International journal of oncology最新文献

{"title":"Long non‑coding RNA ABHD11‑AS1 inhibits colorectal cancer progression through interacting with EGFR to suppress the EGFR/ERK signaling pathway.","authors":"Shiming Tan, Shizhen Li, Longzheng Xia, Xianjie Jiang, Zongyao Ren, Qiu Peng, Mingjing Peng, Wenjuan Yang, Xuemeng Xu, Linda Oyang, Mengzhou Shen, Jiewen Wang, Haofan Li, Nayiyuan Wu, Yanyan Tang, Qianjin Liao, Jinguan Lin, Yujuan Zhou","doi":"10.3892/ijo.2025.5726","DOIUrl":"10.3892/ijo.2025.5726","url":null,"abstract":"<p><p>Long non‑coding (lnc)RNAs participate in colorectal cancer (CRC) occurrence and progression. The present study aimed to investigate whether lncRNA ABHD11‑AS1 regulates malignant biological behavior of CRC cells. Bioinformatic analysis, reverse transcription‑quantitative PCR and <i>in situ</i> hybridization revealed that ABHD11‑AS1 expression was decreased in CRC samples and associated with an unfavorable prognosis. ABHD11‑AS1 overexpression significantly decreased proliferation, migration and invasion of CRC cells, whereas ABHD11‑AS1 inhibition had the opposite effects. ABHD11‑AS1 interacted with EGFR to inhibit EGFR phosphorylation and attenuate EGFR/ERK signaling, which in turn suppressed the malignant biological behavior of CRC cells. The tumor suppressor function of ABHD11‑AS1 was attenuated by the EGFR agonist NSC228155. Finally, resveratrol (RSV) inhibited CRC cell proliferation, migration and invasion, which may be associated with RSV‑induced decrease in SPT6 homolog, histone chaperone and transcription elongation factor protein expression and increase in ABHD11‑AS1 transcript levels. ABHD11‑AS1 inhibited the phosphorylation of EGFR and decreased EGFR/ERK signaling by interacting with EGFR, thereby delaying the progression of CRC. The ABHD11‑AS1/EGFR/ERK axis may be a novel therapeutic target for preventing CRC progression.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414251","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":"Pathogenetic development, diagnosis and clinical therapeutic approaches for liver metastasis from colorectal cancer (Review).","authors":"Zhenhua Jin, Yin Li, Hao Yi, Menghui Wang, Chaofeng Wang, Shaokun Du, Wenjuan Zeng, Zhen Zong","doi":"10.3892/ijo.2025.5728","DOIUrl":"10.3892/ijo.2025.5728","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a prevalent malignancy and a significant proportion of patients with CRC develop liver metastasis (CRLM), which is a major contributor to CRC‑related mortality. The present review aimed to comprehensively examine the pathogenetic development and diagnosis of CRLM and the clinical therapeutic approaches for treatment of this disease. The molecular mechanisms underlying CRLM were discussed, including the role of the tumour microenvironment and epithelial‑mesenchymal transition. The present review also highlighted the importance of early detection and the current challenges in predicting the development of CRLM. Various treatment strategies were reviewed, including surgical resection, chemotherapy and immunotherapy, and the potential of novel therapies, such as selective internal radiation therapy and Traditional Chinese Medicine. Despite recent advancements in treatment options, the treatment of CRLM remains a therapeutic challenge due to the complexity of the liver microenvironment and the heterogeneity of CRC. The present review emphasized the need for a multidisciplinary approach and the integration of emerging therapies to improve patient outcomes.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414256","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":"Emerging role of bile acids in colorectal liver metastasis: From molecular mechanism to clinical significance (Review).","authors":"Zhaoyu Li, Lingjun Deng, Mengting Cheng, Xiandong Ye, Nanyan Yang, Zaiwen Fan, Li Sun","doi":"10.3892/ijo.2025.5730","DOIUrl":"10.3892/ijo.2025.5730","url":null,"abstract":"<p><p>Liver metastasis is the leading cause of colorectal cancer (CRC)‑related mortality. Microbiota dysbiosis serves a role in the pathogenesis of colorectal liver metastases. Bile acids (BAs), cholesterol metabolites synthesized by intestinal bacteria, contribute to the metastatic cascade of CRC, encompassing colorectal invasion, migration, angiogenesis, anoikis resistance and the establishment of a hepatic pre‑metastatic niche. BAs impact inflammation and modulate the immune landscape within the tumor microenvironment by activating signaling pathways, which are used by tumor cells to facilitate metastasis. Given the widespread distribution of BA‑activated receptors in both tumor and immune cells, strategies aimed at restoring BA homeostasis and blocking metastasis‑associated signaling are of importance in cancer therapy. The present study summarizes the specific role of BAs in each step of colorectal liver metastasis, elucidating the association between BA and CRC progression to highlight the potential of BAs as predictive biomarkers for colorectal liver metastasis and their therapeutic potential in developing novel treatment strategies.