Oncology reports最新文献_第10页

[Retracted] Inhibition of neddylation modification by MLN4924 sensitizes hepatocellular carcinoma cells to sorafenib. 【撤回】MLN4924抑制类化修饰可使肝癌细胞对索拉非尼增敏。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-03-01 Epub Date: 2025-01-17 DOI: 10.3892/or.2025.8866

Zelong Yang, Jie Zhang, Xiaotong Lin, Di Wu, Guixi Li, Chunlian Zhong, Lei Fang, Peng Jiang, Liangyu Yin, Leida Zhang, Ping Bie, Chuan-Ming Xie

{"title":"[Retracted] Inhibition of neddylation modification by MLN4924 sensitizes hepatocellular carcinoma cells to sorafenib.","authors":"Zelong Yang, Jie Zhang, Xiaotong Lin, Di Wu, Guixi Li, Chunlian Zhong, Lei Fang, Peng Jiang, Liangyu Yin, Leida Zhang, Ping Bie, Chuan-Ming Xie","doi":"10.3892/or.2025.8866","DOIUrl":"10.3892/or.2025.8866","url":null,"abstract":"Following the publication of the above article, the authors noticed that they had inadvertently included a duplication of the same data in Fig. 3C, portraying colony formation experiments, where the results from differently performed experiments were intended to have been shown, and requested that a corrigendum be published to present the data in this figure accurately. Having investigated this matter in the Editorial Office, however, additional panels of overlapping data were identified, comparing between Figs. 2 and 3; moreover, a pair of overlapping data panels were also identified examining the Transwell migration assay data in Fig. 5A. The Editor of Oncology Reports has considered the authors' request to publish a corrigendum, but has decided to decline this request on account of the additional errors that have been identified; rather, the article is to be be retracted from the Journal on the basis of an overall lack of confidence in the presented data. Upon receiving this decision from the Editor, the authors did not provide a satisfactory reply. The Editor apologizes to the readership of the Journal for any inconvenience caused. [Oncology Reports 41: 3257‑3269, 2019; DOI: 10.3892/or.2019.7098].","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11747261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009122","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

Protein regulator of cytokinesis 1 regulates autophagy in hepatitis B virus‑associated liver cancer development. 细胞分裂1蛋白调节自噬在乙型肝炎病毒相关肝癌的发展。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-03-01 Epub Date: 2025-01-24 DOI: 10.3892/or.2025.8869

Jingjing Huang, Xianzhi Cheng, Chuang Wang, Fangyan Gong

{"title":"Protein regulator of cytokinesis 1 regulates autophagy in hepatitis B virus‑associated liver cancer development.","authors":"Jingjing Huang, Xianzhi Cheng, Chuang Wang, Fangyan Gong","doi":"10.3892/or.2025.8869","DOIUrl":"10.3892/or.2025.8869","url":null,"abstract":"Hepatitis B protein x (HBx) is considered a critical contributor to hepatitis B virus (HBV)‑associated liver cancer development. Protein regulator of cytokinesis 1 (PRC1) has been implicated in hepatocarcinogenesis. However, the clinical relevance, biological functions and related regulatory mechanisms of PRC1 in HBV‑associated liver cancer have not yet been clarified. PRC1 expression profiles in liver cancer were obtained from The Cancer Genome Atlas and Gene Expression Profiling Interactive Analysis database and through reverse transcription‑quantitative polymerase chain reaction and immunohistochemistry assays. A series of in vitro and in vivo assays were used to explore the function of the PRC1 gene and the possible mechanisms through which it affects HBV‑associated liver cancer. PRC1 was overexpressed in HBV‑positive liver cancer tissues. Functional studies in vitro demonstrated that HBx induced the expression of the PRC1 gene, which promoted cell autophagy and enhanced viability, invasion and migration. Furthermore, the knockdown of the PRC1 gene or treatment with the autophagosome inhibitor 3‑methyladenine blocked the HBx‑induced autophagic flux, disrupted the formation of autophagosomes, and promoted cell apoptosis. Liver cancer xenograft animal model experiments revealed that inhibition of autophagy by 3‑methyladenine or silencing of the PRC1 gene attenuated HBx‑induced malignant behavior in vivo. The absence of autophagy inhibited the expression of Bcl‑2, induced the expression of Bax, and regulated the levels of Th1 and Th2 cytokines. These results elucidate a mechanism wherein the PRC1 gene participates in the occurrence and development of HBV‑associated liver cancer by modulating autophagy. PRC1 could be a potential therapeutic target for liver cancer.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11795243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391408","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

