World Journal of Gastrointestinal Oncology最新文献

{"title":"Efficacy of adjuvant chemotherapy in stage II colon cancer patients with twelve or more lymph nodes retrieve.","authors":"Yu Huo, Yue-Yang Zhang, Shuai Jiao, Zhong-Yuan Bai, Wen-Qi Bai, Hai-Tao Zhou, Xu Guan","doi":"10.4251/wjgo.v17.i9.108470","DOIUrl":"10.4251/wjgo.v17.i9.108470","url":null,"abstract":"<p><strong>Background: </strong>The National Comprehensive Cancer Network guidelines recommend adjuvant chemotherapy (ACT) for patients with stage II colon cancer who have undergone curative surgery when fewer than 12 lymph nodes (LNs) are retrieved. This study seeks to further examine the requirement for ACT in individuals who had 12 or more LNs harvested.</p><p><strong>Aim: </strong>To investigate if stage II colon cancer patients with 12 or more LNs retrieved benefit from ACT.</p><p><strong>Methods: </strong>This retrospective cohort study included individuals diagnosed with stage II colon cancer who underwent surgery between 2008 and 2017 from the Surveillance, Epidemiology, and End Results (SEER) registry and a Chinese multicenter database. All patients had at least 12 LNs retrieved. The key endpoint was overall survival (OS). Cox regression analysis was performed to assess independent OS predictors. Propensity score matching controlled for confounders, and Kaplan-Meier analysis evaluated the impact of ACT on survival.</p><p><strong>Results: </strong>A total of 32742 patients with stage II colon cancer from the SEER cohort and 3153 patients from the Chinese cohort were included. The average number of LNs retrieved was 20.0 (15.0, 26.0) in the SEER cohort and 18.0 (15.0, 22.0) in the Chinese cohort. No-ACT remained an independent risk factor in both cohorts (hazard ratio = 1.589, 95% confidence interval: 1.485-1.700 and hazard ratio = 1.865, 95% confidence interval: 1.465-2.375, respectively). In the SEER cohort, patients in the ACT group consistently demonstrated better 5-year OS rates both before and after propensity score matching (79.4% <i>vs</i> 66.1% and 79.4% <i>vs</i> 69.4%, both <i>P</i> < 0.0001). Similarly, these findings were further validated in the Chinese cohort (91.2% <i>vs</i> 82.1% and 90.0% <i>vs</i> 82.8%, both <i>P</i> < 0.0001). ACT improved prognosis even in T3 and grade 1/2 patients.</p><p><strong>Conclusion: </strong>This research, based on two large population-based cohorts, demonstrates that stage II colon cancer patients with 12 or more LNs retrieved can still benefit from ACT.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"108470"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation between KAT6A and PD-L1 expression and role of KAT6A in colorectal cancer.","authors":"Zhen-Dong Zhou, Jian-Pei Zhao, Shu-Chun Zheng, Ting-Ting Wang","doi":"10.4251/wjgo.v17.i9.105937","DOIUrl":"10.4251/wjgo.v17.i9.105937","url":null,"abstract":"<p><strong>Background: </strong>Immune checkpoint inhibitors (ICIs) are effective cancer treatments; however, a significant proportion of colorectal cancer (CRC) patients exhibit limited responses to ICI therapy. KAT6A has been strongly associated with cancer initiation and progression.</p><p><strong>Aim: </strong>To examine the role of KAT6A in CRC progression and immune evasion.</p><p><strong>Methods: </strong>The functional role of KAT6A was evaluated through genetic knockdown, pharmacological inhibition (WM-3835), and CRISPR/dCas9-mediated epigenetic editing in CRC cells. T cell-mediated apoptosis was assessed using co-culture models, and H3K23pr was measured <i>via</i> chromatin immunoprecipitation assays. PD-L1 expression at mRNA and protein levels was analyzed under KAT6A knockdown conditions.</p><p><strong>Results: </strong>KAT6A suppression reduced CRC cell proliferation, invasion, and migration. Pharmacological or epigenetic disruption of KAT6A phenocopied these effects, with dose-dependent reductions in H3K23pr (28.4% residual at 10 μM) and PD-L1 expression. KAT6A knockdown enhanced T cell-mediated apoptosis, evidenced by increased expression of granzyme B and perforin. Mechanistically, KAT6A loss decreased H3K23pr and reduced RNA polymerase II occupancy on the PD-L1 promoter, leading to suppressed PD-L1 transcription. CRISPR/dCas9-mediated H3K23pr editing at the PD-L1 promoter directly modulated immune evasion, confirming its causal role. Overexpression of PD-L1 mitigated the inhibitory effects of KAT6A knockdown on CRC progression and immune evasion.