Anti-Cancer Drugs最新文献_第10页

aYAP1-2 contributes to bFGF-induced proliferation In gastric cancer. aYAP1-2参与bfgf诱导的胃癌增殖。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-02-01 Epub Date: 2024-12-03 DOI: 10.1097/CAD.0000000000001668

Hui Chen, Di-Kai Xue, Yi-Xuan Wang, Tian-Fang Jiang

{"title":"aYAP1-2 contributes to bFGF-induced proliferation In gastric cancer.","authors":"Hui Chen, Di-Kai Xue, Yi-Xuan Wang, Tian-Fang Jiang","doi":"10.1097/CAD.0000000000001668","DOIUrl":"10.1097/CAD.0000000000001668","url":null,"abstract":"Gastric cancer (GC) is one of the leading causes of cancer-related deaths in humans worldwide. Fibroblast growth factor family (FGFs) and the Hippo signaling pathway play an important role in the epithelial-mesenchymal transition (EMT) process of GC. YAP1, a key mediator of the Hippo pathway, plays an important role in tumor genesis. Alternative splicing of human YAP1 mRNA results in two major isoforms: YAP1-1, which contains a single WW domain, and YAP1-2, which contains two WW domains, respectively. There are significant differences in post-transcriptional regulation and function. Basic FGF (bFGF) treatment promoted the EMT process of most GC cell lines, and the proliferation ability was enhanced. This process may be related to the upregulation of YAP1, the proliferation ability of GC was significantly alleviated upon YAP1 knockdown. bFGF treatment can induce EMT of GC through YAP1-2 and enhance their proliferative ability. In this process, bFGF may enhance the nuclear localization of YAP1-2.In the mouse model of intraperitoneal implantation tumorigenesis, it was shown that under the action of bFGF, the expressing YAP1-2 cell lines could form larger tumors than the expressing YAP1-1, but both of them were larger than the YAP1 knockdown. Our results show that YAP1-2 is the main subtype of bFGF-induced EMT and proliferation of GC cells.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"97-103"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11670903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Induction of neuronal differentiation in glioma cells by histone deacetylase inhibitors based on Connectivity Map discovery. 基于连接图谱发现的组蛋白去乙酰化酶抑制剂诱导胶质瘤细胞的神经元分化。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-02-01 Epub Date: 2024-12-24 DOI: 10.1097/CAD.0000000000001667

Zhao-Qi Tang, Hong-Bin Xu, Chang Cao, Yue-Jin Liu, Yan-Rong Ye, Yun Shen

{"title":"Induction of neuronal differentiation in glioma cells by histone deacetylase inhibitors based on Connectivity Map discovery.","authors":"Zhao-Qi Tang, Hong-Bin Xu, Chang Cao, Yue-Jin Liu, Yan-Rong Ye, Yun Shen","doi":"10.1097/CAD.0000000000001667","DOIUrl":"10.1097/CAD.0000000000001667","url":null,"abstract":"Neuron conversion leads to proliferation inhibition of glioma cells and may be an effective strategy to combat glioma and prevent recurrence. In this study, drug repositioning based on Connectivity Map (CMap) was conducted to discover drugs that could induce the differentiation of glioma cells into neuron-like cells, complemented by in vitro experimental validation. Downregulated neuronal genes in glioma were identified by the Human Protein Atlas database and the GeneCards database, and enrichment analysis and Gene Expression Profiling Interactive Analysis (GEPIA) were performed to ensure their reliability before they were uploaded to CMap for drug screening. The potential drug targets were screened through GEPIA and validated by the Chinese Glioma Genome Atlas database. Cell morphology, proliferation, and neuronal marker expression were detected to evaluate the differentiation-inducing effect of the selected drugs. The bioinformatics analysis identified histone deacetylase (HDAC) inhibitors as potential drugs. HDAC1/3/7 showed the relationship with neuronal genes, and HDAC1 showed the highest level of inverse correlation with neuronal gene expression and had the highest hazard ratio. In vitro study showed that both the pan-HDAC inhibitor belinostat, class I and class IIa HDAC inhibitor valproic acid, and selective HDAC1 inhibitor parthenolide induce morphology alteration, proliferation inhibition, expression of neuronal markers including microtubule-associated protein 2, neuronal nuclei antigen, and synaptophysin in U87 cells. This study suggests that the HDAC inhibitors belinostat, valproic acid, and parthenolide can induce glioma cells to differentiate into neuron-like cells, with HDAC1/3/7 being the likely drug targets and HDAC1 potentially playing an important role in this.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"104-113"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Sorafenib as maintenance therapy in FLT3+ acute myeloid leukemia post allogeneic transplantation: a case report. 索拉非尼作为同种异体移植后FLT3+急性髓性白血病的维持疗法：病例报告。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-02-01 Epub Date: 2024-11-26 DOI: 10.1097/CAD.0000000000001672

