International journal of oncology最新文献

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Unveiling vitamin C: A new hope in the treatment of diffuse large B‑cell lymphoma (Review). 揭示维生素C:弥漫性大B细胞淋巴瘤治疗的新希望(综述)
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-05-02 DOI: 10.3892/ijo.2025.5746
Chunxiao Ren, Yaqiong Li, Mingrui Li, Yuqun Wang
{"title":"Unveiling vitamin C: A new hope in the treatment of diffuse large B‑cell lymphoma (Review).","authors":"Chunxiao Ren, Yaqiong Li, Mingrui Li, Yuqun Wang","doi":"10.3892/ijo.2025.5746","DOIUrl":"https://doi.org/10.3892/ijo.2025.5746","url":null,"abstract":"<p><p>Lymphoma is a malignancy of the immune system, which originates from lymphatic tissues and lymph nodes. Diffuse large B‑cell lymphoma (DLBCL) is a common type of non‑Hodgkin lymphoma, occurring in 30‑40% of all cases, which has persistent clinical challenges. The treatment of DLBCL is challenging due to its diverse genetic and biological characteristics and complex clinical physiology. Despite advancements in overall prognosis, 20‑25% of patients continue to experience relapse and 10‑15% of patients experience refractory disease. Vitamin C is a water‑soluble vitamin with antioxidant properties and notable pharmacological activity, with potential applications in cancer therapy. Pharmacological doses of vitamin C (1‑4 g/kg) can induce apoptosis in malignant cells by inhibiting and/or reversing gene mutations that are associated with hematological malignancies. For example, 10‑25% of patients with myeloid malignancies have tet methylcytosine dioxygenase 2 (TET2) gene mutations and vitamin C can regulate blood stem cell frequency and leukemia production by enhancing TET2 function. Consequently, pharmacological doses of vitamin C can inhibit the development and progression of hematological malignancies. Therefore, the present review aimed to investigate the role of vitamin C in the pathophysiology and treatment of DLBCL, whilst highlighting the potential challenges and future perspectives.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019529","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}
引用次数: 0
Current updates on the structural and functional aspects of the CRISPR/Cas13 system for RNA targeting and editing: A next‑generation tool for cancer management (Review). 用于RNA靶向和编辑的CRISPR/Cas13系统的结构和功能方面的最新进展:下一代癌症管理工具(综述)。
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-05-01 Epub Date: 2025-05-09 DOI: 10.3892/ijo.2025.5748
Khaled S Allemailem, Arshad Husain Rahmani, Nahlah Makki Almansour, Fahad M Aldakheel, Ghadah Mohammad Albalawi, Ghadeer Mohammed Albalawi, Amjad Ali Khan
{"title":"Current updates on the structural and functional aspects of the CRISPR/Cas13 system for RNA targeting and editing: A next‑generation tool for cancer management (Review).","authors":"Khaled S Allemailem, Arshad Husain Rahmani, Nahlah Makki Almansour, Fahad M Aldakheel, Ghadah Mohammad Albalawi, Ghadeer Mohammed Albalawi, Amjad Ali Khan","doi":"10.3892/ijo.2025.5748","DOIUrl":"https://doi.org/10.3892/ijo.2025.5748","url":null,"abstract":"<p><p>For centuries, a competitive evolutionary race between prokaryotes and related phages or other mobile genetic elements has led to the diversification of Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) and CRISPR‑associated sequence (Cas) genome‑editing systems. Among the different CRISPR/Cas systems, the CRISPR/Cas9 system has been widely studied for its precise DNA manipulation; however, due to certain limitations of direct DNA targeting, off‑target effects and delivery challenges, researchers are looking to perform transient knockdown of gene expression by targeting RNA. In this context, the more recently discovered type VI CRISPR/Cas13 system, a programmable single‑subunit RNA‑guided endonuclease system that has the capacity to target and edit any RNA sequence of interest, has emerged as a powerful platform to modulate gene expression outcomes. All the Cas13 effectors known so far possess two distinct ribonuclease activities. Pre‑CRISPR RNA processing is performed by one RNase activity, whereas the two higher eukaryotes and prokaryotes nucleotide‑binding domains provide the other RNase activity required for target RNA degradation. Recent innovative applications of the type VI CRISPR/Cas13 system in nucleic acid detection, viral interference, transcriptome engineering and RNA imaging hold great promise for disease management. This genome