene body and their methylation level positively correlated to DLL3 expression. Multivariate Cox regression analysis revealed that DLL3 was an independent protective factor for UM patients. High DLL3 expression significantly prolonged the overall survival and disease-free survival of UM patients. DLL3 also showed a promising power to distinguish CM from normal tissues. Functional annotation exhibited that DLL3 may suppress UM progression through modulating immune activities and down-regulating various signaling pathways. External datasets, biospecimens, and cell lines further validated the aberrant expression and prognostic role of DLL3 in ocular melanoma.ConclusionMethylation-driven gene DLL3 could serve as a new potential diagnostic and prognostic biomarker in ocular melanoma. Our findings may contribute to improving the clinical outcomes of patients with UM or CM.

Gastric cancer (GC) is a disease characterized by high molecular and phenotypic heterogeneity and represents a leading cause of cancer-related death worldwide. The tumor immune microenvironment (TIME) affects the response to immunotherapy and the prognosis of patients with GC. Explorations of the TIME in GC and characterization of molecular subtypes might enhance personalized treatment and facilitate clinical decision-making. In this study, two molecular subtypes were defined through unsupervised consensus clustering based on immune-related dysregulated genes. Then, patients with different molecular subtypes of GC were shown to have distinct differences in sensitivity to immune checkpoint blockers (ICBs). The immune-related prognostic signature was established utilizing least absolute shrinkage and selection operator (LASSO)-Cox regression analysis. Three independent external cohorts and the IMvigor210 cohort were introduced to validate the robustness of IPRS. scRNA-seq data of GC samples were used to decipher the underlying mechanisms of how IPRS contributes to the TIME. GC biospecimens were collected for RT-qPCR to further validate our findings. In summary, we characterized the abnormal TIME of GC and constructed a reliable immune-related prognostic signature correlating with the response to immunotherapy. This study may provide new strategies for developing individualized treatments for patients with GC.

The development of multifunction nanoplatforms integrating accurate diagnosis and efficient therapy is of great significance for the precise treatment of tumors. Gold nanoparticles (AuNPs) possessing hallmark features of computed tomography (CT) imaging and photothermal conversion capability hold great potential in tumor theranostics. In this study, taking the advantages of outstanding biocompatibility, interesting anti-inflammatory and immunomodulatory properties, and abundant amino acid residues of silk fibroin (SF), a multifunctional Gd-hybridized AuNP nanoplatform was constructed using SF as a stabilizer and reductant via a facile one-pot biomimetic method, denoted as Gd:AuNPs@SF. The obtained Gd:AuNPs@SF possessed fascinating biocompatibility and excellent photothermal conversion efficiency. Functionalized with Gd, Gd:AuNPs@SF exhibited super tumor-contrasted imaging performance in magnetic resonance (MR) and CT imaging modalities. Moreover, Gd:AuNPs@SF, with strong NIR absorbance, demonstrated that it could effectively kill tumor cells in vitro, and was also proved to successfully ablate tumor tissues through MR/CT imaging-guided photothermal therapy (PTT) without systemic toxicity in Pan02 xenograft C57BL/6 mouse models. We successfully synthesized Gd:AuNPs@SF for MR/CT dual-mode imaging-guided PTT via a facile one-pot biomimetic method, and this biomimetic strategy can also be used for the construction of other multifunction nanoplatforms, which is promising for precise tumor theranostics.

Bile acid reflux and subsequent caudal-related homeobox 2 (CDX2) activation contribute to gastric intestinal metaplasia (IM), a precursor of gastric cancer; however, the mechanism underlying this phenomenon is unclear. Here, we demonstrate that alkylation repair homolog protein 5 (ALKBH5), a major RNA N6-adenosine demethylase, is required for bile acid-induced gastric IM. Mechanistically, we revealed the N6-methyladenosine (m6A) modification profile in gastric IM for the first time and identified ZNF333 as a novel m6A target of ALKBH5. ALKBH5 was shown to demethylate ZNF333 mRNA, leading to enhanced ZNF333 expression by abolishing m6A-YTHDF2-dependent mRNA degradation. In addition, ALKBH5 activated CDX2 and downstream intestinal markers by targeting the ZNF333/CYLD axis and activating NF-κB signaling. Reciprocally, p65, the key transcription factor of the canonical NF-κB pathway, enhanced the transcription activity of ALKBH5 in the nucleus, thus forming a positive feedforward circuit. Furthermore, ALKBH5 levels were positively correlated with ZNF333 and CDX2 levels in IM tissues, indicating significant clinical relevance. Collectively, our findings suggest that an m6A modification-associated positive feedforward loop between ALKBH5 and NF-κB signaling is involved in generating the IM phenotype of gastric epithelial cells. Targeting the ALKBH5/ZNF333/CYLD/CDX2 axis may be a useful therapeutic strategy for gastric IM in patients with bile regurgitation.

Stomach adenocarcinoma (STAD) is one of the most common cancers in the world. However, the prognosis of STAD remains poor, and the therapeutic effect of chemotherapy and immunotherapy varies from person to person. MicroRNAs (miRNAs) play vital roles in tumor development and metastasis and can be used for cancer diagnosis and prognosis. In this study, hsa-miR-100-5p was identified as the only dysregulated miRNA in STAD samples through an analysis of three miRNA expression matrices. A weighted gene co-expression network analysis (WGCNA) was performed to select hsa-miR-100-5p-related genes. A least absolute shrinkage and selection operator (LASSO) Cox regression analysis was performed to establish a miR-100-5p-related prognostic signature. Kaplan–Meier analyses, nomograms, and univariate and multivariate Cox regression analyses were used to evaluate the prognostic signature, which was subsequently identified as an independent risk factor for STAD patients. We investigated the tumor immune environment between low- and high-risk groups and found that, among component types, M2 macrophages contributed the most to the difference between these groups. A drug sensitivity analysis suggested that patients with high-risk scores may be more sensitive to docetaxel and cisplatin chemotherapy and that patients in the low-risk group may be more likely to benefit from immunotherapy. Finally, external cohorts were evaluated to validate the robustness of the prognostic signature. In summary, this study may provide new ideas for developing more individualized therapeutic strategies for STAD patients.

