American journal of cancer research最新文献

{"title":"GSG2 promotes aerobic glycolysis and colorectal cancer progression via the MDM2-p53 axis.","authors":"Hua Pan, Jipeng Liu, Taifu Xiao, Jun Huang","doi":"10.62347/WEGW4871","DOIUrl":"https://doi.org/10.62347/WEGW4871","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is the third most common type of cancer worldwide and ranks among the leading causes of cancer-related deaths. During tumor progression, post-translational modifications, mainly the ubiquitin-proteasome system, are critical mediators of cellular metabolic reprogramming, including the metabolic changes of tumor development. Although TP53 mutations occur in approximately half of all CRC cases and could define their genetic makeup, precise therapeutic vulnerabilities remain largely unknown for the subgroup with wild-type p53. This study investigated the significant expression of Germ Cell-Specific Gene 2 (GSG2) in CRC. We demonstrated GSG2 is strongly increased in malignant colorectal tissues compared with adjacent benign tissues, and this high expression strongly predicts poor patient survival. Additionally, the results indicate that removing GSG2 effectively suppresses tumor growth in both in vitro systems and in vivo xenograft models. Mechanistically, GSG2 directly binds to the E3 ligase MDM2, and promoted MDM2-mediated ubiquitination and degradation of p53 in p53 wild-type CRC cells. Consequently, GSG2 enhances the cellular metabolic program, reprogramming glucose use toward aerobic glycolysis to meet the energy needs of uncontrolled growth. Thus, our findings reveal a novel way that p53 is silenced in cancers with wild-type TP53. GSG2 demonstrate control of the MDM2-p53 axis to promote the Warburg effect and drive CRC progression via p53 suppression.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3066-3083"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757482","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":"Integrating in silico modeling and experimental validation to determine the anti-breast cancer mechanisms of mulberry leaf bioactive compounds.","authors":"Jun Zhang, Guoxin Zhao, Renping Zhang, Zhengyu Fu, Xinru Chen, Jiong Wu","doi":"10.62347/PLVO6071","DOIUrl":"https://doi.org/10.62347/PLVO6071","url":null,"abstract":"<p><p>Breast cancer (BRCA) is the most prevalent malignancy and leading cause of cancer-related death in women. To elucidate the anti-BRCA mechanisms of mulberry leaves (ML), the present study used an integrated strategy combining network pharmacology, molecular docking and in vitro validation. The active components of ML, their putative targets and BRCA-related proteins were screened from public databases (Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, and Encyclopedia of Traditional Chinese Medicine). A protein-protein interaction network was constructed using Cytoscape, followed by Gene Ontology (GO) biological function and Kyoto Encyclopedia of Genes and Genes (KEGG) pathway analyses through the Database for Annotation, Visualization and Integrated Discovery. Molecular docking was then conducted to assess the binding affinities of key compounds to prioritized targets. In vitro assays (MTT, wound healing and flow cytometry) were performed to evaluate the effects of ML on MDA-MB-231 cell proliferation, migration, apoptosis and cell cycle progression. Western blotting was conducted to validate core target proteins. In total, nine bioactive ML compounds (such as quercetin and stigmasterol) were identified, targeting six core proteins [tumor protein p53, estrogen receptor 1 (ESR1), catenin β1, AKT serine/threonine kinase 1, MYC proto-oncogene/BHLH transcription factor and telomerase reverse transcriptase]. GO analysis revealed enrichment in 'nucleoplasm', 'enzyme binding' and 'cellular response to hypoxia' terms, whilst KEGG pathway analysis results highlighted 'cancer-related pathways' (such as PI3K/AKT). Stigmasterol exhibited the strongest binding affinity to ESR1 (in silico). In vitro, ML extract significantly suppressed MDA-MB-231 proliferation and migration, induced apoptosis and triggered G₂/M arrest. Western blotting confirmed the downregulation of oncoproteins (TP53, AKT1, ESR1 and JUN). The results of the present study suggest that ML can inhibit the proliferation and migration of BRCA cells whilst inducing their apoptosis by regulating the expression of key proteins. This provides a scientific basis for the in-depth exploration of the anti-BRCA mechanism of ML.