editing system can also be employed by the Specific High Sensitivity Enzymatic Reporter Unlocking platform to identify any tumor DNA. The discovery of this system has added a new dimension to targeting, tracking and editing circulating microRNA/RNA/DNA/cancer proteins for the management of cancer. However, there is still a lack of thorough understanding of the mechanisms underlying some of their functions. The present review summarizes the recent updates on the type VI CRISPR/Cas system in terms of its structural and mechanistic properties and some novel applications of this genome‑editing tool in cancer management. However, some issues, such as collateral degradation of bystander RNA, impose major limitations on its <i>in vivo</i> application. Furthermore, additional challenges and future prospects for this genome editing system are described in the present review.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144023004","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}
引用次数: 0
Current developments of pharmacotherapy targeting heme oxygenase 1 in cancer (Review). 靶向血红素加氧酶1在癌症中的药物治疗进展(综述)。
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-04-01 Epub Date: 2025-02-21 DOI: 10.3892/ijo.2025.5732
Xiaohu Ouyang, Jingbo Wang, Xiaoyuan Qiu, Desheng Hu, Jing Cui
{"title":"Current developments of pharmacotherapy targeting heme oxygenase 1 in cancer (Review).","authors":"Xiaohu Ouyang, Jingbo Wang, Xiaoyuan Qiu, Desheng Hu, Jing Cui","doi":"10.3892/ijo.2025.5732","DOIUrl":"10.3892/ijo.2025.5732","url":null,"abstract":"<p><p>Malignant tumors are non-communicable diseases that impact human health and quality of life. Identifying and targeting the underlying genetic drivers is a challenge. Heme oxygenase-1 (HO-1), a stress-inducible enzyme also known as heat shock protein 32, plays a crucial role in maintaining cellular homeostasis. It mitigates oxidative stress-induced damage and exhibits anti-apoptotic properties. HO-1 is expressed in a wide range of malignancies and is associated with tumor growth. However, the precise role of HO-1 in tumor development remains controversial. Drugs, both naturally occurring and chemically synthesized, can inhibit tumor growth by modulating HO-1 expression in cancer cells. The present review aimed to discuss biological functions of HO-1 pharmacological therapies targeting HO-1.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Tumor‑associated neutrophils: Critical regulators in cancer progression and therapeutic resistance (Review). 肿瘤相关中性粒细胞:癌症进展和治疗耐药性的关键调节因子(综述)。
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-04-01 Epub Date: 2025-02-28 DOI: 10.3892/ijo.2025.5734
Rui Hou, Xi Wu, Cenzhu Wang, Hanfang Fan, Yuhan Zhang, Hanchi Wu, Huiyu Wang, Junli Ding, Huning Jiang, Junying Xu
{"title":"Tumor‑associated neutrophils: Critical regulators in cancer progression and therapeutic resistance (Review).","authors":"Rui Hou, Xi Wu, Cenzhu Wang, Hanfang Fan, Yuhan Zhang, Hanchi Wu, Huiyu Wang, Junli Ding, Huning Jiang, Junying Xu","doi":"10.3892/ijo.2025.5734","DOIUrl":"10.3892/ijo.2025.5734","url":null,"abstract":"<p><p>Cancer is the second leading cause of death among humans worldwide. Despite remarkable improvements in cancer therapies, drug resistance remains a significant challenge. The tumor microenvironment (TME) is intimately associated with therapeutic resistance. Tumor‑associated neutrophils (TANs) are a crucial component of the TME, which, along with other immune cells, play a role in tumorigenesis, development and metastasis. In the current review, the roles of TANs in the TME, as well as the mechanisms of neutrophil‑mediated resistance to cancer therapy, including immunotherapy, chemotherapy, radiotherapy and targeted therapy, were summarized. Furthermore, strategies for neutrophil therapy were discussed and TANs were explored as potential targets for cancer treatment. In conclusion, the need to explore the precise roles, recruitment pathways and mechanisms of action of TANs was highlighted for the purpose of developing therapies that precisely target TANs and reverse drug resistance.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522802","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}
引用次数: 0
AGTR1 potentiates the chemotherapeutic efficacy of cisplatin in esophageal carcinoma through elevation of intracellular Ca2+ and induction of apoptosis. AGTR1 通过升高细胞内 Ca2+ 和诱导细胞凋亡增强顺铂对食管癌的化疗效果。
