Anti-Cancer Drugs最新文献

{"title":"Albumin-based nanocarriers loaded with novel Zn(II)-thiosemicarbazone compounds chart a new path for precision breast cancer therapy.","authors":"Ferdane Danişman-Kalindemirtaş, Dilşad Özerkan, İshak Afşin Kariper, Gökçe Erdemir Cilasun, Bahri Ülküseven, Serap Erdem-Kuruca","doi":"10.1097/CAD.0000000000001679","DOIUrl":"10.1097/CAD.0000000000001679","url":null,"abstract":"<p><p>This study explores the therapeutic potential of albumin-bound Zn(II)-thiosemicarbazone compounds (Alb-ZnTcA, Alb-ZnTcB) against breast cancer cells. Previous research indicates that these compounds hinder cancer cell proliferation by blocking DNA synthesis, promoting oxidative stress to induce apoptosis, and disrupting the cell cycle to inhibit cellular division. This study focuses on the loading and characterization of these potentially chemically unstable compounds on bovine serum albumin-based nanocarriers. Accordingly, unlike previous studies using albumin nanoparticles, in this study, ultraviolet light was used to precisely bind the therapeutic agent to albumin during the integration of thiosemicarbazones, achieving controlled nanoparticle size to control nanoparticle size. The mean diameter of Alb-ZnTcA nanoparticles was 32 nm, while Alb-ZnTcB exhibited an average diameter of 43 nm. Notably, Alb-ZnTcA displayed the highest cytotoxicity toward breast cancer cells, suggesting an optimal size for cellular uptake. Additionally, albumin-bound compounds showed enhanced cytotoxicity at lower concentrations, potentially minimizing adverse side effects. Apoptosis analysis indicated that both Alb-ZnTcA and Alb-ZnTcB induce cell death predominantly through apoptosis, effectively preventing the uncontrolled proliferation of cancer cells. These findings demonstrate the potential of Zn(II)-thiosemicarbazone compounds loaded on albumin-based nanocarriers for breast cancer treatment. The increased potency of Alb-ZnTcA and Alb-ZnTcB compared to free compounds, along with their ability to activate apoptotic signaling pathways in MCF-7 breast cancer cells, highlights a promising approach for future cancer therapies. This study suggests that albumin-bound Zn(II)-thiosemicarbazone compounds could offer a targeted and effective strategy in breast cancer treatment, leveraging the advantages of nanocarrier-based delivery systems.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"208-219"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943241","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}

{"title":"The impact of bevacizumab intraperitoneal perfusion combined with paclitaxel and platinum-based chemotherapy on serum stromal-derived factor-1α (SDF-1α) and chemokine ligand 5 (CXCL-5) levels in patients with ovarian cancer after tumor cell debulking surgery.","authors":"Liangliang Wang, Shanshan Ma, Huiwen Su, Dandan Nie, Lihua Wang","doi":"10.1097/CAD.0000000000001663","DOIUrl":"10.1097/CAD.0000000000001663","url":null,"abstract":"&lt;p&gt;&lt;p&gt;The aim of this study is to investigate the impact of bevacizumab intraperitoneal perfusion combined with paclitaxel and platinum-based chemotherapy on serum stromal-derived factor-1α (SDF-1α) and chemokine ligand 5 (CXCL-5) levels in patients with ovarian cancer after tumor cell debulking surgery. This clinical study was conducted on a cohort of 89 ovarian cancer patients who underwent tumor debulking surgery at our hospital from February 2020 to February 2021. The patients were divided into two groups using a random number table: the control group ( n  = 44) received postoperative treatment with paclitaxel and platinum-based chemotherapy, while the research group ( n  = 45) received additional treatment with intraperitoneal perfusion of bevacizumab in addition to the control group's treatment regimen. The analysis included an assessment of the clinical efficacy of both groups, changes in tumor biomarker levels before and after treatment, serum levels of SDF-1α and CXCL-5, T-lymphocyte subset levels, treatment-related adverse reactions, and a 2-year prognosis and survival assessment. The research group showed better performance compared to the control group in terms of disease remission rate (80.00% vs. 59.09%) and treatment effectiveness rate (95.56% vs. 75.00%) ( P  &lt; 0.05). Before treatment, the levels of tumor biomarkers between the two groups were compared ( P  &gt; 0.05). After treatment, the levels of serum ferritin, carbohydrate antigen 125, carbohydrate antigen 199, and human epididymis protein 4 in both groups significantly decreased compared to before treatment, with the research group having lower levels ( P  &lt; 0.05). Before treatment, serum levels of SDF-1α and CXCL-5 between the two groups were compared ( P  &gt; 0.05). After treatment, however, the levels of SDF-1α and CXCL-5 significantly decreased compared to before treatment, with the research group having lower levels than the control group ( P  &lt; 0.05). Before treatment, there was no difference in T-lymphocyte levels between the two groups ( P  &gt; 0.05). In the control group, there was no significant change in T-lymphocyte levels before and after treatment ( P  &gt; 0.05). In the research group, however, after treatment, each indicator increased compared to before treatment, and posttreatment levels of all indicators were higher than those in the control group ( P  &lt; 0.05). The adverse reactions were compared between the two groups ( P  &gt; 0.05). The research group had a longer average survival time than the control group, with 1-year and 2-year survival rates higher than the control group ( P  &lt; 0.05). There was, however, no significant difference between the two groups in terms of local recurrence and metastasis ( P  &gt; 0.05). In conclusion, bevacizumab intraperitoneal perfusion combined with paclitaxel and platinum-based chemotherapy shows better clinical efficacy in the treatment of ovarian cancer after tumor cell debulking surgery. It can significantly reduce the levels of ser","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"232-237"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930340","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}