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2899-2918"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757215","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":"Predictive value of conventional ultrasonographic features combined with clinical factors for capsular invasion in papillary thyroid carcinoma with Hashimoto's thyroiditis.","authors":"Chengcheng Yu, Xiaojie Liu, Borui Yu, Jinming Zhao","doi":"10.62347/PXJQ7157","DOIUrl":"https://doi.org/10.62347/PXJQ7157","url":null,"abstract":"<p><p>This retrospective study aimed to investigate the predictive value of conventional ultrasonographic features combined with clinical factors for capsular invasion in patients with papillary thyroid carcinoma (PTC) with concurrent Hashimoto's thyroiditis (HT). A total of 262 patients with pathologically confirmed PTC and concurrent HT who underwent surgery at our institution from January 2018 to June 2024 were included as the training cohort. Patients were divided into capsular invasion and non-capsular invasion groups according to postoperative pathological findings. Clinical characteristics, conventional ultrasonographic features, and preoperative serum thyroid-stimulating hormone (TSH) levels were compared between the two groups. Univariate and multivariate logistic regression analyses were performed to identify independent predictors of capsular invasion, and a nomogram model was constructed based on the selected variables. The predictive performance of the model was evaluated using receiver operating characteristic curves, calibration curves, decision curve analysis, and clinical impact curves. Univariate analysis showed that age, tumor diameter, postoperative lymph node metastasis, lesion margin, and blood flow signal were significantly associated with capsular invasion. Multivariate logistic regression analysis further identified age ≥55 years, larger tumor diameter, ill-defined lesion margin, and abundant blood flow signal as independent predictors of capsular invasion. The combined nomogram model achieved an area under the curve of 0.706 in the training cohort and 0.804 in the external validation cohort, showing better predictive performance than any single factor alone. Calibration curves, decision curve analysis, and clinical impact curves suggested acceptable model calibration and potential clinical utility. These findings indicate that a nomogram incorporating age, tumor diameter, lesion margin, and blood flow signal may provide a practical preoperative tool for estimating the risk of capsular invasion in patients with PTC and HT.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2848-2860"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148761431","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":"A novel circular RNA hsa_circ_0020123 exerts oncogenic properties through suppression of miR-144 in non-small cell lung cancer [Retraction].","authors":"","doi":"10.62347/EZTV1194","DOIUrl":"https://doi.org/10.62347/EZTV1194","url":null,"abstract":"<p><p>[This retracts the article on p. 1387 in vol. 8, PMID: 30210911.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3201"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148762843","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":"Dichloromethane fraction from Ficus hispida L.f. fruit extract suppresses lung cancer through cell cycle arrest and TNF-induced apoptosis.","authors":"Juan Yang, Wenming Wu, Jiahui Peng, Xiaoyu Liu, Dongmei Ying, Xinyi Zhou, Junan Wang, Youfa Duan, Wenchao Xiong, An Jin","doi":"10.62347/EKIX8621","DOIUrl":"https://doi.org/10.62347/EKIX8621","url":null,"abstract":"<p><p><i>Ficus hispida</i> L.f., a traditional medicinal plant widely distributed in South and Southeast Asia, has long been used in ethnomedicine to treat respiratory disorders, inflammation and tumor-related conditions. Although previous studies have suggested that <i>F. hispida</i> possesses cytotoxic and anti-inflammatory activities, the <i>in vivo</i> antitumor efficacy and underlying mechanisms of its fruit-derived dichloromethane extract remain unclear. This study aimed to investigate the anti-lung cancer activity of the dichloromethane extract of <i>F. hispida</i> fruits (FHF-DE) using integrated phytochemical, cellular, transcriptomic and <i>in vivo</i> approaches. FHF-DE inhibited the proliferation of multiple human lung cancer cell lines (including H1299, A549, H1975, H460, and PC9 cells) as well as murine Lewis lung carcinoma (LLC) line. Flow cytometry indicated