Role of miRNA‑145‑5p in cancer (Review). miRNA - 145 - 5p在癌症中的作用（综述）。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-03-01 Epub Date: 2025-01-31 DOI: 10.3892/or.2025.8872

Zeshan Chen, Yijue Qin

引用次数: 0

Cysteine‑ and glycine‑rich protein 2: A vital regulator that inhibits necroptosis glioma cell by activating the JAK‑STAT1 pathways. 富含半胱氨酸和甘氨酸的蛋白2：通过激活JAK - STAT1途径抑制坏死性上睑胶质瘤细胞的重要调节因子。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-03-01 Epub Date: 2025-02-07 DOI: 10.3892/or.2025.8873

Dongsheng Lv, Xu Han, Liang Hao, Zhimin Sun, Aobo Zhang, Jing Liu, Liang Liu, Liqiang Liu

{"title":"Cysteine‑ and glycine‑rich protein 2: A vital regulator that inhibits necroptosis glioma cell by activating the JAK‑STAT1 pathways.","authors":"Dongsheng Lv, Xu Han, Liang Hao, Zhimin Sun, Aobo Zhang, Jing Liu, Liang Liu, Liqiang Liu","doi":"10.3892/or.2025.8873","DOIUrl":"10.3892/or.2025.8873","url":null,"abstract":"Cysteine‑ and glycine‑rich protein 2 (CSRP2) are closely associated with tumor invasion and metastasis. CSRP2 is significantly upregulated in glioma tissues and is associated with the clinical stage of the tumor. Overexpression of CSRP2 in glioma cells promotes the proliferation and metastasis of cancer cells, whereas CSRP2 knockdown inhibits the biological functions of tumor cells. Transcriptome sequencing of CSRP2‑knockdown U251M cells revealed that silencing of CSRP2 inhibited the JAK‑STAT1 signaling pathway, and differentially expressed genes were significantly enriched in cell processes related to necroptosis. Experiments on necroptosis in glioma cells using flow cytometry, Hoechst 33342/PI dual staining and transmission electron microscopy indicated that CSRP2 overexpression inhibited necroptosis in glioma cells. Western blotting results showed that overexpression of CSRP2 activated the JAK‑STAT1 signaling pathway, while the addition of the pathway inhibitor ruxolitinib promoted the phosphorylation of necroptosis proteins RIPK1, RIPK3 and MLKL. Therefore, it was hypothesized that CSRP2 maintains JAK‑STAT1 activation by inhibiting the protein inhibitor of activated STAT1, which then inhibits the necrotizing apoptosis of glioma cells.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11826106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143365493","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

Negative regulation of cannabinoid receptor 2‑induced tumorigenic effect by sphingosine‑1‑phosphate receptor 5 activation. 鞘氨醇- 1 -磷酸受体5激活对大麻素受体2诱导的致瘤作用的负调控。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-03-01 Epub Date: 2025-02-07 DOI: 10.3892/or.2025.8874