</p><p><strong>Conclusion: </strong>KAT6A drives CRC progression and immune evasion by promoting histone H3 propionylation to epigenetically activate PD-L1 expression. Targeting KAT6A or its downstream H3K23pr-PD-L1 axis represents a promising therapeutic strategy to overcome ICI resistance in CRC.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"105937"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145114162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rapamycin suppresses small bowel adenocarcinoma HUTU 80 cells proliferation by inhibiting hypoxia-inducible factor-1α mediated metabolic reprogramming.","authors":"Bao-Peng Pu, Peng-Hui Wang, Kai-Kai Guo, Chun Liu, Si-Run Chen, Xiao-Meng Li, Shi-Min Chen, Xiang-Zhou Zeng, Chang Gao","doi":"10.4251/wjgo.v17.i9.109378","DOIUrl":"10.4251/wjgo.v17.i9.109378","url":null,"abstract":"<p><strong>Background: </strong>Small bowel adenocarcinoma (SBA) is a rare malignant tumor of gastrointestinal tract. Currently, there is no standard treatment approach for late-stage SBA, which lead to poor outcome and prognosis. Rapamycin is an immunosuppressive agent that has been reported to inhibit the proliferation of tumor cells. However, whether rapamycin inhibit the growth of SBA remains to be investigated.</p><p><strong>Aim: </strong>To observe the inhibitory effect of rapamycin on small intestinal adenocarcinoma cells.</p><p><strong>Methods: </strong>Methylthiazolyldiphenyl-tetrazolium bromide assay, colony formation assay, cell cycle analysis, and glycolysis assay were used to observe the phenotypic changes of rapamycin-treated HUTU 80 cells. RNA sequencing and untargeted ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) metabolomics were also used to find the potential targets of action of rapamycin in inhibiting HUTU 80 cells proliferation, and validate potential targets by quantitative polymerase chain reaction and western blotting. The construction of a subcutaneous HUTU 80 xenograft in BALB/c nude mice was used to explore the tumor suppression effect of rapamycin.</p><p><strong>Results: </strong>Rapamycin inhibited HUTU 80 cell proliferation <i>in vitro</i> and <i>in vivo</i>. Rapamycin inhibited the migration, invasion, and glycolysis of HUTU 80 cells, and induced cell cycle arrest. RNA sequencing and untargeted UHPLC-MS/MS metabolomic analysis indicated that the mechanism of rapamycin action was linked to the hypoxia-inducible factor (HIF)-1α signaling pathway and the related gluconeogenesis/glycolysis pathways. Subsequent experiments found that rapamycin downregulated the messenger RNA expression of HIF-1α and its downstream target genes, <i>LDHA</i>, <i>PDK1</i> and <i>VEGF</i>. Additionally, rapamycin inhibited expression of phosphorylated mammalian target of rapamycin (mTOR), phosphorylated-70 kDa ribosomal protein S6 kinase (p70S6k), phosphorylated eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) and HIF-1α proteins <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Conclusion: </strong>Downregulation of mTOR/p70S6k/4E-BP1/HIF-1α signaling pathway activation, leading to decreased glycolysis and cell cycle arrest, may be the pivotal mechanism by which rapamycin inhibits SBA.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"109378"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145114300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and safety of transarterial chemoembolization with chemotherapy, PD-1/PD-L1 inhibitors, and tyrosine kinase inhibitors in unresectable intrahepatic cholangiocarcinoma.","authors":"Xiao Chen, Xi-Heng Sun, Yue Xiao, Dan Zhang, Xiao-Yan Lu, Cheng-Lei Fu, Chun Bi, Xia Wang","doi":"10.4251/wjgo.v17.i9.103816","DOIUrl":"10.4251/wjgo.v17.i9.103816","url":null,"abstract":"<p><strong>Background: </strong>Chemotherapy, targeted therapy, and immunotherapy have all been shown to achieve some efficacy in treating intrahepatic cholangiocarcinoma (ICC). However, these systemic treatments have not provided optimal results for some patients. Therefore, the combination of transarterial chemoembolization (TACE) and hepatic artery infusion chemotherapy or other local interventional therapy methods is being considered for the treatment of liver tumors.</p><p><strong>Aim: </strong>To evaluate the efficacy and safety of combining chemotherapy, targeted therapy, and immunotherapy, with or without TACE, in patients with ICC.