G0/G1 arrest in LLC cells and S-phase arrest in H1975 cells. FHF-DE also promoted apoptotic cell death, as indicated by increased Bax expression, decreased Bcl-2 expression, and caspase-3 activation. Transcriptome sequencing and reverse transcription-quantitative (RT-q) PCR analyses indicated enrichment of the TNF signaling pathway, with increased TNF-<i>α</i> and related gene expression (e.g., IRF1, BIRC3). In an LLC allograft mouse model, daily oral administration of FHF-DE (200-400 mg/kg) significantly suppressed tumor growth, without evident hepatotoxicity or nephrotoxicity in H&E staining. This <i>in vivo</i> finding demonstrates the antitumor efficacy of FHF-DE, although, molecular validation of the proposed mechanism in tumor tissues was not performed. Collectively, our in vitro data demonstrate that FHF-DE induces apoptosis and cell cycle arrest in lung cancer cells, with transcriptomic and pharmacological data suggesting a functional association with TNF-related signaling pathways. However, definitive mechanistic proof of direct TNFR1 engagement or extrinsic apoptotic pathway activation, particularly in vivo, requires further investigation. The present study provides preclinical evidence supporting further pharmacological and toxicological evaluation of <i>F. hispida</i> fruit-derived extracts as natural-product-based candidates for lung cancer intervention.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3084-3101"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757229","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":"Orthodontic treatment outcomes and safety for secondary dentofacial deformities after childhood cancer therapy: a systematic review and meta-analysis.","authors":"Hualiang Sun, Xiaohong Liu, Jianshu Yang, Jingzi Zhao","doi":"10.62347/VGIP2111","DOIUrl":"https://doi.org/10.62347/VGIP2111","url":null,"abstract":"<p><strong>Aims: </strong>To systematically evaluate the treatment outcomes and safety of orthodontic intervention for secondary dentofacial deformities after childhood cancer therapy, with particular emphasis on occlusal outcomes, oral health-related quality of life, treatment-related complications, and dental developmental abnormalities relevant to orthodontic management.</p><p><strong>Methods: </strong>A comprehensive search of PubMed, Embase, Cochrane Library, Web of Science, Scopus, and CINAHL was performed using terms related to cancer, orthodontic treatment, and treatment outcomes. Eligible studies included observational or comparative clinical studies reporting either treatment efficacy outcomes (e.g., w-PAR, ICON, and oral health-related quality of life) or treatment safety/sequelae outcomes (e.g., treatment-related complications and dental developmental abnormalities). Risk of bias was assessed using the Newcastle-Ottawa Scale. For efficacy outcomes, pooled standardized mean differences with 95% confidence intervals were calculated; for safety/sequelae outcomes, pooled risk ratios with 95% confidence intervals were estimated. Random-effects models were applied in Stata, and heterogeneity was assessed using Cochran's Q and the I² statistic.</p><p><strong>Results: </strong>Ten studies published between 2001 and 2023 were included. For w-PAR, the pooled effect showed a significant overall change (SMD = -1.12, 95% CI -2.22 to -0.01; I² = 98.5%), driven mainly by the immediate post-treatment subgroup. For ICON, the pooled effect was also significant (SMD = 0.68, 95% CI 0.12 to 1.24; I² = 97.5%), with the stronger signal observed at follow-up beyond 3 weeks. Oral health-related quality of life, assessed by OHIP-14, showed a small but significant overall improvement (SMD = 0.26, 95% CI 0.03 to 0.49), with moderate heterogeneity (I² = 54.3%). In contrast, survivors experienced a significantly higher risk of complications during orthodontic treatment than comparison groups (RR = 2.44, 95% CI 1.07-5.58; I² = 36.7%). The pooled relative risk of dental developmental abnormalities relevant to orthodontic planning was not significantly different overall (RR = 1.11, 95% CI 0.40-3.08), although heterogeneity was considerable (I² = 90.3%).</p><p><strong>Conclusion: </strong>Orthodontic intervention in survivors of childhood cancer may be associated with improvements in occlusal outcomes and oral health-related quality of life; however, the evidence for treatment efficacy remains uncertain, largely due to substantial between-study heterogeneity. At the same time, survivors appear to have a significantly increased risk of treatment-related complications.