Oncology reports最新文献

{"title":"Targeting adenocarcinoma and enzalutamide‑resistant prostate cancer using the novel anti‑androgen inhibitor ADA‑308.","authors":"Shaghayegh Nouruzi, Fraser Johnson, Sahil Kumar, Olena Sivak, Nakisa Tabrizian, Milla Koistinaho, Anu Muona, Amina Zoubeidi","doi":"10.3892/or.2024.8791","DOIUrl":"10.3892/or.2024.8791","url":null,"abstract":"<p><p>Prostate cancer (PCa) is the leading cause of cancer‑related death among men worldwide. PCa often develops resistance to standard androgen deprivation therapy and androgen receptor (AR) pathway inhibitors, such as enzalutamide (ENZ). Therefore, there is an urgent need to develop novel therapeutic strategies for this disease. The efficacy of ADA‑308 was evaluated through <i>in vitro</i> assessments of AR activity and cell proliferation, alongside <i>in vivo</i> studies. ADA‑308 has emerged as a promising candidate, demonstrating potent inhibition of AR‑sensitive adenocarcinoma as well as ENZ‑resistant PCa cell lines. The results of the study revealed that ADA‑308 effectively blocked AR activity, including its nuclear localization, and inhibited cell proliferation <i>in vitro</i>. Furthermore, ADA‑308 demonstrated notable efficacy <i>in vivo</i>, with a robust antitumor response in ENZ‑resistant models. These findings establish the role of ADA‑308 as a potent AR inhibitor that overcomes resistance to AR‑targeted therapies and highlights its potential as a novel therapeutic approach in advanced PCa management.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11332584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917275","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 potential mechanism of tumor immune escape: Regulation and application of soluble natural killer group 2 member D ligands (Review).","authors":"Shuhao Huang, Zihao Qin, Feiyang Wang, Yiping Kang, Biqiong Ren","doi":"10.3892/or.2024.8796","DOIUrl":"10.3892/or.2024.8796","url":null,"abstract":"<p><p>The immune system is integral to the surveillance and eradication of tumor cells. Interactions between the natural killer group 2 member D (NKG2D) receptor and its ligands (NKG2DLs) are vital for activating NKG2D receptor‑positive immune cells, such as natural killer cells. This activation enables these cells to identify and destroy tumor cells presenting with NKG2DLs, which is an essential aspect of tumor immunity. However, tumor immune escape is facilitated by soluble NKG2DL (sNKG2DL) shed from the surface of tumor cells. The production of sNKG2DL is predominantly regulated by metalloproteinases [a disintegrin and metalloproteinases (ADAM) and matrix metalloproteinase (MMP) families] and exosomes. sNKG2DL not only diminish immune recognition on the tumor cell surface but also suppress the function of immune cells, such as NK cells, and reduce the expression of the NKG2D receptor. This process promotes immune evasion, progression, and metastasis of tumors. In this review, an in‑depth summary of the mechanisms and factors that influence sNKG2DL production and their contribution to immune suppression within the tumor microenvironment are provided. Furthermore, due to the significant link between sNKG2DLs and tumor progression and metastasis, they have great potential as novel biomarkers. Detectable via liquid biopsies, sNKG2DLs could assess tumor malignancy and prognosis, and act as pivotal targets for immunotherapy. This could lead to the discovery of new drugs or the enhancement of existing treatments. Thus, the application of sNKG2DLs in clinical oncology was explored, offering substantial theoretical support for the development of innovative immunotherapeutic strategies for sNKG2DLs.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11358674/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000447","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":"Metformin suppresses esophageal cancer progression through the radiation‑induced cellular senescence of cancer‑associated fibroblasts.","authors":"Yuya Sugimoto, Koichi Okamoto, Hiroto Saito, Takahisa Yamaguchi, Jun Kinoshita, Keishi Nakamura, Takahisa Takino, Yoshio Endo, Itasu Ninomiya, Tetsuo Ohta, Noriyuki Inaki","doi":"10.3892/or.2024.8788","DOIUrl":"10.3892/or.2024.8788","url":null,"abstract":"<p><p>Senescent cells are known to secrete proteins, including inflammatory cytokines and damage‑associated molecular patterns. This phenomenon is known as the senescence‑associated secretory phenotype (SASP). SASP in cancer stromal fibroblasts is involved in cancer growth and progression. Conversely, metformin, an antidiabetic drug, has been reported to inhibit SASP induction by inhibiting the activation of NF‑κB, a regulator of SASP. To date, at least to the best of our knowledge, there have been no reports regarding cellular senescence in fibroblasts and tumor progression via the SASP‑mediated paracrine pathway. The present study thus aimed to elucidate the induction mechanisms of SASP in radiation‑induced fibroblasts and to determine its effects on cancer progression via the paracrine pathway. Furthermore, the present study aimed to determine whether controlling SASP using metformin suppresses cancer