Oncology reports最新文献

{"title":"[Retracted] Inhibition of 5‑lipoxygenase triggers apoptosis in pancreatic cancer cells.","authors":"Guo-Xiong Zhou, Xiao-Ling Ding, Sheng-Bao Wu, Hai-Feng Zhang, Wei Cao, Li-Shuai Qu, Hong Zhang","doi":"10.3892/or.2024.8853","DOIUrl":"https://doi.org/10.3892/or.2024.8853","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the Editor's attention that Fig. 3 on p. 664, showing TUNEL assay data relating to apoptosis of the cell line under investigation in this paper, contained apparent anomalies, including repeated patternings of certain cells both within and between the data panels, such that it would have been difficult to have attributed these anomalies to coincidence. After having conducted an independent investigation in the Editorial Office, the Editor of <i>Oncology Reports</i> has determined that the above paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the 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 regrets any inconvenience that has been caused to the readership of the Journal. [Oncology Reports 33: 661‑668, 2015; DOI: 10.3892/or.2014.3650].</p>","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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818627","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":"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":"<p><p>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 <i>in vitro</i>, 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.</p>","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":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antibody‑drug conjugates in prostate cancer: Emerging strategies to enhance therapeutic index and current clinical landscape (Review).","authors":"Chadanfeng Yang, Limei Wang, Chen Gong, Dihao Lv, Haihao Li, Yinglong Huang, Jiting Li, Wujie Chen, Shi Fu, Zhiyong Tan, Mingxia Ding","doi":"10.3892/or.2024.8854","DOIUrl":"10.3892/or.2024.8854","url":null,"abstract":"<p><p>The global incidence of prostate cancer (PCa) is rising. Localized PCa can be managed through surgical intervention or radiotherapy, but certain patients may experience recurrence or develop metastatic disease following localized treatment. Despite aggressive therapeutic approaches, the majority of metastatic patients with PCa will eventually progress to metastatic castration‑resistant PCa, with limited treatment alternatives and a dismal prognosis. The treatment options for advanced PCa are continuously evolving, yet there remains a demand for further innovative therapeutic approaches. Antibody‑drug conjugates (ADCs) represent a novel class of targeted medications comprising a humanized monoclonal antibody, a linker and a cytotoxic payload. ADCs primarily bind to antigens that are upregulated on the surface of PCa cells but are minimally expressed on normal cells. At present, a variety of targets for ADCs have been identified in the treatment of PCa, encompassing prostate‑specific membrane antigen, STEAP family member 1, trophoblast cell‑surface antigen 2, CD46, B7‑H3, tissue factor and delta‑like protein 3, each with one or more specific ADC that has shown encouraging results in the PCa field. In the present review, the developmental course, composition and mechanism of action of ADCs are explored, with a specific focus on recently published studies and ongoing trials aimed at investigating the efficacy and safety of ADCs in treating PCa. Lastly, ongoing challenges in ADC development and corresponding strategies to combat them are discussed.</p>","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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818692","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":"Interactions between ferroptosis and tumour development mechanisms: Implications for gynaecological cancer therapy (Review).","authors":"Peiting Wu, Jianlin Chen, Hui Li, Haiyuan Lu, Yukun Li, Juan Zhang","doi":"10.3892/or.2024.8851","DOIUrl":"10.3892/or.2024.8851","url":null,"abstract":"<p><p>Ferroptosis is a form of programmed cell death that is distinct from apoptosis. The mechanism involves redox‑active metallic iron and is characterized by an abnormal increase in iron‑dependent lipid reactive oxygen species, which results in high levels of membrane lipid peroxides. The relationship between ferroptosis and gynaecological tumours is complex. Ferroptosis can regulate tumour proliferation, metastasis and chemotherapy resistance, and targeting ferroptosis is a promising antitumour approach. Ferroptosis interacts with mechanisms related to tumorigenesis and development, such as macrophage polarization, the neutrophil trap network, mitochondrial autophagy and cuproptosis. The present review examines recent information on the interaction between the molecular mechanism of ferroptosis and other tumour‑related mechanisms, as well as the involvement of ferroptosis in gynaecological tumours, to identify implications for gynaecological cancer therapy.