</p><p><strong>Methods: </strong>We recruited 83 patients with unresectable ICC from July 2021 to December 2023 at the Affiliated Hospital of Xuzhou Medical University. Forty-one patients received TACE combined with chemotherapy, tyrosine kinase inhibitors, and programmed death 1 (PD-1)/programmed cell death ligand 1 (PD-L1) inhibitors (experimental group), whereas 42 patients were treated with chemotherapy, tyrosine kinase inhibitors, and PD-1/PD-L1 inhibitors (control group). Short-term efficacy was assessed using the modified response evaluation criterion, and the objective response rate, disease control rate, progression-free survival, and incidence of adverse events were compared between groups.</p><p><strong>Results: </strong>The objective response rate in the experimental group was greater than that in the control group (39.0% <i>vs</i> 19.0%, <i>P</i> < 0.05). The disease control rate in the experimental group was significantly greater than that in the control group (75.6% <i>vs</i> 52.4%, <i>P</i> < 0.05). The median progression-free survival times were 14.3 months in the experimental group and 12.7 months in the control group (<i>P</i> < 0.05). All 41 patients in the experimental group developed postembolization syndrome. Among the symptoms, fever and pain were significantly more common in the experimental group than in the control group (85.4% <i>vs</i> 11.9%, <i>P</i> < 0.001 and 58.5% <i>vs</i> 9.5%, <i>P</i> < 0.001). No grade 4 or 5 treatment-related adverse events were observed in either group.</p><p><strong>Conclusion: </strong>In patients with unresectable ICC, TACE combined with chemotherapy, tyrosine kinase inhibitors, and PD-1/PD-L1 inhibitors has good efficacy and high safety, indicating potential benefits for these patients.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"103816"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145114317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Medical travel patterns for hepatocellular carcinoma treatment in South Korea: National Health Insurance data from 2013 to 2021.","authors":"Sungmin Kim, Naeun Kim, Hyung-Sik Lee, Mina Kim, Hoseob Kim, Youngmin Choi","doi":"10.4251/wjgo.v17.i9.109060","DOIUrl":"10.4251/wjgo.v17.i9.109060","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) remains a significant public health concern in South Korea even though the incidence rates are declining. While medical travel for cancer treatment is common, its patterns and influencing factors for patients with HCC are unknown.</p><p><strong>Aim: </strong>To assess medical travel patterns and determinants and their policy implications among patients with newly diagnosed HCC in South Korea.</p><p><strong>Methods: </strong>This retrospective cohort study used the National Health Insurance Service database to identify patients with newly diagnosed HCC from 2013 to 2021. Medical travel was defined as receiving initial treatment outside one's residential region. Patient characteristics and regional trends were analyzed, and factors influencing medical travel were identified using logistic regression analysis.</p><p><strong>Results: </strong>Among 64808 patients 52.4% received treatment in the capital. This proportion increased to 67.4% when including the surrounding metropolitan area. Medical travel was significantly more common among younger and wealthier patients. Patients with greater comorbidity burden or liver cirrhosis were less likely to travel. While geographic distance influenced travel patterns, high-volume academic centers in the capital attracted patients nationwide regardless of proximity.</p><p><strong>Conclusion: </strong>This nationwide study highlighted the centralization of HCC care in the capital. This observation indicates that regional cancer hubs should be strengthened and promoted for equitable healthcare access.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"109060"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145114173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between uric acid and colon cancer risk: Dose-response analysis and mechanisms.","authors":"Teng-Fei Sun, Ke-Xin Fan, Yu-Xin Luo, Jia Song, Zhuo-Xiao Han, Xiao-Lan Zhang","doi":"10.4251/wjgo.v17.i9.107651","DOIUrl":"10.4251/wjgo.v17.i9.107651","url":null,"abstract":"<p><strong>Background: </strong>Uric acid (UA), a key antioxidant metabolite, demonstrates dual roles in cancer. Unfortunately, studies on its role in colon cancer risk are uncommon, and the limited results are inconsistent.</p><p><strong>Aim: </strong>To elucidate the association between UA and colon cancer risk and its mechanisms.