Alicia Martín Roldán, Carolina Alarcón-Payer, María Del Mar Sánchez Suárez, Alberto Jiménez Morales

引用次数: 0

YKL-06-061 exerts antitumor effect through G1/S phase arrest by downregulating c-Myc and inhibition of metastasis via SIK1 upregulation in pancreatic cancer. YKL-06-061在胰腺癌中通过下调c-Myc和上调SIK1抑制转移，通过G1/S期阻滞发挥抗肿瘤作用。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-02-01 Epub Date: 2024-12-24 DOI: 10.1097/CAD.0000000000001673

Chao-Yang Zeng, Wen-Die Wang, Yue Shang, Shuo-Han Xi, Li-Ping Li, Shu-Zhen Chen

{"title":"YKL-06-061 exerts antitumor effect through G1/S phase arrest by downregulating c-Myc and inhibition of metastasis via SIK1 upregulation in pancreatic cancer.","authors":"Chao-Yang Zeng, Wen-Die Wang, Yue Shang, Shuo-Han Xi, Li-Ping Li, Shu-Zhen Chen","doi":"10.1097/CAD.0000000000001673","DOIUrl":"10.1097/CAD.0000000000001673","url":null,"abstract":"Pancreatic cancer ranks fourth among cancer-related deaths with a low 5-year overall survival rate of less than 13%. At present, treatment of pancreatic cancer is still based on chemotherapy, but the efficacy is limited. Thus, a novel therapeutic agent for pancreatic cancer therapy is urgently needed. A library of compounds was screened, and YKL-06-061, a selective inhibitor of salt-inducible kinases (SIKs), was discovered for its ability of inhibiting the proliferation and metastasis of pancreatic cancer cells in vitro and reducing the growth of xenografts in nude mice in vivo . The results from transcriptome analysis showed that YKL-06-061 influenced the mRNA levels of many genes related to c-Myc and SIK1 signals. Based on this, it was found that YKL-06-061 induced cell cycle arrest at the G1 phase and decreased the levels of c-Myc, CDK4, and cyclin D1 protein. At the same time, YKL-06-061 inhibited invasion and metastasis of cancer cells, increased the levels of SIK1 and E-cadherin protein, and lowered vimentin and ZEB-1. Moreover, YKL-06-061 effectively enhanced the antiproliferation of gemcitabine or doxorubicin in pancreatic cancer cells in a synergistic manner. Collectively, these findings implicate YKL-06-061 as a promising therapeutic agent for patients with pancreatic cancer.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"114-125"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

A rare EGFR exon 19 insertion mutation in metastatic lung adenocarcinoma: a favorable response to afatinib. 转移性肺腺癌中一种罕见的EGFR外显子19插入突变：对阿法替尼的有利反应。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-02-01 Epub Date: 2024-12-24 DOI: 10.1097/CAD.0000000000001671

İsmet Seven, Fahriye Tuğba Köş, Hayriye Tatli Doğan, Mustafa Hayri Kişlal, Serhat Sekmek, İrfan Karahan, Selin Aktürk Esen, Doğan Uncu