</p>","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/PMC11638741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786169","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":"Targeted therapy‑associated cardiotoxicity in patients with stage‑IV lung cancer with or without cardiac comorbidities.","authors":"Yanmei Peng, Dong Li, Jason A Wampfler, Yung-Hung Luo, Ashok V Kumar, Zhong Gu, Nikhila Kosuru, Nathan Y Yu, Zhichao Wang, Konstantinos Leventakos, Vinicius Ernani, Ping Yang","doi":"10.3892/or.2024.8858","DOIUrl":"https://doi.org/10.3892/or.2024.8858","url":null,"abstract":"<p><p>Targeted drugs have revolutionized the treatment of advanced non‑small cell lung cancer (NSCLC). However, the understanding of how cardiac comorbidity and toxicity affect the clinical outcomes of patients following targeted therapy remains limited. In a 14‑year cohort, cardiac comorbidities and toxicities among patients with stage‑IV NSCLC treated with targeted therapy were identified. The cardiotoxicities were compared in three patient groups: Cardiac, other and no comorbidities. Survival analysis employed Cox Proportional Hazard Models. In the prospectively followed 3,767 patients with stage‑IV NSCLC, 701 received targeted therapy; of which 133 (19.0%) had cardiac comorbidity, 504 (71.9%) had other comorbidities and 64 (9.1%) had none. In total, 15 patients (2.1%) developed cardiotoxicity after taking drugs targeting epidermal growth factor receptor, anaplastic lymphoma kinase (<i>ALK</i>), c‑ros oncogene 1 (<i>ROS1</i>) or vascular endothelial growth factor/receptor (<i>VEGF</i>)/<i>VEGFR</i>, and all 15 had comorbidities: 10 cardiac and 5 other comorbidities. Cardiac comorbidity was associated with a 7.5‑fold higher risk of targeted therapy‑related cardiotoxicity than other comorbidities (7.5 vs. 1.0%; P<0.001). Patients with or without cardiotoxicity had a median survival time of 4.7 or 1.9 years, respectively, and patients with cardiotoxicity had a lower risk of death (hazard ratio, 0.45; 95% confidence interval, 0.25‑0.81) than those without (P=0.003), when adjusting for comorbidities. In the 164 patients that received osimertinib, 32 (19.5%) had cardiac comorbidity and a 1.7‑fold higher risk of death than the 121 (73.8%) patients with other comorbidities. In the 74 patients treated with <i>ALK/ROS1</i> inhibitors, cardiotoxicity was 14 times more common in patients with heart disease (30.0%) than those without (2.1%) (P=0.001). Cardiotoxicity was uncommon in patients with targeted drug‑treated stage‑IV NSCLC but was more prevalent in those with cardiac comorbidity and appeared to be a protector for longer survival. However, in osimertinib‑treated patients, cardiac comorbidity increased mortality.</p>","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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865050","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":"<i>SPRR1A</i> is a potential therapeutic target for osteosarcoma: <i>in vitro</i> and <i>in vivo</i> evaluations using generated artificial osteosarcoma cancer stem cell‑like cells.","authors":"Tomohiro Miyamoto, Naomasa Fukase, Teruya Kawamoto, Shuichi Fujiwara, Hitomi Hara, Ryoko Sawada, Yuta Nakamatsu, Yutaka Mifune, Kenichiro Kakutani, Yuichi Hoshino, Shinya Hayashi, Tomoyuki Matsumoto, Takehiko Matsushita, Michiyo Koyanagi-Aoi, Takashi Aoi, Toshiyuki Takemori, Shunsuke Yahiro, Ryosuke Kuroda, Toshihiro Akisue","doi":"10.3892/or.2024.8857","DOIUrl":"https://doi.org/10.3892/or.2024.8857","url":null,"abstract":"<p><p>Cancer stem cells (CSCs) have been implicated as critical mediators in the progression, chemoresistance and metastatic capabilities of diverse malignancies, including osteosarcoma (OS). The authors have succeeded in generating CSC‑like cells (MG‑OKS) from the OS cell line MG‑63 by transducing defined factors. A significant increase in small proline‑rich protein 1A (SPRR1A) expression, a cross‑linked envelope protein in keratinocytes, was observed in MG‑OKS cells. Therefore, SPRR1A could be involved in tumor initiation, growth and poor OS progression. However, its