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844338/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467930","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":"[Retracted] Zinc finger protein‑like 1 is a novel neuroendocrine biomarker for prostate cancer.","authors":"Neshat Masud, Afaf Aldahish, Kenneth A Iczkowski, Ajay Kale, Girish V Shah","doi":"10.3892/ijo.2025.5722","DOIUrl":"10.3892/ijo.2025.5722","url":null,"abstract":"<p><p>Following the publication of this paper, a concerned reader drew to the attention of the Editorial Office that, for the photomicrographs shown in Fig. 2B on p. 8, the same image had apparently been selected to represent the images for cerebrum and cerebellum from the brain. Secondly, the same image for the prostate tissue in Fig. 2B was used as the 'Matched normal' data in Fig. 3C on p. 9, and thirdly, the si3 and si3+CT images selected for Fig. 7B on p. 13 appeared to be derived from the same original source. Finally, after having performed an independent analysis of the data in the Editorial Office, it was noted that, for the wound healing assay data shown in Fig. 8E on p. 14, overlapping sections were identified comparing the CT and Overexp panels in the lower panel of images in this figure, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original source. After having considered these issues, owing to the number of instances of apparently misassembled data that have been identified in this paper, and also on the basis of an overall lack of confidence in the presented data, the Editor of <i>International Journal of Oncology</i> has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 62: 38, 2023; DOI: 10.3892/ijo.2023.5486].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364693","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":"Norchelerythrine from <i>Corydalis incisa</i> (Thunb.) Pers. promotes differentiation and apoptosis by activating DNA damage response in acute myeloid leukemia.","authors":"Ji-Eun Lee, Byeol-Eun Jeon, Chan-Seong Kwon, Hyeon-Young Kim, Tae-Jin Kim, Youngseob Seo, Sang Hun Lee, Ho-Jin Shin, Sang-Woo Kim","doi":"10.3892/ijo.2025.5723","DOIUrl":"10.3892/ijo.2025.5723","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is the most prevalent form of leukemia in adults. The cornerstone of first‑line chemotherapy for AML has poor survival rates, underscoring the urgent need for development of novel therapeutic agents. Differentiation therapy targets the blockade of differentiation in myeloid progenitor cells. The present study screened 100 plant extracts native to South Korea to search for those with differentiation‑inducing activity in AML. Differentiation‑inducing activity was assessed by measuring CD11b expression using fluorescence activated cell sorting. Of these, <i>Corydalis incisa</i> (Thunb.) Pers. (CIP) exhibited the highest efficacy. CIP induced myeloid differentiation, decreased viability and increased cell apoptosis and cell cycle arrest in HL‑60, U937 and THP‑1 cells. Furthermore, ultra‑performance liquid chromatography‑quadrupole time‑of‑flight mass spectrometry identified norchelerythrine as the primary anti‑leukemic compound in CIP. Norchelerythrine induced differentiation and promoted cell cycle arrest and apoptosis, mirroring the tumor‑suppressive effects of CIP, and notably decreased cell viability in patients with various genetic abnormalities. The present mechanistic study showed that norchelerythrine stimulated reactive oxygen species generation, leading to activation of DNA damage signaling and upregulation of p21^cip1, a cyclin‑dependent kinase inhibitor. Overall, norchelerythrine isolated from CIP may be a novel therapeutic option in AML.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364695","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":"Unleashing the power of urine‑based biomarkers in diagnosis, prognosis and monitoring of bladder cancer (Review).","authors":"Xuebin Wan, Dan Wang, Xiaoni Zhang, Mingyan Xu, Yuying Huang, Wenjian Qin, Shifu Chen","doi":"10.3892/ijo.2025.5724","DOIUrl":"10.3892/ijo.2025.5724","url":null,"abstract":"<p><p>Bladder cancer (BCa) is a prevalent malignant neoplasm of the urinary tract with high incidence rate, frequent recurrence and rapid disease progression. Conventional approaches for diagnosing, prognosticating and monitoring BCa often rely on invasive procedures such as cystoscopy and tissue biopsy, which are associated with high costs and low patient compliance for follow‑up. Liquid biopsies have advantages, such as being non‑invasive, real‑time, and reproducible, in obtaining diverse biomarkers derived from