{"title":"Transformation of lung adenocarcinoma to small cell lung cancer following osimertinib treatment: a case report and literature review.","authors":"Linwu Kuang, Peng Wang, Lin Zhou, Yangkai Li","doi":"10.1097/CAD.0000000000001686","DOIUrl":"10.1097/CAD.0000000000001686","url":null,"abstract":"<p><p>Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) effectively treat EGFR-mutant lung adenocarcinoma, demonstrating initial efficacy but eventually leading to acquired resistance. Small cell transformation is a rare resistance mechanism to EGFR-TKIs in lung adenocarcinoma, which can complicate clinical diagnosis and treatment. We present a patient with lung adenocarcinoma who underwent a prior pneumonectomy and adjuvant chemotherapy and was treated with osimertinib after the recurrence of lung cancer. Small cell transformation occurred approximately 20 months after starting osimertinib treatment. After this transformation, the patient underwent lung radiotherapy and cisplatin-etoposide chemotherapy, which stabilized the disease. Following the confirmation of small cell lung cancer (SCLC) via thyroid puncture, treatments with irinotecan, irinotecan plus atezolizumab, thyroid radiotherapy, adrenal radiotherapy, and head radiotherapy were sequentially administered, yet the disease continued to progress. The patient succumbed to the disease in May 2023 because of progression and organ failure, with an overall survival of 52.7 months, including 16 months post small cell transformation. This case highlights the possibility of osimertinib causing lung adenocarcinoma to transform into SCLC and underscores rebiopsies' importance in identifying resistance mechanisms to EGFR-TKIs. Increased levels of neuron-specific enolase and pro-gastrin releasing peptide can signal early transformation into SCLC.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"253-259"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943251","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}

{"title":"WISP1 inhibition of YAP phosphorylation drives breast cancer growth and chemoresistance via TEAD4 activation.","authors":"Tingting Dong, Li Liu, Yikai You, Jin Liu, Fuchao Wang, Shimeng Li, Zhenghong Yu","doi":"10.1097/CAD.0000000000001687","DOIUrl":"10.1097/CAD.0000000000001687","url":null,"abstract":"<p><p>Wnt1-inducible signaling pathway protein 1 (WISP1) promotes breast cancer. The Hippo signaling pathway demonstrates a potential connection with WISP1, necessitating an exploration of their interaction. This study hypothesized that WISP1 boosts breast cancer by modulating the Hippo signaling pathway. The Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases were used to analyze WISP1 expression and Hippo signaling in breast cancer patients. WISP1, yes-associated protein (YAP), and domain family member 4 (TEAD4) were overexpressed or silenced in breast cancer cells. Epithelial-mesenchymal transition (EMT), and chemoresistance of breast cancer cells were evaluated. Immunofluorescence, PCR, immunoprecipitation, and western blot were used to detect the expression of WISP1 and key Hippo signaling factors and their interactions. Enrichment analysis indicated activation of WISP1 and Hippo signaling pathway and correlated with a worse prognosis in breast cancer. WISP1 overexpression facilitated EMT and chemotherapy resistance in breast cancer. Importantly, overexpression of WISP1 promoted YAP's nuclear translocation. TEAD4 expression in YAP precipitates from nuclear of WISP1-overexpressing MCF-7 cells increased. The promoting effect of WISP1 on breast cancer was counteracted by silencing YAP or TEAD4. Moreover, in WISP1 small interfering RNA-transfected MCF-7 cells, p-YAP expression increased, while interaction between YAP and TEAD4 decreased. WISP1 silencing led to ubiquitin increase and TEAD reduction in the p-YAP precipitates. In conclusion, WISP1 promotes YAP nuclear translocation and binding with TEAD4 by inhibiting YAP phosphorylation, reducing ubiquitin recruitment, and participating in transcriptional regulation in breast cancer.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"157-176"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942616","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}