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-04-01 Epub Date: 2025-03-14 DOI: 10.3892/ijo.2025.5738
Kang Liu, Jun Bie, Ruolan Zhang, Rong Xiong, Lihong Peng, Yi Luo, Siyun Yang, Gang Feng, Guiqin Song
{"title":"AGTR1 potentiates the chemotherapeutic efficacy of cisplatin in esophageal carcinoma through elevation of intracellular Ca<sup>2+</sup> and induction of apoptosis.","authors":"Kang Liu, Jun Bie, Ruolan Zhang, Rong Xiong, Lihong Peng, Yi Luo, Siyun Yang, Gang Feng, Guiqin Song","doi":"10.3892/ijo.2025.5738","DOIUrl":"10.3892/ijo.2025.5738","url":null,"abstract":"<p><p>Cisplatin is one of the principal chemotherapeutic agents used for esophageal cancer (EC) treatment; however, EC mortality remains high. It is therefore imperative to find new therapeutic targets and approaches to potentiate the chemotherapeutic efficacy of cisplatin. Angiotensin II receptor type 1 (AGTR1) is a potential therapeutic target in multiple cancer types. In the present study, RNA‑sequencing analysis of EC and normal esophageal tissues was performed and AGTR1 was identified as a differentially expressed gene that is markedly downregulated in recurrent and metastasized EC. AGTR1 upregulation in the esophageal squamous cell carcinoma cell lines, KYSE‑150 and EC109, promoted their chemosensitivity to cisplatin both <i>in vitro</i> and <i>in vivo</i>. Additionally, AGTR1 suppressed the metastasis‑relevant traits of EC cells, as evidenced by the reduced migration, invasion and wound healing of EC cells with higher AGTR1 expression levels. Moreover, AGTR1 overexpression in EC cells upregulated intracellular Ca<sup>2+</sup> levels, reduced ATP levels and mitochondrial membrane potentials, which was accompanied by enhanced mitochondrial pathway apoptosis. Notably, either AGTR1 overexpression or treatments with the calcium channel blocker, fendiline, caused Ca<sup>2+</sup> influx and promoted mitochondria‑dependent apoptosis in KYSE‑150 cells <i>in vitro</i>. These effects were augmented when both AGTR1 overexpression and fendiline stimulation were imposed in the absence or presence of cisplatin treatments. Furthermore, fendiline administration enhanced the chemosensitivity of cisplatin in an EC xenograft mouse model. Collectively, these findings offer an alternative treatment option and provide mechanistic insights into using fendiline to potentiate the chemotherapy efficacy of cisplatin in treating EC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623730","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}
引用次数: 0
[Retracted] Feroniellin A‑induced autophagy causes apoptosis in multidrug‑resistant human A549 lung cancer cells. [撤回]Feroniellin A诱导的自噬导致多药耐药人A549肺癌细胞凋亡。
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-04-01 Epub Date: 2025-03-07 DOI: 10.3892/ijo.2025.5736
Chutima Kaewpiboon, Serm Surapinit, Waraporn Malilas, Eong Moon, Preecha Phuwapraisirisan, Santi Tip-Pyang, Randal N Johnston, Sang Seok Koh, Wanchai Assavalapsakul, Young-Hwa Chung
{"title":"[Retracted] Feroniellin A‑induced autophagy causes apoptosis in multidrug‑resistant human A549 lung cancer cells.","authors":"Chutima Kaewpiboon, Serm Surapinit, Waraporn Malilas, Eong Moon, Preecha Phuwapraisirisan, Santi Tip-Pyang, Randal N Johnston, Sang Seok Koh, Wanchai Assavalapsakul, Young-Hwa Chung","doi":"10.3892/ijo.2025.5736","DOIUrl":"10.3892/ijo.2025.5736","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that a pair of data panels (namely, the A549T‑eto/FERO, 1 mM and FERO, 12 h panels) in the cell viability experiments shown in Fig. 1B on p. 1235 were partially overlapping, where the data had apparently been derived from the same original source. After having performed an independent review of the data in the Editorial Office, also in Fig. 1B, another pair of overlapping data panels were identified; moreover, strikingly similar data for the α‑P‑glycoprotein blots had been included in different figures (Figs. 1C and 3B), and there appeared to be a splicing event/break in the continuity of the α‑actin bands shown for the control data in Figs. 1C and 3B that wasn't apparent elsewhere for the proteins of interest shown in these figure parts. Owing to these possible anomalies and the duplications of the data that have been identified in this paper, the Editor of <i>International Journal of Oncology</i> has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 44: 1233‑1242, 2014; DOI: 10.3892/ijo.2014.2297].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572320","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}