Yuna Kim, Sungho Ghil

{"title":"Negative regulation of cannabinoid receptor 2‑induced tumorigenic effect by sphingosine‑1‑phosphate receptor 5 activation.","authors":"Yuna Kim, Sungho Ghil","doi":"10.3892/or.2025.8874","DOIUrl":"10.3892/or.2025.8874","url":null,"abstract":"G protein‑coupled receptors (GPCR), also known as seven‑transmembrane proteins, serve a role in transmitting extracellular information into the cellular environment. Type 2 cannabinoid receptors (CB2) and type 5 sphingosine‑1‑phosphate receptor (S1P5) are GPCRs that are activated by biolipids and involved in tumor progression in various cancer types. At present, effects of crosstalk between CB2 and S1P5 receptors on tumor cell proliferation and migration in gliomas are not fully understood. The present study screened S1Ps for potential interactions with CB2 using bioluminescence resonance energy transfer analysis. S1P5 interacted strongly and specifically with CB2. 293T cells were transfected with CB2 tagged with Venus and S1P5 tagged with mCherry to investigate the cellular localization of both receptors. After 24 h, Confocal microscopy analysis revealed that, in the absence of agonists, both receptors were predominantly localized at the plasma membrane. Notably, both receptors were co‑internalized from the membrane to the cytoplasm upon individual and combined activation. The effects of co‑activation of both receptors on tumor progression were investigated using U‑87 MG, the human glioblastoma cell line. Activation of CB2 induced an increase in cell migration and proliferation, which were downregulated following the co‑activation of S1P5. Furthermore, activation of S1P5 significantly attenuated the upregulation of tumor progression‑related genes, including zinc finger protein 91, activating transcription factor 3, Ki67, basic transcription factor 3, and p21, induced by CB2 activation. This suggests that S1P5 exerts a negative regulatory effect on CB2‑mediated tumor progression. The present findings provide evidence of the crosstalk between CB2 and S1P5.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364544","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

Heteronemin suppresses EGF‑induced proliferation through the PI3K/PD‑L1 signaling pathways in cholangiocarcinoma. 在胆管癌中，Heteronemin通过PI3K/PD - L1信号通路抑制EGF诱导的增殖。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-03-01 Epub Date: 2025-01-10 DOI: 10.3892/or.2025.8865

Yu-Chen S H Yang, Chung-Che Tsai, Yung-Ning Yang, Feng-Cheng Liu, Sheng-Yang Lee, Jen-Chang Yang, Dana R Crawford, Hsien-Chung Chiu, Mei-Chin Lu, Zi-Lin Li, Yi-Chen Chen, Tin-Yi Chu, Jacqueline Whang-Peng, Hung-Yun Lin, Kuan Wang

{"title":"Heteronemin suppresses EGF‑induced proliferation through the PI3K/PD‑L1 signaling pathways in cholangiocarcinoma.","authors":"Yu-Chen S H Yang, Chung-Che Tsai, Yung-Ning Yang, Feng-Cheng Liu, Sheng-Yang Lee, Jen-Chang Yang, Dana R Crawford, Hsien-Chung Chiu, Mei-Chin Lu, Zi-Lin Li, Yi-Chen Chen, Tin-Yi Chu, Jacqueline Whang-Peng, Hung-Yun Lin, Kuan Wang","doi":"10.3892/or.2025.8865","DOIUrl":"10.3892/or.2025.8865","url":null,"abstract":"Epidermal growth factor (EGF) binds with its surface receptor to stimulate gene expression and cancer cell proliferation. EGF stimulates cancer cell growth via phosphoinositide 3‑kinase (PI3K) and programmed cell death ligand 1 (PD‑L1) pathways. As an integrin αvβ3 antagonist, heteronemin exhibits potent cytotoxic effects against cancer cells. It inhibits critical signal transduction pathways promoted by the EGF. In the current study, EGF‑induced signal activation and proliferative effects were investigated in cholangiocarcinoma cells and its molecular targets using qPCR and western blotting analyses. In addition, cell viability assays were performed to assess the growth effects of EGF and heteronemin. Heteronemin reversed the effects of EGF and was further enhanced by blockage of PI3K's activity. In summary, EGF stimulates cholangiocarcinoma cell growth. On the other hand, heteronemin inhibited PI3K activation and PD‑L1 expression to reverse the stimulative effects of EGF‑induced gene expression and proliferation in cholangiocarcinoma cells.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952657","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