Pancreatic ductal adenocarcinoma (PDAC) is one of most lethal cancers and is projected to be the second leading cause of cancer deaths in the United States by 2030. The lack of effective treatment and increased incidence in PDAC encourage a deeper knowledge of PDAC progression. By analyzing a long noncoding RNA (lncRNA) dataset, we found that increased LINC00941 expression led to poor outcomes in PDAC patients. Furthermore, in vitro and in vivo experiments revealed that LINC00941 promoted PDAC cancer cell growth by enhancing aerobic glycolysis. Mechanistically, LINC00941 was found to interact with mammalian STE20-like protein kinase 1 (MST1), which facilitated the protein phosphatase 2A (PP2A)-mediated dephosphorylation of MST1, resulting in Hippo pathway activation and consequently, enhanced glycolysis in PDAC. These results suggest that LINC00941 plays a key role in regulating PDAC tumorigenesis, potentially highlighting novel avenues for PDAC therapy.

Pancreatic adenocarcinoma is one of the most lethal diseases with a 5-year survival rate of about 8%. ASXL2 is an epigenetic regulator associated with various tumors including colorectal cancer, breast cancer, and myeloid leukemia. However, the role of ASXL2 in pancreatic cancer remains unclear. This is the first research focusing on the prognostic value of ASXL2 in pancreatic cancer. In this research, we aimed to explore the correlation between ASXL2 and the prognosis, as well as other features in PAAD. We obtained gene expression profiles of PAAD and normal tissues from TCGA, GEO, and Xena databases. TIMER and CIBERSORT algorithms were employed to investigate the effect of ASXL2 on tumor microenvironment. GSEA along with GO and KEGG enrichment analyses were conducted to uncover the biological functions of ASXL2. The response to various chemotherapeutic drugs was estimated by algorithms in R package "pRRophetic", while the sensitivity to immunotherapy was quantified by TIDE score. We found that ASXL2 was upregulated in the PAAD samples and elevated expression of ASXL2 was linked to poor overall survival. ASXL2 DNA methylation contributed to ASXL2 expression. Functional annotation indicated that ASXL2 was mainly involved in inflammatory response and epithelial mesenchymal transition. Patients with high ASXL2 expression were more likely to benefit from immune checkpoint blockade, gemcitabine, and mitomycin-C. Finally, external datasets and biospecimens were used and the results further validated the aberrant expression of ASXL2 in PAAD samples. In summary, our results highlight that ASXL2 is a potential prognostic and predictive biomarker in pancreatic cancer.

Objective: Colorectal cancer is one of the most common malignant tumors worldwide. ASXL2 is an enhancer of the trithorax and polycomb genes, which have been proven to act in many tumor types. The role of ASXL2 in the occurrence and development of tumors has been extensively studied in recent years. However, the relationship between ASXL2 and the prognosis of CRC is still unclear.Materials and Methods: In this study, quantitative real-time polymerase chain reaction (qRT-PCR), Western blot analysis and immunohistochemistry (IHC) were used to examine the expression of ASXL2 in CRC tissues. Cells were transfected with siRNAs or lentivirus to regulate the expression of ASXL2. The effects of ASXL2 on the proliferation of CRC cells were determined by CCK8 assay.Results: This study demonstrated that ASXL2 was significantly more highly expressed in CRC specimens than in normal adjacent tissues. The upregulation of ASXL2 was related to advanced clinical stage. Patients who exhibited high expression levels of ASXL2 had poorer overall survival, whereas those with low expression of ASXL2 survived longer. Multivariate Cox regression analysis revealed that ASXL2 expression could be considered an independent prognostic factor for CRC. Inhibition or overexpression of ASXL2 markedly influenced the proliferation of CRC cells.Conclusion: These results showed that ASXL2 could induce cell proliferation, which was associated with poor prognosis of CRC patients, suggesting that ASXL2 might be a new therapeutic target for CRC.

Background: Colorectal cancer is one of the most common malignant tumors worldwide. ASXL2 is an enhancer of trithorax and polycomb gene, which have been proved to act in many tumor types. The role of ASXL2 in the occurrence and development of tumors have been extensively studied in recent years. However the relationship between ASXL2 and the prognosis of CRC is still unclear. Methods: In this study, quantitative real-time polymerase chain reaction (qRT-PCR), Western blot analysis and immunohistochemistry (IHC) were used to examine the expression of ASXL2 in CRC tissues. Cells were transfected with siRNAs or lentivirus to regulate the expression of ASXL2. The effects of ASXL2 on proliferation of CRC cells were determined by CCK8 assay. Results: This study demonstrated that ASXL2 was significantly more expressed in CRC specimens relative to the normal adjacent tissues. The upregulation of ASXL2 was related to advanced clinical stages. Patients who exhibited high expression levels of ASXL2 had poorer overall survival, whereas those with low expression of ASXL2 survived longer. Multivariate Cox regression analysis revealed ASXL2 expression could be considered as an independent prognostic factor for CRC. Inhibition or overexpression of ASXL2 markedly influenced the proliferation of CRC cells. Conclusion: These results showed that ASXL2 could induce cell proliferation which is associated with poor prognosis of CRC patients and might be a new therapeutic target for CRC.