cellular, molecular, proteomic and genetic signatures in urine or plasma samples. Although plasma‑based biomarkers have been clinically validated, urine provides greater specificity for directly assessing biological materials from urological sources. The present review summarizes advancements and current limitations in urinary protein, genetic and epigenetic biomarkers for disease progression and treatment response of BC, compares performance and application scenarios of urine and blood biomarkers and explores how urinary biomarkers may serve as an alternative or complementary tool to traditional diagnostic methods. The integration of urine‑based or plasma‑based biomarkers into existing diagnostic workflows offers promising avenues for improving accuracy and efficiency of diagnosis in the management of BCa. Notably, the emergence of synthetic biomarkers and urine metabolites, combined with artificial intelligence or bioinformatic technologies, has promise in the screening of potential targets. Continued research and validation efforts are needed to translate these findings into routine clinical practice, ultimately improving patient outcomes and decreasing the burden of BCa.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364697","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":"Curcumin inhibits the activity of ubiquitin ligase Smurf2 to promote NLRP3‑dependent pyroptosis in non‑small cell lung cancer cells.","authors":"Yunzhu Xi, Saili Zeng, Xiaowu Tan, Xiaoyu Deng","doi":"10.3892/ijo.2025.5727","DOIUrl":"10.3892/ijo.2025.5727","url":null,"abstract":"<p><p>Non‑small cell lung cancer (NSCLC) is a malignant tumor of significant clinical relevance. Curcumin has been investigated for its potential anticancer properties, as it has been reported to act through multiple cancer‑related targets and pathways. The present study aimed to explore the effects of curcumin in NSCLC using both <i>in vitro</i> and <i>in vivo</i> models. NSCLC cell lines (specifically, A549 and NCI‑H1299 cells), and a mouse tumor model established through the subcutaneous injection of A549 cells, were utilized to evaluate the effects of curcumin intervention. The effects of treatment with curcumin on NOD‑like receptor pyrin domain‑containing 3 (NLRP3) ubiquitination, cell pyroptosis and pyroptosis‑associated factors were also evaluated. In addition, Smad ubiquitination regulatory factor 2 (Smurf2) was analyzed via a series of knockdown and overexpression experiments, both <i>in vitro</i> and <i>in vivo</i>, aimed at investigating its association with curcumin and NLRP3. The results obtained from these experiments showed that curcumin inhibited NSCLC cell growth, promoted pyroptosis and reduced the level of NLRP3 ubiquitination. NLRP3 knockdown reversed the curcumin‑induced increase in pyroptosis‑associated factors both <i>in vitro</i> and <i>in vivo</i>. Additionally, Smurf2 interacted with NLRP3 and alterations in Smurf2 expression levels influenced NLRP3 ubiquitination and cell pyroptosis. Moreover, molecular docking analysis demonstrated that curcumin could bind directly to Smurf2, which subsequently led to an inhibition of Smurf2 activity. Knockdown of Smurf2 enhanced curcumin's ability to stabilize NLRP3 and to promote pyroptosis, whereas Smurf2 overexpression negated these effects. In the <i>in vivo</i> animal model, curcumin treatment led to reduced tumor volumes and weights, in addition to a decreased expression level of Ki67 and increased expression levels of NLRP3 and pyroptosis‑associated factors. Similarly, these effects were enhanced or reversed by Smurf2 knockdown or overexpression, respectively. In conclusion, the findings of the present study showed that curcumin inhibited Smurf2 activity, thereby promoting NLRP3‑dependent pyroptosis in NSCLC cells. In addition, these findings have provided mechanistic insights into the role of curcumin in NSCLC, opening an avenue for its potential therapeutic application.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414246","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":"[Corrigendum] Upregulated NTF4 in colorectal cancer promotes tumor development via regulating autophagy.","authors":"Zhou Yang, Yusheng Chen, Xiyi Wei, Dejun Wu, Zhijun Min, Yingjun Quan","doi":"10.3892/ijo.2025.5725","DOIUrl":"10.3892/ijo.2025.5725","url":null,"abstract":"<p><p>Following the publication of the above article, the authors subsequently realized that, during the process of collating the raw data, Fig. 1 [the immunohistochemical (IHC) results for stage IV colorectal cancer (CRC)], Fig. 2A (the control β‑actin blots) and Fig. 5C and D (both the images selected for the clone formation assays, and the histograms showing the quantification of the data) were inadvertently assembled incorrectly. These errors arose as a consequence of the affected files having been named similarly to those of the correct panels. The revised versions of Figs. 1, 2 and 5, now featuring the correct IHC data for stage IV CRC in Fig. 1, the correct control western blots in Fig. 2 and the correct colony formation assay data (and quantification thereof) in Fig. 5, are shown on the next three pages. Note that the correction of these figures does not affect the key findings of the study (either the existing published results or the conclusions reached from the results). The authors thank the Editor of <i>International Journal of Oncology</i> for granting them the opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 56: 1442‑1454, 2020; DOI: 10.3892/ijo.2020.5027].