</p><p><strong>Methods: </strong>Multivariate logistic regression analysis evaluated the association between UA levels and colon cancer risk. Non-linear relationships were illustrated using restricted cubic splines. The threshold effect was performed to identify cut-off points. Human colon cancer cell lines (HCT-116 and HT29) were exposed to UA for 48 hours. Cell viability was assessed <i>via</i> the cell counting kit-8 assay. The evaluation of cell migration involved wound healing and transwell migration assays. HCT-116 cells were exposed to 4 mg/dL UA for 48 hours. The impact of the subsequent treatment with a phosphoinositide 3-kinases (PI3K) agonist and UA was assessed.</p><p><strong>Results: </strong>After adjusting for potential confounders, an inverse association was observed between UA and colon cancer risk (odds ratio = 0.65, <i>P</i> < 0.05). A non-linear relationship was identified, with a 4.79 mg/dL cut-off point (<i>P</i> < 0.05). UA inhibited colon cancer cell proliferation and migration. These effects were mediated by the induction of reactive oxygen species and the suppression of the PI3K/protein kinase B/mammalian target of rapamycin pathway.</p><p><strong>Conclusion: </strong>UA acts as a protective agent against colon cancer by inhibiting cell proliferation and migration through increased reactive oxygen species production and modulation of the PI3K/protein kinase B/mammalian target of rapamycin pathway.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"107651"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145114315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibroblast growth factor 19-fibroblast growth factor receptor 4 axis: From oncogenesis to targeted-immunotherapy in advanced hepatocellular carcinoma.","authors":"Tian-Ao Zhan, Feng Xia, Hong-Wei Huang, Jun-Cheng Zhan, Xin-Kang Liu, Qi Cheng","doi":"10.4251/wjgo.v17.i9.108649","DOIUrl":"10.4251/wjgo.v17.i9.108649","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality globally, with limited therapeutic progress for advanced stages. The aberrant fibroblast growth factor 19 (FGF19)-fibroblast growth factor receptor 4 (FGFR4) axis promotes oncogenesis and is linked to targeted-immunotherapy of HCC. Multi-kinase inhibitors (MKIs) enhance anti-tumor effects by targeting this axis and FGF19 overexpression upregulates programmed cell death ligand 1 in tumor microenvironment. Clinical studies have demonstrated the efficacy of selective FGFR4 inhibitors in HCC treatment, with enhanced anti-tumor effects when combined with MKIs or immune checkpoint inhibitors. Phase I clinical trials of Irpagratinib (ABSK-011) demonstrated an objective response rate of 43.5%, which increased to 55.6% combined with atezolizumab. FGF19 also serves as a biomarker for HCC. This review systematically summarizes the literature retrieved from PubMed and other databases using search terms \"HCC\", \"fibroblast growth factor 19\", \"fibroblast growth factor receptor 4\", \"FGFR4 inhibitor\", \"targeted therapy\", \"multi-kinase inhibitor\", \"immunotherapy\", \"immune checkpoint inhibitor\", and \"biomarker\". It also firstly synthesizes combination strategies and underlying mechanisms between FGFR4 inhibitors and targeted-immunotherapy, addressing critical gaps in existing reviews. Additionally, we discuss the potential of FGF19 as a predictive biomarker, integrating mechanistic and clinical evidence to advance precision HCC therapeutics.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"108649"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444330/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Postoperative immune checkpoint inhibitors plus anti-angiogenesis for hepatitis B virus-associated hepatocellular carcinoma: Analyzing the evidence and future prospects.","authors":"Arunkumar Krishnan, Diptasree Mukherjee","doi":"10.4251/wjgo.v17.i9.106801","DOIUrl":"10.4251/wjgo.v17.i9.106801","url":null,"abstract":"<p><p>A recent study by Lu <i>et al</i> examined the potential benefits of postoperative combined therapy (PCT) using anti-programmed cell death protein-1/PD-ligand-1 and anti-vascular endothelial growth factor agents for patients with hepatitis B virus-associated hepatocellular carcinoma (HBV-HCC). At the same time, the findings offer important insights; however, several methodological and statistical limitations should be noted. These limitations include selection bias from the study's retrospective design, variability in treatment regimens, a small sample size, and inadequate monitoring of hepatitis B virus (HBV) reactivation. The study's conclusions about PCT efficacy warrant cautious interpretation due to unresolved biases. Prospective trials with biomarker stratification are critical to confirm these preliminary findings. These findings underscore the need for prospective, biomarker-driven trials to validate the efficacy of PCT. Future research should prioritize standardized regimens, HBV reactivation monitoring, and global collaborations to optimize therapeutic strategies for HBV-HCC.