引用次数: 0

Myositis associated with pembrolizumab presenting with myastheniform symptoms: two case reports. 与派姆单抗相关的肌炎表现为肌无力样症状：两例报告

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-02-01 Epub Date: 2024-12-24 DOI: 10.1097/CAD.0000000000001665

Şule Deveci, Mustafa Uzun, Pinar Özçelik, Sebile Serranur Tümer Doğukan, Zeliha Matur

{"title":"Myositis associated with pembrolizumab presenting with myastheniform symptoms: two case reports.","authors":"Şule Deveci, Mustafa Uzun, Pinar Özçelik, Sebile Serranur Tümer Doğukan, Zeliha Matur","doi":"10.1097/CAD.0000000000001665","DOIUrl":"10.1097/CAD.0000000000001665","url":null,"abstract":"Immune checkpoint inhibitors (ICIs), such as pembrolizumab, have revolutionized cancer treatment by enhancing the immune system's response to malignancies. However, these therapies are associated with immune-related adverse events (irAEs), including neuromuscular complications such as myasthenia gravis, myositis, and myocarditis. We describe two male patients, aged 67 and 68, with small cell and non-small cell lung cancers, who developed progressive neuromuscular symptoms, including ptosis, diplopia, and generalized weakness, after receiving pembrolizumab. Clinical, biochemical, imaging, and electrophysiological findings confirmed the diagnosis of myositis with myastheniform features, with one case also involving myocarditis. Both patients underwent treatments with intravenous immunoglobulin (IVIg), pyridostigmine, and corticosteroids. The first patient, despite aggressive treatment including plasma exchange and rituximab, succumbed to complications from aspiration pneumonia. The second patient showed partial response to pyridostigmine and IVIg but later died due to metastatic cancer progression. A literature review revealed 52 cases of pembrolizumab-associated myositis with myastheniform symptoms, emphasizing its high morbidity and the need for vigilant monitoring. Pembrolizumab-associated myositis with myastheniform symptoms, especially when accompanied by myocarditis, presents a significant clinical challenge with high mortality. Early recognition and aggressive management of these irAEs are crucial to improving outcomes in cancer patients receiving ICIs.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":"36 2","pages":"143-150"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Prophylactic role of pentoxifylline against paclitaxel-induced neuropathy among patients with breast cancer: a randomized-controlled trial. 喷托非利兰对紫杉醇诱发的乳腺癌患者神经病变的预防作用：随机对照试验。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-02-01 Epub Date: 2024-10-16 DOI: 10.1097/CAD.0000000000001666

Mariam A Kidwani, Hasnaa Osama, Ahmed Hassan, Mohamed E A Abdelrahim

{"title":"Prophylactic role of pentoxifylline against paclitaxel-induced neuropathy among patients with breast cancer: a randomized-controlled trial.","authors":"Mariam A Kidwani, Hasnaa Osama, Ahmed Hassan, Mohamed E A Abdelrahim","doi":"10.1097/CAD.0000000000001666","DOIUrl":"10.1097/CAD.0000000000001666","url":null,"abstract":"Paclitaxel-induced peripheral neuropathy (PN) is a significant clinical concern for which no approved treatment is currently available. The purpose of this trial was to investigate the neuro-prophylactic impact of pentoxifylline against paclitaxel-induced PN in patients diagnosed with breast cancer (BC). BC patients who were assigned to paclitaxel chemotherapy were randomly allocated to pentoxifylline or a control group for 12 weeks. The main outcomes included the assessment of PN incidence according to the defined Common Terminology Criteria for Adverse Events, quality of life (QoL) using the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-NTx) scale, and neuropathic pain using the scale of self-reported Leeds Assessment for Neuropathic Symptoms and Signs (s-LANSS). The code of the clinical trial registration is NCT06562998. The current study included a total of 72 patients allocated into pentoxifylline arm ( n = 35) and placebo arm ( n = 37). By the 12 th week, the prevalence of PN (grade 2 or 3) was significantly lower in the pentoxifylline arm 10/35 (28.6%) compared to 24/37 (64.9%) of the controls ( P value = 0.016). The total FACT/GOG-NTx score indicated a considerably worse QoL in the control group [98.18 (10.2) vs. 81.43 (14.8) for pentoxifylline and the control group, respectively, P < 0.001] with a mean difference of -16.75 [95% confidence interval (CI): -23.97 to -9.53]. S-LANSS scale showed significantly higher scores after 6 weeks [13.72 (5.86) vs. 17.52 (3.16), P = 0.002] and 12 weeks [17.84 (4.25) vs. 23.80 (1.00), P < 0.001] for pentoxifylline and control group, respectively. In conclusion, the use of pentoxifylline showed a significant reduction in paclitaxel-induced PN, which improved their QoL.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"126-134"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Prognostic impact of elevated C-reactive protein and procalcitonin in patients with extensive-stage small cell lung cancer. 广泛期小细胞肺癌患者 C 反应蛋白和降钙素原升高的预后影响。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-02-01 Epub Date: 2024-11-27 DOI: 10.1097/CAD.0000000000001670