specific role in OS remains unclear. The present study aimed to evaluate the role of SPRR1A in OS both <i>in vitro</i> and <i>in vivo</i> using MG‑OKS cells. Three experimental groups were established: MG‑OKS cells transfected with SPRR1A small interfering (si)RNA (siMG‑OKS), untransfected MG‑OKS cells and MG‑OKS cells transfected with scrambled siRNA (scMG‑OKS) as controls. SPRR1A expression, morphological changes, cell proliferation and migration were assessed in these groups. RNA sequencing was performed to examine the genetic changes caused by SPRR1A suppression. To evaluate tumorigenicity <i>in vivo</i>, cells from each group were subcutaneously transplanted into the backs of nude mice. Tumor volume and Ki‑67 expression were assessed and compared among the three groups at four weeks post‑transplantation. The siMG‑OKS group exhibited altered cell morphology, reduced cell proliferation and decreased migratory abilities <i>in vitro</i>. RNA sequencing revealed suppression of genes involved in cell adhesion in the siMG‑OKS group. Furthermore, the <i>in vivo</i> tumorigenicity of siMG‑OKS was lower than that of the other two experimental groups. These findings suggest that SPRR1A is one of the key cell adhesion‑related molecules involved in OS progression, potentially serving as a therapeutic target for this refractory tumor. However, further research is needed to fully elucidate the mechanisms by which SPRR1A influences OS pathogenesis and to explore its clinical potential.</p>","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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865049","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":"[Retracted] Hypoxia‑induced overexpression of DEC1 is regulated by HIF‑1α in hepatocellular carcinoma.","authors":"Wanshan Ma, Xiaohong Shi, Sumei Lu, Linlin Wu, Yunshan Wang","doi":"10.3892/or.2024.8850","DOIUrl":"10.3892/or.2024.8850","url":null,"abstract":"<p><p>Further to the publication of the above paper, a concerned reader drew to our attention that, in Figs. 1A and 4A, the same loading controls for the RT‑PCR experiments portrayed had apparently been incorporated into these figures, even though the experimental results (i.e., for the DEC1 bands) were otherwise different. In addition, the control GAPDH bands featured in the western blots in Figs. 3A and 3B for the SMMC‑7721 and BRL‑7402 cell lines respectively were strikingly similar, albeit the bands appeared to have been vertically flipped in Fig. 3A relative to Fig. 3B, and possibly stretched. The Editorial Office subsequently investigated this matter, and were able to confirm the concerns of the reader. After having considered the various issues that have been brought to light with this paper, in spite of a request from the authors that a Corrigendum be published, the Editor of <i>Oncology Reports</i> has determined that the article should be retracted on account of a lack of overall 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 reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 30: 2957‑2962, 2013; DOI: 10.3892/or.2013.2774].</p>","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/PMC11632655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786157","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":"Biological implications of decoding the extracellular matrix of vulva cancer.","authors":"Mohammad Emranul Islam, Kala Chand Debnath, Rohan Moniruzzaman, Kohei Okuyama, Shajedul Islam, Harsh Nitin Dongre","doi":"10.3892/or.2024.8852","DOIUrl":"10.3892/or.2024.8852","url":null,"abstract":"<p><p>The present review aimed to elucidate the roles of extracellular matrix (ECM) components in the progression of vulvar squamous cell carcinoma (VSCC) and explore potential therapeutic avenues for this type of malignancy. This exploration holds promise for identifying precise molecular targets within the ECM milieu, thus facilitating the development of innovative therapeutic modalities tailored to disrupt these interactions and ultimately improve patient outcomes in VSCC. The dysregulated ECM serves as a potent driver of SCC tumor progression, orchestrating key processes such as angiogenesis, inflammation and stromal cell behavior. Yet, the exploration of ECM role in VSCC is still in its early stages. Recent research highlights the critical role of ECM organization and expression within the tumor microenvironment (TME) in influencing key aspects of VSCC, including tumor staging, grading, metastasis, invasion and patient survival. Cancer‑associated fibroblasts play a pivotal role in this dynamic by engaging in reciprocal interactions with VSCC cells, leading to significant ECM alterations and creating an immune‑suppressive TME. This hinders antitumor immunity and fosters therapeutic resistance in VSCC treatment. The dysregulated ECM in VSCC drives tumor progression, metastasis and affects patient survival. Targeting ECM, along with emerging therapies such as immune checkpoint blockade, offers promise for improved VSCC treatment outcomes.