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3010-3024"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759075","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":"Incidence and risk factors of infections in lung cancer patients receiving immunotherapy combined with chemotherapy: a real-world retrospective study.","authors":"Jing Zou, Guanghai Ji, Lei Yan, Jinyong Li, Yanxia Zhang, Dingfang Pi","doi":"10.62347/OIJD3060","DOIUrl":"https://doi.org/10.62347/OIJD3060","url":null,"abstract":"<p><p>This single-center, real-world retrospective cohort study assessed the incidence, risk factors, and clinical risk stratification of infections in lung cancer (LC) patients receiving immune checkpoint inhibitors (ICIs) combined with chemotherapy. This study comprised a cohort of 616 consecutive LC patients who received ICI-based chemotherapy during hospitalization between January 2020 and December 2025. LASSO regression followed by multivariable logistic regression was used to identify independent risk factors. Optimal cutoffs for score construction were determined using receiver operating characteristic (ROC) curve analysis combined with the Youden index, and internal validation was performed with 1,000 bootstrap resamples. The overall infection rate was 9.09% (56/616), with pulmonary infection being the most common site (64.29%), and gram-negative bacteria being most predominant (50.00%) Among culture-positive specimens, CRKP, MRSA, and CRPA accounted for 40.00%, 33.33%, and 25.00% of their respective species. Multivariable analyses identified ECOG performance status ≥2 (OR=3.993, 95% CI: 1.520-10.926, P=0.005), C-reactive protein (CRP) (OR=1.114, 95% CI: 1.079-1.159, P<0.05) as independent risk factors. In summary, infections appear to be a major complication in LC patients receiving ICIs combined with chemotherapy, often involving drug-resistant pathogens. A scoring system based on seven routinely available clinical parameters demonstrated good discrimination and internal stability in bootstrap validation, potentially aiding in the identification of high-risk patients for preventive measures.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2707-2724"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759172","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":"Chenodeoxycholic acid suppresses colorectal cancer by activating Farnesoid X receptor.","authors":"Jun Xie, Yiding He, Chenhao Xu, Sihao Wang, Guangchuan Qu, Yilin Ren, Tong Wang, Yuzheng Xue","doi":"10.62347/BZHD6251","DOIUrl":"https://doi.org/10.62347/BZHD6251","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a major cause of cancer-related mortality worldwide. Therefore, it is critical to identify accurate biomarkers for improving early diagnosis and clinical outcomes. In our study, serum was collected from 90 healthy controls and 98 CRC patients after 8-hour fasting, followed by the measurement of chenodeoxycholic acid (CDCA) levels using ELISA. Cell proliferation and metastasis were assessed using MTT, colony-forming, and transwell assays. Farnesoid X receptor (FXR) was silenced with shFXR lentivirus, and its expression in tumors was analyzed by RT-qPCR. The result revealed that serum CDCA levels were significantly lower in CRC patients compared to healthy controls. Lower CDCA levels were associated with advanced TNM stage, differentiation status, and lymph node metastasis. FXR mRNA was significantly downregulated in CRC tumors and was negatively correlated with tumor aggressiveness. Serum CDCA levels were positively correlated with tumor FXR mRNA expression, and higher FXR expression was associated with better 5-year overall survival. CDCA treatment significantly suppressed CRC cell proliferation and migration in a dose- and time-dependent manner, whereas FXR knockdown attenuated these inhibitory effects. These findings indicated that CDCA suppressed CRC progression by activating FXR and inhibiting Wnt/β-catenin signaling. This highlights the potential of CDCA and FXR as therapeutic targets for CRC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"2801-2813"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148762859","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":"Targeting FAM64A: a promising strategy to halt liver cancer angiogenesis and enhance immunity.","authors":"Liping Bai, Xueyan Yang, Lixian Bai, Zhongkun Ren, Hong Gong, Yinghui Zhang, Han Chen, Zhijian