İrfan Buğday, Mevlüde İnanç, Metin Özkan, Oktay Bozkurt, Ramazan Coşar, Sedat Tarik Firat, Emel Mutlu, Murat Eser, Ahmet Kürşad Dişli, Muhammet Cengiz

{"title":"Prognostic impact of elevated C-reactive protein and procalcitonin in patients with extensive-stage small cell lung cancer.","authors":"İrfan Buğday, Mevlüde İnanç, Metin Özkan, Oktay Bozkurt, Ramazan Coşar, Sedat Tarik Firat, Emel Mutlu, Murat Eser, Ahmet Kürşad Dişli, Muhammet Cengiz","doi":"10.1097/CAD.0000000000001670","DOIUrl":"10.1097/CAD.0000000000001670","url":null,"abstract":"Small cell lung cancer (SCLC) constitutes around 15% of lung cancer cases and stands as the primary cause of cancer-related fatalities in men and the second leading cause in women globally. In this study, our objective was to evaluate the levels of C-reactive protein (CRP) and procalcitonin (PCT) in newly diagnosed extensive-stage SCLC patients without evidence of infection. We aimed to demonstrate that elevated CRP and PCT levels may not solely indicate infection but could also be elevated in malignancies. Furthermore, we sought to correlate these marker levels with patient and disease characteristics to elucidate the relationship between these inflammation markers and disease progression. A total of 115 patients who were pathologically and radiologically diagnosed with extensive-stage SCLC between January 2020 and December 2022 and who had received no prior treatment were included in the study. The Kaplan-Meier analysis revealed a median progression-free survival (PFS) of 7.46 months [95% confidence interval (CI), 6.85-8.07] and a median overall survival (OS) of 10.50 months (95% CI, 8.69-12.30) for all patients. In the group with elevated PCT, the median PFS was 6.73 months (95% CI, 3.92-9.54), whereas it was 7.86 months (95% CI, 7.13-8.59) in the group with normal PCT ( P = 0.002). Similarly, the median OS was 9.10 months (95% CI, 5.61-12.58) in the elevated PCT group and 11.66 months (95% CI, 9.59-13.74) in the normal PCT group ( P = 0.006). Patients with elevated procalcitonin (PRC) levels at the time of diagnosis exhibited shorter PFS and OS durations compared to patients with normal PRC levels. Furthermore, elevated CRP has also been demonstrated to correlate with poorer prognosis in extensive-stage SCLC.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"135-139"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Identification and validation of mitochondria-related LncRNA signatures as a novel prognostic model for glioma. 线粒体相关LncRNA标记作为胶质瘤新预后模型的鉴定和验证。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2025-01-14 DOI: 10.1097/CAD.0000000000001677