</p>","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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818700","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":"[Retracted] Upregulation of estrogen receptor mediates migration, invasion and proliferation of endometrial carcinoma cells by regulating the PI3K/AKT/mTOR pathway.","authors":"Xinxin Hou, Meng Zhao, Tong Wang, Guiyu Zhang","doi":"10.3892/or.2024.8856","DOIUrl":"https://doi.org/10.3892/or.2024.8856","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned reader drew to the Editor's attention that a couple of the figures in this paper contained overlapping sections, where data which were intended to show the results from differently performed experiments had been derived from the same original source. First, regarding the cell transfection experiments in Fig. 1, the Con, ERα and ERβ data panels in Fig. 1A all contained overlapping sections of data; secondly, comparing the data panels for the cell migration and invasion assays shown in Fig. 5, three pairs of panels were also found to contain overlapping data. In view of the fact that these identifications were made in terms of overlapping data panels, the Editor of <i>Oncology Reports</i> has decided that this paper 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. [Oncology Reports 31: 1175‑1182, 2014; DOI: 10.3892/or.2013.2944].</p>","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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865048","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":"Bcl‑xL‑specific BH3 mimetic A‑1331852 suppresses proliferation of fluorouracil‑resistant colorectal cancer cells by inducing apoptosis.","authors":"Akira Kato, Hiroki Takahashi, Hiroyuki Asai, Shuhei Uehara, Shinnosuke Harata, Yoshiaki Fujii, Kaori Watanabe, Takeshi Yanagita, Takuya Suzuki, Hajime Ushigome, Kazuyoshi Shiga, Yushi Yamakawa, Ryo Ogawa, Akira Mitsui, Yoichi Matsuo, Shuji Takiguchi","doi":"10.3892/or.2024.8859","DOIUrl":"https://doi.org/10.3892/or.2024.8859","url":null,"abstract":"<p><p>BH3 mimetics are small‑molecule inhibitors of the antiapoptotic Bcl‑2 family and have therapeutic efficacy against hematological malignancies. BH3 mimetic A‑1331852 suppresses colorectal cancer cell proliferation. Progressive resistance to the widely used anticancer agent fluorouracil (5‑FU) is a key reason for colorectal cancer recurrence; therefore, the present study tested if A‑1331852 can suppress the proliferation of 5‑FU‑resistant colorectal cancer cells. A 5‑FU‑resistant colorectal cancer cell line was derived from HCT116 cells and compared with the parental line. Expression levels of the antiapoptotic Bcl‑2 proteins Bcl‑xL and myeloid cell leukemia 1 (Mcl‑1) were determined via western blotting, proliferation in the presence of 5‑FU and following small interfering (si)RNA‑mediated Bcl‑xL or Mcl‑1 knockdown was assessed by WST‑1 assay and sensitivity to A‑1331852‑induced apoptosis was assessed via western blotting and DNA fragmentation assay. In addition, a xenograft mouse model of 5‑FU‑resistant colorectal cancer was established via subcutaneous inoculation of 5‑FU‑resistant HCT116 cells to examine the <i>in vivo</i> antitumor efficacy of A‑1331852. Compared with the parental line, 5‑FU‑resistant cells overexpressed Bcl‑xL. Knockdown of Bcl‑xL by siRNA and treatment with A‑1331852 suppressed proliferation and induced the apoptosis of both 5‑FU‑resistant and parental HCT116 cells, but the potency of both effects was stronger in 5‑FU‑resistant than parental HCT116 cells. Furthermore, A‑1331852 suppressed the growth of xenograft tumors derived from 5‑FU‑resistant cells by inducing apoptosis. Overall, the present findings suggested that Bcl‑xL upregulation contributes to 5‑FU resistance of colorectal cancer and targeted inhibition by A‑1331852 may be an effective treatment strategy.</p>","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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882699","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}