[Corrigendum] ND‑09 inhibits chronic myeloid leukemia K562 cell growth by regulating BCR‑ABL signaling. [勘误]ND‑09通过调节BCR‑ABL信号抑制慢性髓系白血病K562细胞生长。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-03-01 Epub Date: 2025-01-31 DOI: 10.3892/or.2025.8870

Yan-Hong Liu, Man Zhu, Pan-Pan Lei, Xiao-Yan Pan, Wei-Na Ma

{"title":"[Corrigendum] ND‑09 inhibits chronic myeloid leukemia K562 cell growth by regulating BCR‑ABL signaling.","authors":"Yan-Hong Liu, Man Zhu, Pan-Pan Lei, Xiao-Yan Pan, Wei-Na Ma","doi":"10.3892/or.2025.8870","DOIUrl":"10.3892/or.2025.8870","url":null,"abstract":"Subsequently to the publication of the above article, and a Corrigendum that has already been published with the intention of showing a corrected version of Fig. 2A (DOI: 10.3892/or.2023.8518; published online on March 3, 2023), the authors have subsequently realized that other errors were featured in certain of the published figures. First, the authors realized that Fig. 3 on p. 5 was incorrectly assembled: specifically, the flow cytometric data included in Figs. 3A and 3B were inadvertently assembled incorrectly. Additionally, the authors note that the control GAPDH data were duplicated in Figs. 5A and 5B, 6A and 6B, and 7A and 7B on p. 7 and 8. These errors occurred on account of the fact that the authors chose to use the same GAPDH bands for quantitative analysis, which they subsequently realize was not an appropriate course of action; the original GAPDH bands pertaining to the correct experiments are now included in each of these figures. The revised versions of Figs. 3, 5, 6 and 7 are shown on the next two pages. Note that the revisions made to Figs. 3, 5, 6 and 7 in this paper do not have a major impact on the reported results, and neither do they affect the overall conclusions reported in the study. All the authors agree to the publication of this corrigendum. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this additional Corrigendum; furthermore, they apologize for any inconvenience caused to the readership of the Journal. [Oncology Reports 46: 136, 2021; DOI: 10.3892/or.2021.8087].","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11795229/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067232","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] Inhibition of 5‑lipoxygenase triggers apoptosis in pancreatic cancer cells. [撤稿】抑制 5-脂氧合酶可引发胰腺癌细胞凋亡。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-02-01 Epub Date: 2024-12-13 DOI: 10.3892/or.2024.8853

Guo-Xiong Zhou, Xiao-Ling Ding, Sheng-Bao Wu, Hai-Feng Zhang, Wei Cao, Li-Shuai Qu, Hong Zhang

引用次数: 0

Regulation of pancreatic cancer cells by suppressing KIN17 through the PI3K/AKT/mTOR signaling pathway. 通过PI3K/AKT/mTOR信号通路抑制KIN17调控胰腺癌细胞。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-02-01 Epub Date: 2025-01-10 DOI: 10.3892/or.2025.8864

Qiuyan Li, Yuxia Yang, Xiaocong Lin, Lok Ting Chu, Helian Chen, Linsong Chen, Jinjing Tang, Tao Zeng