Kaihan Deng, Wei Zhao, Lin Dai, Zixuan Jing, Lixin Ma

{"title":"Identification and validation of mitochondria-related LncRNA signatures as a novel prognostic model for glioma.","authors":"Kaihan Deng, Wei Zhao, Lin Dai, Zixuan Jing, Lixin Ma","doi":"10.1097/CAD.0000000000001677","DOIUrl":"10.1097/CAD.0000000000001677","url":null,"abstract":"A predictive model for long-term survival is needed, and mitochondrial dysfunction is a key feature of cancer metabolism, though its link to glioma is not well understood. The aim of this study was to identify the molecular characteristics associated with glioma prognosis and explore its potential function. We analyzed RNA-seq data from The Cancer Genome Atlas and identified differentially expressed mitochondrial long noncoding RNAs (lncRNAs) using R's 'limma' package. A prognostic model was developed using 10 selected lncRNAs and validated with Cox regression and least absolute shrinkage and selection operator algorithm. The model's efficacy was assessed using Kaplan-Meier and receiver operating characteristic curve analyses, and its correlation with immune cell profiles and drug sensitivity was explored. A 10-mitochondria-related LncRNA signature was generated. The median risk score values are used to classify glioma samples into low-risk and high-risk groups. In breast patients, the signature-based risk score demonstrated a more potent ability to predict survival than conventional clinicopathological features. Furthermore, we noted a substantial disparity in the number of immune cells, including B cells, CD8+T cells, and macrophages, between the two groups. In addition, the high-risk group exhibited lower half-maximal inhibitory concentration values for specific chemotherapy medications, including bortezomib, luminespib, rapamycin, and 5-fluorouracil. Our study elucidates the diagnostic and prognostic value of mitochondria-related-lncRNAs in the promotion, suppression, and treatment of glioma.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

KLF4 activates LATS2 to promote cisplatin sensitivity in ovarian cancer through DNA damage. KLF4 通过 DNA 损伤激活 LATS2，促进卵巢癌对顺铂的敏感性。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-01-01 Epub Date: 2024-09-27 DOI: 10.1097/CAD.0000000000001662

Ling Ma, Xiaoting Zhao, Xiang Lu, Jiahui Shen, Jiankang Huang

{"title":"KLF4 activates LATS2 to promote cisplatin sensitivity in ovarian cancer through DNA damage.","authors":"Ling Ma, Xiaoting Zhao, Xiang Lu, Jiahui Shen, Jiankang Huang","doi":"10.1097/CAD.0000000000001662","DOIUrl":"10.1097/CAD.0000000000001662","url":null,"abstract":"We aimed to investigate the role of large tumor suppressor kinase 2 (LATS2) in cisplatin (DDP) sensitivity in ovarian cancer. Bioinformatic analysis explored LATS2 expression, pathways, and regulators. Quantitative reverse transcription-PCR measured LATS2 and KLF4 mRNA levels. Dual-luciferase and chromatin immunoprecipitation assays confirmed their binding relationship. Cell viability, half maximal inhibitory concentration (IC 50 ) values, cell cycle, and DNA damage were assessed using CCK-8, flow cytometry, and comet assays. Western blot analyzed protein expression. The effect of LATS2 on the sensitivity of ovarian cancer to DDP was verified in vivo . LATS2 and KLF4 were downregulated in ovarian cancer, with LATS2 enriched in cell cycle, DNA replication, and mismatch repair pathways. KLF4, an upstream regulator of LATS2, bound to its promoter. Overexpressing LATS2 increased G1-phase cells, reduced cell viability and IC 50 values, and induced DNA damage. Silencing KLF4 alone showed the opposite effect on LATS2 overexpression. Knocking out LATS2 reversed the effects of KLF4 overexpression on cell viability, cell cycle, IC 50 values, and DNA damage in ovarian cancer cells. Inhibiting LATS2 inactivated the Hippo-YAP signaling pathway. In vivo experiments showed that overexpression of LATS2 enhanced the sensitivity of ovarian cancer to DDP. KLF4 activates LATS2 via DNA damage to enhance DDP sensitivity in ovarian cancer, providing a potential target for improving treatment outcomes.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"49-61"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142374909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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