Ma","doi":"10.62347/HFGX2343","DOIUrl":"https://doi.org/10.62347/HFGX2343","url":null,"abstract":"<p><p>Liver cancer, a primary malignancy of liver cells, exhibits high morbidity and mortality. Family with sequence similarity 64, member A (FAM64A) acts as an oncogene and modulates tumor progression in multiple cancers. However, the specific role of FAM64A in liver cancer development remains poorly elucidated. Thus, this work uncovered the action of FAM64A on liver cancer pathogenesis and cancer immunity and reveals the underlying mechanism. In this study, the FAM64A expression in liver cancer and its association with the overall survival were investigated using bioinformatics analysis. Tumor tissues and adjacent normal tissues were obtained from 64 liver cancer cases. Cell viability, invasion, and angiogenesis were assessed by CCK-8 method, Transwell invasion assay, and tube formation assay, respectively. The secretion levels of IFN-γ, IL-2, IL-10 and TGF-β were tested utilizing the ELISA assay. A xenograft tumor was created to monitor tumor growth <i>in vivo</i>. Results revealed that FAM64A expression was elevated in liver cancer. Clinically, high FAM64A levels correlated with shorter overall survival. Silencing of FAM64A restricted the malignant phenotypes of liver cancer cells, including proliferation, invasion, angiogenesis and immune escape. Furthermore, FAM64A knockdown restricted the activation of the VEGFA/AKT signaling. Conversely, VEGFA overexpression offset the above influences of FAM64A on liver cancer cells. Moreover, silenced FAM64A suppressed tumor growth, decreased CD31 and PD-L1 levels, increased CD8 and IFN-γ level, and reduced activation of the VEGFA/AKT signaling. Taken together, FAM64A is up-regulated in liver cancer and closely correlated with poor prognosis. Silenced FAM64A restrained proliferation ability, invasion capacity, angiogenesis and immune escape of liver cancer cells through inactivating the VEGFA/AKT signaling. FAM64A may be a valuable candidate target for liver cancer therapy.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3102-3118"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148756973","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":"CAAP1 suppresses tumor growth and metastasis via interacting with EIF3I in high-grade serous ovarian carcinoma.","authors":"Chunyan Wang, Liyang Liang, Lei Kuang, Sisi Liu, Weiwei Qian, Chunlei Zhang","doi":"10.62347/HYOR3386","DOIUrl":"https://doi.org/10.62347/HYOR3386","url":null,"abstract":"<p><p>High-grade serous ovarian cancer (HGSOC) is frequently diagnosed at advanced stages with refractory peritoneal metastases, resulting in a dismal prognosis. Caspase activity and apoptosis inhibitor 1 (CAAP1), an apoptosis regulator with debated functions, has an unexplored role in HGSOC progression. Herein, the prognostic value of CAAP1 was evaluated using The Cancer Genome Atlas (TCGA) database and clinical tissue samples. The effects of CAAP1 on HGSOC cell proliferation, migration, and apoptosis resistance were examined via cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) incorporation, wound healing, Transwell, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays. A subcutaneous xenograft model was employed to verify the tumor-suppressive role of CAAP1 in vivo. Furthermore, liquid chromatography-tandem mass spectrometry (LC-MS/MS) and co-immunoprecipitation (Co-IP) were performed to identify and validate CAAP1-interacting proteins, with Western blotting utilized to assess downstream signaling alterations. Our results demonstrated that CAAP1 downregulation was significantly correlated with poor prognosis in HGSOC patients. Functionally, CAAP1 knockdown promoted HGSOC cell proliferation, migration, and apoptosis resistance, whereas CAAP1 overexpression exerted opposite inhibitory effects. In vivo experiments corroborated that CAAP1 overexpression effectively suppressed tumor growth. Mechanistically, CAAP1 was found to interact with eukaryotic translation initiation factor 3 subunit I (EIF3I) to modulate the expression of cancer-related proteins. Collectively, this study establishes that CAAP1 functions as a tumor suppressor in HGSOC by binding to EIF3I, thereby restraining tumor growth and metastasis.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 7","pages":"3136-3149"},"PeriodicalIF":3.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13468234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148756970","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}