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"106801"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145114184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Importance of the pattern of lymph node metastasis in upper and lower gastric cancer.","authors":"Parbatraj Regmi, Sagar Mani Regmi, Anish Paudyal","doi":"10.4251/wjgo.v17.i9.103144","DOIUrl":"10.4251/wjgo.v17.i9.103144","url":null,"abstract":"<p><p>The article by Yuan <i>et al</i> accessed the clinicopathologic and prognostic significance of the patterns of lymph node (LN) metastasis in upper and lower gastric cancer (GC). In this article, we will analyze both the strengths and limitations of this paper. The study's methodology seems appropriate and proper statistical analyses were applied to identify significant variables. The authors applied the Cox regression model to identify independent risk factors and Kaplan-Meier survival curves to assess prognosis. The researchers found notable differences in clinicopathologic variables between patients with upper and lower GC. Additionally, they identified specific LN stations more prone to metastasis in different Siewert classifications of GC. Despite the study's detailed analysis, it would have been beneficial to explore whether there were survival differences among upper GC patients based on the Siewert classification. Furthermore, the study should have addressed potential confounding factors that might have influenced the results. A more comprehensive analysis could have been achieved by comparing survival outcomes based on LN metastasis patterns. Overall, this article is relevant and provides valuable insights into the significance of LN metastasis patterns in upper GC patients.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"103144"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145114225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcription factor 3 enhances hepatocellular carcinoma metastasis by upregulating matrix metalloproteinase-11.","authors":"Hong-Peng Tian, Tian-Hao Wu, Guang-Jun Zhang, Sheng-Jie Li","doi":"10.4251/wjgo.v17.i9.110527","DOIUrl":"10.4251/wjgo.v17.i9.110527","url":null,"abstract":"<p><strong>Background: </strong>Transcription factor 3 (TCF3) has a vital role in tumor occurrence and progression. However, the specific functions and underlying mechanisms of dysregulated TCF3 in hepatocellular carcinoma (HCC) have not been not thoroughly characterized. Thus, we explored the roles of TCF3 in HCC.</p><p><strong>Aim: </strong>To explore the roles of TCF3 in HCC.</p><p><strong>Methods: </strong>TCF3 knockdown and overexpression models were developed <i>via</i> lentiviral vectors in HCC cells. Transwell and <i>in vivo</i> metastasis experiments were performed to measure the effects of TCF3 on HCC cell metastasis. Then, reverse transcription-quantitative polymerase chain reaction, serial deletion, western blotting, site-directed mutagenesis, chromatin immunoprecipitation, and dual-luciferase reporter assays were done to determine the pathomechanisms.</p><p><strong>Results: </strong>TCF3 levels were markedly elevated in HCC samples and correlated with poor prognosis. Furthermore, overexpression of TCF3 promoted HCC cell invasion as well as migration, while TCF3 knockdown repressed HCC cell growth. In addition, TCF3 interacted with the promoter region of matrix metalloproteinase-11 (MMP11), facilitating the transcriptional activation of MMP11 mRNA, which consequently enhanced the expression of MMP11. MMP11 knockdown repressed TCF3-associated HCC cell migration and invasion, while its overexpression attenuated the TCF3 knockdown-mediated repression of HCC growth. In human-derived HCC samples, TCF3 was positively correlated with MMP11 expression levels.</p><p><strong>Conclusion: </strong>TCF3 was significantly upregulated in HCC. TCF3 overexpression enhanced HCC cell invasion and metastasis through transactivation of MMP11 expression. TCF3 could be a prognostic biomarker and regulator of HCC metastasis.</p>","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":"17 9","pages":"110527"},"PeriodicalIF":2.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145114246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}