progression. A well‑differentiated esophageal cancer cell line established by the authors' department and fibroblasts isolated and cultured from the non‑cancerous esophageal mucosa of resected esophageal cancer cases were used for the experiments. Fibroblasts were irradiated with 8 Gy radiation, and the changes in the expression of the senescence markers, SA‑β‑gal, p21, p16 and NF‑κB were evaluated using immunofluorescent staining and western blot analysis in the presence or absence of metformin treatment. The culture supernatants of irradiated fibroblasts treated with metformin and those treated without metformin were collected and added to the cancer cells to evaluate their proliferative, invasive and migratory abilities. Vimentin and E‑cadherin expression levels were also evaluated using immunofluorescent staining and western blot analysis. The expression levels of p16, p21 and NF‑κB in irradiated fibroblasts were attenuated by treatment with metformin. Supernatants collected from irradiated fibroblasts exhibited the proliferative activity of esophageal cancer cells, and the promotion of migratory and invasion abilities, which may be due to epithelial‑mesenchymal transition and changes in cell morphology. These reactions were confirmed to be suppressed by the addition of the supernatant of cultured fibroblasts pre‑treated with metformin. On the whole, the present study demonstrates that fibroblasts in the cancer stroma may be involved in tumor progression through cellular senescence.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11332583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875488","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":"DNA methylation and mRNA expression of ZNF577 as biomarkers for the detection and prognosis of lung adenocarcinoma.","authors":"Batkhishig Munkhjargal, Kazuya Kondo, Shiho Soejima, Bilguun Tegshee, Michiko Yamashita, Naoya Kawakita, Hiroaki Toba, Hiromitsu Takizawa","doi":"10.3892/or.2024.8790","DOIUrl":"10.3892/or.2024.8790","url":null,"abstract":"<p><p>Despite advances in science and technology, lung cancer remains a major public health issue. The discovery of early diagnostic and prognostic markers is still needed to reduce the mortality rate of lung cancer, which is the highest among all cancer types. Aberrations in the DNA methylation system have an important role in human cancer and are promising for the development of early diagnostic and prognostic markers. The present study focused on zinc finger protein (ZNF)577, whose encoding gene was indicated to exhibit promoter hypermethylation together with 9 other genes in lung adenocarcinoma (LADC) in a previous study by our group. ZN577 is a member of the ZNG family and its functional role has so far remained elusive. LADC tissue samples surgically resected at Tokushima University Hospital (Tokushima, Japan) between April 1999 and November 2013 were collected. A total of 73 tumors and 27 paired tumor-adjacent normal tissues were examined for DNA methylation and mRNA expression of ZNF577. A total of 149 LADC tissue samples were collected and evaluated by immunohistochemistry (IHC) for the tissue expression of ZNF577. High methylation (n=27, P<0.0001) and low mRNA expression levels (n=27, P<0.031) of ZNF577 were identified in LADC tissues, and it was demonstrated that methylation levels were inversely correlated with mRNA expression levels (P=0.0116, ρ=-0.2515). Among the LADC tissues, lepidic-patterned samples had lower methylation levels of ZNF577 than other pathological types. In addition, mRNA expression levels of ZNF577 were significantly higher in females, non-smokers and stage I samples. Overall survival [P<0.0001; area under curve (AUC)=0.8658] and disease-free survival (DFS; P<0.0004; AUC=0.7232) rates were significantly higher in the ZNF577 high mRNA expression group than in the ZNF577 low mRNA expression group. Among the 149 LADC samples examined by IHC, 105 were negative and 44 were positive for the tissue expression of ZNF577. Cox regression analysis showed poorer DFS (hazard ratio: 3.917; P=0.023) in patients with lower expression of ZNF577. In conclusion, higher methylation levels of ZNF577 were observed in LADC tissues than in normal lung tissue and low mRNA expression of ZNF577 was associated with unfavorable prognosis.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917273","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}