引用次数: 0
Fucoxanthin suppresses pancreatic cancer progression by inducing bioenergetics metabolism crisis and promoting SLC31A1‑mediated sensitivity to DDP. 岩藻黄素通过诱导生物能量代谢危机和促进SLC31A1介导的对DDP的敏感性来抑制胰腺癌的进展。
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-04-01 Epub Date: 2025-03-07 DOI: 10.3892/ijo.2025.5737
Fugen Shangguan, Nengfang Ma, Yang Chen, Yuansi Zheng, Ting Ma, Jing An, Jianhu Lin, Hailong Yang
{"title":"Fucoxanthin suppresses pancreatic cancer progression by inducing bioenergetics metabolism crisis and promoting SLC31A1‑mediated sensitivity to DDP.","authors":"Fugen Shangguan, Nengfang Ma, Yang Chen, Yuansi Zheng, Ting Ma, Jing An, Jianhu Lin, Hailong Yang","doi":"10.3892/ijo.2025.5737","DOIUrl":"10.3892/ijo.2025.5737","url":null,"abstract":"<p><p>Pancreatic cancer (PC) is one of the most malignant tumors, with a 5‑year survival rate <10%. Chemosynthetic drugs are widely used in the treatment of PC; however, their toxicity and side effects often reduce the quality of life for patients. MTT and colony formation assay were performed to detect cell growth and viability in PC cells. Levels of ROS in whole cell and mitochondria were analyzed through flow cytometry. ATP production was evaluated using an ATP Assay Kit. Cellular bioenergetics were analyzed with a Seahorse XFe96 Analyzer, and changes in target molecules were monitored by western blotting. The present study reports that fucoxanthin (FX), a carotenoid derived from aquatic brown seaweed, significantly inhibits PC by inhibiting cell proliferation and inducing cell death via the non‑classical pathway. FX switches mitochondrial respiration to aerobic glycolysis in PC cells. Furthermore, FX decreases whole‑cell ATP levels, which indicates that promotion of glycolysis does not compensate for FX‑induced ATP depletion in mitochondria. Moreover, FX decreased the reduced glutathione/oxidized glutathione ratio observed under glucose‑limited conditions. These alterations caused by FX may decrease metabolic flexibility, indicating higher sensitivity to glucose‑limited (GL) conditions. FX increased the cytotoxicity of cisplatin (DDP) and the expression of solute carrier family 31 member 1 (SLC31A1) in PC cells. Furthermore, the knockdown of SLC31A1 can attenuate cytotoxicity caused by the combination of FX and DDP. It was inferred that FX increased the sensitivity of PC cells to DDP), potentially by upregulating SLC31A1 expression. In conclusion, FX exhibited potent antitumor effects by reprogramming energy metabolism and inducing a distinct form of regulated cell death. Therefore, combining FX with GL treatment or DDP presents a promising therapeutic strategy for PC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572330","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}
引用次数: 0
[Retracted] Selenium‑binding protein 1 may decrease gastric cellular proliferation and migration. 【缩回】硒结合蛋白1可能降低胃细胞增殖和迁移。
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-04-01 Epub Date: 2025-02-21 DOI: 10.3892/ijo.2025.5731
Chenjing Zhang, Wen Xu, Wensheng Pan, Nana Wang, Guogang Li, Xiaoyuan Fan, Xiang Xu, Shengrong Shen, Undurti N Das
{"title":"[Retracted] Selenium‑binding protein 1 may decrease gastric cellular proliferation and migration.","authors":"Chenjing Zhang, Wen Xu, Wensheng Pan, Nana Wang, Guogang Li, Xiaoyuan Fan, Xiang Xu, Shengrong Shen, Undurti N Das","doi":"10.3892/ijo.2025.5731","DOIUrl":"10.3892/ijo.2025.5731","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the flow cytometric plots shown in Fig. 9A on p. 1628, a pair of data panels showed a surprisingly high level of partially overlapping data, given that the results from differently performed experiments were intended to have been shown in these figure parts. Upon performing an independent analysis of the data in this paper, a series of further issues concerning the data were noted; first in Fig. 9B, a separate pair of flow cytometric plots appeared to have been duplicated in their entireties. In addition, two pairs of data panels in Fig. 6A and B (showing the senescence of gastric cancer cells) contained overlapping sections of data; the control panels for the migration assay data in Fig. 7A and B were overlapping, albeit the orientation of the overlapping data sections was different. Owing to the large number of duplications of data, and other potential anomalies, that were identified in this paper, the Editor of <i>International Journal of Oncology</i> has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 42: 1620‑1629, 2013; DOI: 10.3892/ijo.2013.1850].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467932","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}