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414244","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":"Telomeres and telomerase in mesothelioma: Pathophysiology, biomarkers and emerging therapeutic strategies (Review).","authors":"Dimitrios Andreikos, Demetrios A Spandidos, Vasiliki Epameinondas Georgakopoulou","doi":"10.3892/ijo.2025.5729","DOIUrl":"10.3892/ijo.2025.5729","url":null,"abstract":"<p><p>Malignant mesothelioma (MM) is a rare but aggressive cancer linked to asbestos exposure and characterized by advanced‑stage disease at presentation. Despite advances in treatment, prognosis remains abysmal, highlighting the imperative for the development of novel biomarkers and treatment approaches. Telomere biology plays a pivotal role in the tumorigenic process and has emerged as a key area in oncology research. Short telomeres have been associated with genomic instability, and substantially shorter telomere length (TL) has been identified in MM, showcasing the potential of TL in risk assessment, early detection, and disease progression monitoring. MM predominantly maintains TL through telomerase activity (TA), which in research has been identified in >90% of MM cases, underscoring the potential of TA as a biomarker in MM. Telomerase reverse transcriptase (TERT) polymorphisms may serve as valuable biomarkers, with research identifying associations between single nucleotide polymorphisms (SNPs) and the risk and prognosis of MM. Additionally, TERT promoter mutations have been associated with poor prognosis and advanced‑stage disease, with the non‑canonical functions of TERT hypothesized to contribute to the development of MM. TERT promoter mutations occur in ~12% of MM cases; C228T, C250T and A161C are the most common, while the distribution and frequency differ depending on histological subtype. Research reveals the promise of the various approaches therapeutically targeting telomerase, with favorable results in pre‑clinical models and inconclusive findings in clinical trials. The present review examines the role of telomere biology in MM and its implications in diagnosis, prognosis, and therapy.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467931","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":"SLC25A1 promotes lymph node metastasis of esophageal squamous cell carcinoma by regulating lipid metabolism.","authors":"Guoquan Zhang, Jingru Wu, Minghao Ji, Xiangyan Liu, Mo Shi","doi":"10.3892/ijo.2025.5721","DOIUrl":"10.3892/ijo.2025.5721","url":null,"abstract":"<p><p>Solute carrier family 25 member 1 (SLC25A1) affects lipid metabolism and energy regulation in multiple types of tumor cell, affecting their proliferation and survival. To the best of our knowledge, however, the impact of SLC25A1 on the proliferation and survival of esophageal squamous cell carcinoma (ESCC) cells has yet to be explored. Here, SLC25A1 expression was detected in ESCC tissues and cell lines. SLC25A1 was silenced or blocked by lentivirus transfection or 2‑[(4‑chloro‑3‑nitrophenyl)sulfonylamino]benzoic acid in ESCC cells. To evaluate the impact of SLC25A1 on <i>in vivo</i> and <i>in vitro</i> proliferation, invasion and migration of ESCC cells, Cell Counting‑Kit, wound healing, colony formation, Transwell, EdU, flow cytometry, tumor xenograft in nude mice, lipid metabolism and energy metabolism detection assays were performed. Reverse transcription‑quantitative PCR and western blot analysis were performed to determine expression of downstream molecules and pathway proteins following the silencing and blockade of SLC25A1. SLC25A1 was significantly overexpressed in ESCC tissue and cell lines. The targeted silencing of SLC25A1 or inhibition of its protein led to a significant decrease in proliferative, invasive and migratory capabilities of ESCC cells, accompanied by increased apoptosis. Additionally, silencing of the SLC25A1 gene significantly inhibited xenograft tumor growth <i>in vivo</i>. The present results indicate that knockdown or blockade of SLC25A1 can significantly impede the malignant biological behavior of ESCC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005174","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}