{"title":"Glioma lateralization: Focus on the anatomical localization and the distribution of molecular alterations (Review).","authors":"Nilgun Tuncel Cini, Manuela Pennisi, Sidika Genc, Demetrios A Spandidos, Luca Falzone, Panayiotis D Mitsias, Aristides Tsatsakis, Ali Taghizadehghalehjoughi","doi":"10.3892/or.2024.8798","DOIUrl":"10.3892/or.2024.8798","url":null,"abstract":"<p><p>It is well known how the precise localization of glioblastoma multiforme (GBM) predicts the direction of tumor spread in the surrounding neuronal structures. The aim of the present review is to reveal the lateralization of GBM by evaluating the anatomical regions where it is frequently located as well as the main molecular alterations observed in different brain regions. According to the literature, the precise or most frequent lateralization of GBM has yet to be determined. However, it can be said that GBM is more frequently observed in the frontal lobe. Tractus and fascicles involved in GBM appear to be focused on the corticospinal tract, superior longitudinal I, II and III fascicles, arcuate fascicle long segment, frontal strait tract, and inferior fronto‑occipital fasciculus. Considering the anatomical features of GBM and its brain involvement, it is logical that the main brain regions involved are the frontal‑temporal‑parietal‑occipital lobes, respectively. Although tumor volumes are higher in the right hemisphere, it has been determined that the prognosis of patients diagnosed with cancer in the left hemisphere is worse, probably reflecting the anatomical distribution of some detrimental alterations such as TP53 mutations, PTEN loss, EGFR amplification, and MGMT promoter methylation. There are theories stating that the right hemisphere is less exposed to external influences in its development as it is responsible for the functions necessary for survival while tumors in the left hemisphere may be more aggressive. To shed light on specific anatomical and molecular features of GBM in different brain regions, the present review article is aimed at describing the main lateralization pathways as well as gene mutations or epigenetic modifications associated with the development of brain tumors.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11358673/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000448","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":"Pituitary tumor‑transforming gene 1 regulates the senescence and apoptosis of oral squamous cell carcinoma in a p21‑dependent DNA damage response manner.","authors":"Suyeon Park, Shihyun Kim, Moon-Young Kim, Sang Shin Lee, Jongho Choi","doi":"10.3892/or.2024.8794","DOIUrl":"10.3892/or.2024.8794","url":null,"abstract":"<p><p>Pituitary tumor‑transforming gene 1 (PTTG1), also known as securin, is a proto‑oncogene involved in the development of various cancers by promoting cell proliferation and mobility. However, its underlying biological mechanisms in oral squamous cell carcinoma (OSCC) progression remain unclear. in the present study, it was sought to elucidate the role of PTTG1 as an oncogene in OSCC progression and was attempted to unravel the underlying mechanism and impact of PTTG1 expression on cell cycle, cell death, and cellular senescence. The effect of double strand break on PTTG1 expression was investigated in OSCC growth. To identify the role of PTTG1 in OSCC growth, the cell viability and senescence was analyzed by EdU and senescence‑associated beta‑galactosidase (SA‑β‑gal) assay, respectively. To verify the DNA damage‑induced senescence of PTTG1, the chromosomal damage in OSCC was analyzed <i>in vitro</i>. Finally, the effect of PTTG1 on tumor growth and gene expression related to cell viability and DNA damaged‑induced senescence was investigated <i>in vivo</i>. PTTG1 expression was compared between OSCC and healthy patient samples (n=32) using reverse transcription‑quantitative PCR and immunohistochemistry; and it was found that PTTG1 expression was upregulated in OSCC. Small interfering RNA‑mediated knockdown of PTTG1 in two OSCC cell lines revealed that PTTG1 downregulation significantly inhibited cell proliferation and arrested the cell cycle pathway as evidenced by changes in checkpoint genes (such as cyclin D1, E and B1). PTTG1 knockdown also increased apoptosis, as evidenced by the upregulation of apoptotic genes [such as cleaved (c‑) Caspase‑7 and c‑poly (ADP‑ribose) polymerase]. Moreover, PTTG1 downregulation promoted cellular senescence, as shown by western blotting and SA‑β‑gal staining. Finally, senescence‑induced DNA damage was observed in OSCC cells, which accelerates genomic instability, through chromosomal damage analysis. Taken together, the present findings suggested that PTTG1 acts as a proto‑oncogene; regulates cell proliferation, cell cycle, cellular senescence and DNA damage in OSCC; and may serve as a novel diagnostic biomarker and potential therapeutic target for OSCC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11338240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000449","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] DJ‑1 is involved in the peritoneal metastasis of gastric cancer through activation of the Akt signaling pathway.","authors":"Zheng-Ming Zhu, Zheng-Rong Li, Yan Huang, Hai-Hong Yu, Xiao-Shan Huang, Yu-Feng Yan, Jiang-Hua Shao, He-Ping Chen","doi":"10.3892/or.2024.8797","DOIUrl":"10.3892/or.2024.8797","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that the western blot data shown for the MMP‑9 experiment in Fig. 4 on p. 1493 were strikingly similar to the western blots shown for the total‑Akt experiments in Fig. 6 on p. 1494. After having re‑examined their original data files, the authors realized that Fig. 6 had been inadvertently assembled incorrectly. The revised version of Fig. 6, containing the correct data for the total‑Akt experiments, is shown below. Note that the corrections made to this figure do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of <i>Oncology Reports</i> for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 31: 1489‑1497, 2014; DOI: 10.3892/or.2013.2961].