引用次数: 0
Epigenetic and epitranscriptomic role of lncRNA in carcinogenesis (Review). lncRNA在肿瘤发生中的表观遗传学和表转录组学作用(综述)。
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-04-01 Epub Date: 2025-02-28 DOI: 10.3892/ijo.2025.5735
Chunfei Dai, Haoyue Qianjiang, Ruishuang Fu, Huimin Yang, Aiqin Shi, Huacheng Luo
{"title":"Epigenetic and epitranscriptomic role of lncRNA in carcinogenesis (Review).","authors":"Chunfei Dai, Haoyue Qianjiang, Ruishuang Fu, Huimin Yang, Aiqin Shi, Huacheng Luo","doi":"10.3892/ijo.2025.5735","DOIUrl":"10.3892/ijo.2025.5735","url":null,"abstract":"<p><p>Long non‑coding RNAs (lncRNAs) are key players in the regulation of gene expression by mediating epigenetic and epitranscriptomic modification. Dysregulation of lncRNAs is implicated in tumor initiation, progression and metastasis. lncRNAs modulate chromatin structure and gene transcription by recruiting epigenetic regulators, including DNA‑ or histone‑modifying enzymes. Additionally, lncRNAs mediate chromatin remodeling and enhancer‑promoter long‑range chromatin interactions to control oncogene expression by recruiting chromatin organization‑associated proteins, thereby promoting carcinogenesis. Furthermore, lncRNAs aberrantly induce oncogene expression by mediating epitranscriptomic modifications, including RNA methylation and RNA editing. The present study aimed to summarize the regulatory mechanisms of lncRNAs in cancer to unravel the complex interplay between lncRNAs and epigenetic/epitranscriptomic regulators in carcinogenesis. The present review aimed to provide a novel perspective on the epigenetic and epitranscriptomic roles of lncRNAs in carcinogenesis to facilitate identification of potential biomarkers and therapeutic targets for cancer diagnosis and treatment.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523462","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}
引用次数: 0
Abnormal expression of CDC25C in NSCLC is influenced by transcriptional and RNA N6‑methyladenosine‑mediated post‑transcriptional regulation. CDC25C在NSCLC中的异常表达受转录和RNA N6甲基腺苷介导的转录后调控的影响。
IF 4.5 3区 医学
International journal of oncology Pub Date : 2025-04-01 Epub Date: 2025-02-21 DOI: 10.3892/ijo.2025.5733
Yuxin Zheng, Kefeng Wang, Wenli Mao, Guojun Zhang, Xiaomin Han, Hualin Li, Yukun Wang
{"title":"Abnormal expression of CDC25C in NSCLC is influenced by transcriptional and RNA N6‑methyladenosine‑mediated post‑transcriptional regulation.","authors":"Yuxin Zheng, Kefeng Wang, Wenli Mao, Guojun Zhang, Xiaomin Han, Hualin Li, Yukun Wang","doi":"10.3892/ijo.2025.5733","DOIUrl":"10.3892/ijo.2025.5733","url":null,"abstract":"<p><p>Non‑small cell lung cancer (NSCLC) exhibits a high incidence and mortality rate worldwide. Elevated cytokinesis cyclin 25 homologous protein C (CDC25C) expression is correlated with a poor prognosis in patients with NSCLC. Transcriptional regulation and post‑transcriptional modification are critical mechanisms governing gene expression, with aberrations in these processes increasingly recognized as pivotal contributors to cancer pathogenesis. The present study elucidated that the transcriptional activator, signal transducer and activator of transcription 3, directly interacts with the CDC25C promoter, thereby modulating its expression. Moreover, multi‑omics analysis was employed to identify the genes involved in the N6‑methyladenosine (m<sup>6</sup>A) methylation‑mediated post‑transcriptional regulation of CDC25C. The findings indicated that downregulation of alkB homolog 5 RNA demethylase in NSCLC leads to a marked increase in the m<sup>6</sup>A modification of CDC25C mRNA. It was also shown that YTH N6‑methyladenosine RNA binding protein (YTHDF) 3 and YTHDF2 compete to bind to CDC25C mRNA, thereby promoting or inhibiting its expression. Thus, the present study revealed that dysregulated expression of the CDC25C gene in NSCLC is influenced by multifaceted regulatory layers encompassing both transcriptional and post‑transcriptional mechanisms.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467933","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}
引用次数: 0
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