{"title":"Regulation of pancreatic cancer cells by suppressing KIN17 through the PI3K/AKT/mTOR signaling pathway.","authors":"Qiuyan Li, Yuxia Yang, Xiaocong Lin, Lok Ting Chu, Helian Chen, Linsong Chen, Jinjing Tang, Tao Zeng","doi":"10.3892/or.2025.8864","DOIUrl":"10.3892/or.2025.8864","url":null,"abstract":"Pancreatic cancer is an aggressive tumor, which is often associated with a poor clinical prognosis and resistance to conventional chemotherapy. Therefore, there is a need to identify new therapeutic markers for pancreatic cancer. Although KIN17 is a highly expressed DNA‑ and RNA‑binding protein in a number of types of human cancer, its role in pancreatic cancer development, especially in relation to progression, is currently unknown. The present study verified the upregulation of KIN17 in pancreatic cancer using The Cancer Genome Atlas and Gene Expression Omnibus databases (GSE15471, GSE71989 and GSE62165), and identified an association between the PI3K/Akt/mTOR pathway and patient prognosis using publicly available datasets (Gene Expression Profiling Interactive Analysis). Immunohistochemistry was performed to determine the association between KIN17 and the pathological features of clinical pancreatic cancer samples. Furthermore, knockdown of KIN17 was shown to inhibit the migration and invasion of pancreatic cancer cells, and to reverse epithelial‑mesenchymal transition in pancreatic cancer cells through downregulation of Vimentin and N‑cadherin, and upregulation of E‑cadherin. Through various cellular experiments, the role of KIIN17 was explored in PI3K/AKT/mTOR activity. KIN17 inhibition was shown to suppress the migration and invasion of pancreatic cancer cells through PI3K/AKT/mTOR‑mediated autophagy. Furthermore, combined with mTOR inhibition, dual inhibition could enhance autophagy, leading to anti‑migratory and anti‑invasion effects in pancreatic cancer. In conclusion, the present study indicated that KIN17 may have a role in carcinogenesis and could serve as a prognostic biomarker of pancreatic cancer, owing to its high expression. In addition, KIN17 may be considered a potential therapeutic target with its knockdown having an inhibitory effect on pancreatic cancer.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952637","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

Regulation of the β‑catenin/LEF‑1 pathway by the siRNA knockdown of RUVBL1 expression inhibits breast cancer cell proliferation, migration and invasion. 通过 siRNA 敲除 RUVBL1 的表达来调节β-catenin/LEF-1 通路，从而抑制乳腺癌细胞的增殖、迁移和侵袭。

IF 3.8 3区医学

Oncology reports Pub Date : 2025-02-01 Epub Date: 2024-12-13 DOI: 10.3892/or.2024.8855

Xin Zhang, Dingyuan Cui, Wei Sun, Guangfei Yang, Wen Wang, Chengrong Mi

{"title":"Regulation of the β‑catenin/LEF‑1 pathway by the siRNA knockdown of RUVBL1 expression inhibits breast cancer cell proliferation, migration and invasion.","authors":"Xin Zhang, Dingyuan Cui, Wei Sun, Guangfei Yang, Wen Wang, Chengrong Mi","doi":"10.3892/or.2024.8855","DOIUrl":"10.3892/or.2024.8855","url":null,"abstract":"RUVBL1 is a protein characterized by its DNA‑dependent ATPase activity and DNA deconjugating enzyme function. It is a member of the ATPase (AAA+) protein family associated with various cellular processes. Available research confirms that the expression of RUVBL1 is upregulated in breast cancer (BRCA) cell lines; however, the mechanisms underlying its functional role in BRCA remain unclear. The β‑catenin/lymphoid enhancer factor‑1 (LEF‑1) pathway plays a crucial role in the occurrence and development of BRCA. The aim of the present study was to investigate whether RUVBL1 regulates the proliferation, migration and invasion of BRCA cells by participating in the β‑catenin/LEF‑1 signaling pathway. Reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analysis were employed to compare the RUVBL1 expression levels between normal mammary epithelial cells (MCF‑10a) and BRCA cell lines (MDA‑MB‑231 and MCF‑7). Scratch, Cell Counting Kit‑8 and Transwell assays were utilized to assess the effects of RUVBL1 knockdown on the proliferation, migration and invasion of BRCA cells. Following the downregulation of RUVBL1 expression in vitro, western blot analysis and RT‑qPCR were conducted to investigate its role in regulating the β‑catenin/LEF‑1 pathway. The aforementioned experiments proved that the knockdown of RUVBL1 expression inhibited BRCA cell proliferative, migratory and invasive capabilities, modulating the β‑catenin/LEF‑1 pathway. Collectively, the findings of the present study provide preliminarily confirmation that RUVBL1 participates in the molecular mechanisms of the β‑catenin signaling pathway, which may provide a novel target for BRCA treatment.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"53 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11667213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818804","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