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11358671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000444","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] MEG3/miR‑21 axis affects cell mobility by suppressing epithelial‑mesenchymal transition in gastric cancer.","authors":"Gang Xu, Lei Meng, Dawei Yuan, Kang Li, Yong Zhang, Chengxue Dang, Kun Zhu","doi":"10.3892/or.2024.8799","DOIUrl":"10.3892/or.2024.8799","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell invasion assay data shown in Fig. 2B on p. 42 and the immunofluorescence data shown in Fig. 4D on p. 44 were strikingly similar to data appearing in other articles written by different authors at different research institutes that were submitted to different journals at around the same time. Moreover, a further investigation of this paper undertaken by the Editorial Office identified a large number of overlapping data panels comparing the Transwell cell migration and invasion assay data and the scratch‑wound assay data both within and between Figs. 2 and 3, where data which were intended to have shown the results from differently performed experiments had apparently been derived from the same original source, including an overlapping section of data within the 'MEG3+mimic' panel in Fig. 3G that would be difficult to attribute to pure chance. Owing to the fact that the contentious data in the above article had already been submitted for publication at around the same time as its submission to <i>Oncology Reports</i>, and given an overall lack of confidence in the presented data, the Editor 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. [Oncology Reports 40: 39‑48, 2018; DOI: 10.3892/or.2018.6424].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11358672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000445","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] MicroRNA‑642a‑5p inhibits colon cancer cell migration and invasion by targeting collagen type I α1.","authors":"Xiaoguang Wang, Zhengwei Song, Biwen Hu, Zhenwei Chen, Fei Chen, Chenxi Cao","doi":"10.3892/or.2024.8795","DOIUrl":"10.3892/or.2024.8795","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the cell invasion assay data shown in Fig. 6B on p. 940, and western blot data featured in Fig. 7B on p. 942, had already appeared in previously published articles written by different authors at different research institutes. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Oncology Reports</i>, the Editor 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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 45: 933‑944, 2021; DOI: 10.3892/or.2020.7905].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11338242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000446","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":"Zinc finger protein 180 induces an apoptotic phenotype by activating METTL14 transcriptional activity in colorectal cancer.","authors":"Liang Xu, Xi-Jie Chen, Qian Yan, Xin-Tao Lei, Hai-Ling Liu, Jing-Ping Xu, Wei-Te Shang, Jing-Lin Huang, Zhi-Ting Chen, Xiao-Li Tan, Han-Jie Lin, Xin-Hui Fu, Li-Sheng Zheng, Ping Lan, Yan Huang","doi":"10.3892/or.2024.8784","DOIUrl":"10.3892/or.2024.8784","url":null,"abstract":"<p><p>Zinc finger protein 180 (ZNF180) is a multifunctional protein that interacts with nucleic acids and regulates various cellular processes; however, the function of ZNF180 in colorectal cancer (CRC) remains unclear. The present study investigated the role and function of ZNF180 in CRC, and aimed to reveal the underlying molecular mechanism. The results revealed that ZNF180 was downregulated in CRC tissues and was associated with a good prognosis in patients with CRC. Additionally, the expression of ZNF180 was downregulated by methylation in CRC. <i>In vivo</i> and <i>in vitro</i> experiments revealed that ZNF180 overexpression was functionally associated with the inhibition of cell proliferation and the induction of apoptosis. Mechanistically, chromatin immunoprecipitation‑PCR and luciferase assays demonstrated that ZNF180 markedly regulated the transcriptional activity of methyltransferase 14, N6‑adenosine‑methyltransferase non‑catalytic subunit (METTL14) by directly binding to and activating its promoter region. Simultaneous overexpression of ZNF180 and knockdown of METTL14 indicated that the reduction of METTL14 could suppress the effects of ZNF180 on the induction of apoptosis. Clinically, the present study observed a significant positive correlation between ZNF180 and METTL14 expression levels, and low expression of ZNF180 and METTL14 predicted a poor prognosis in CRC. Overall, these findings revealed a novel mechanism by which the ZNF180/METTL14 axis may modulate apoptosis and cell proliferation in CRC. This evidence suggests that this axis may serve as a prognostic biomarker and therapeutic target in patients with CRC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141760185","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}