{"title":"High CXCL8 expression predicting poor prognosis in triple-negative breast cancer.","authors":"Sumin Tang, Yuqing Zhang, Liying Song, Kaiyuan Hui, Xiaodong Jiang","doi":"10.1097/CAD.0000000000001678","DOIUrl":"10.1097/CAD.0000000000001678","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is highly prone to early relapse and metastasis following standard treatment. CXCL8 is a key factor in tumor invasion and metastasis, but its role in TNBC prognosis and clinicopathological correlations remains poorly understood. This study investigated CXCL8 expression and its clinical significance in TNBC to develop a prognostic nomogram for guiding intensive treatment and follow-up strategies. Public datasets from the gene expression omnibus public datasets platform were analyzed to assess CXCL8 expression. Additionally, paraffin-embedded TNBC specimens collected from our hospital were examined using immunohistochemistry to explore the relationship between CXCL8 expression and clinicopathological features. Survival analysis was performed to evaluate whether CXCL8 serves as an unfavorable prognostic biomarker for TNBC patients. Univariate Cox regression analysis was conducted to identify prognostic factors. Based on these findings, a nomogram was developed to predict TNBC progression risk. CXCL8 expression was significantly higher in TNBC tissues than in adjacent normal tissues ( P  < 0.05). Among 122 TNBC patients, 46 were CXCL8-positive and 76 were CXCL8-negative. CXCL8 expression was significantly associated with N stage ( P  < 0.05). Progression-free survival (PFS) was markedly shorter in the CXCL8-positive group compared with the CXCL8-negative group ( P  < 0.001). Univariate Cox regression identified N1-3, M1, and CXCL8 positivity as significant risk factors for disease progression. A nomogram incorporating these variables (N, M, and CXCL8) was constructed to predict PFS. Time-dependent receiver operating characteristic curve analysis at 12-, 36-, and 48-month demonstrated strong predictive performance, with area under the curve values of 0.857, 0.839, and 0.795, respectively. CXCL8 is highly expressed in TNBC and promotes lymphatic metastasis, serving as an unfavorable prognostic factor. The developed nomogram offers a valuable tool for guiding personalized treatment and follow-up strategies in TNBC patients.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":"36 3","pages":"246-252"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781556/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063253","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}

{"title":"Research on the mechanism of eugenol in the treatment of liver cancer based on network pharmacology, molecular docking technology, and in vitro experiments.","authors":"Kaiping Liu, Jiuliang Jiang, Zhenyu Yu, Yunhao Wang, Min Wang, Haitao Zhu","doi":"10.1097/CAD.0000000000001675","DOIUrl":"10.1097/CAD.0000000000001675","url":null,"abstract":"<p><p>Eugenol, a phenolic natural product with diverse pharmacological activities, remains unexplored in liver cancer. Using network pharmacology, we investigated eugenol's therapeutic mechanisms in liver cancer. We obtained eugenol's molecular structure from PubChem and screened its targets using similarity ensemble approach in Swiss Target Predictiondatabases. Overlapping genes with liver cancer-related genes from GeneCards were identified. Protein-protein interaction networks, Gene Ontology annotations, and Kyoto Encyclopedia of Genes and Genomes pathway analyses were conducted. A target-pathway network revealed eugenol's interaction with 122 liver cancer-related genes. Molecular docking confirmed eugenol's high affinity for mitochondrial nicotinamide adenine dinucleotide, reduced form (NADH) dehydrogenase 1 (MT-ND1), AKT1, NDUFB7, and NADH dehydrogenase (complex I) subunit S3 (NDUFS3). Expression levels of these targets in normal liver and liver cancer tissues were examined using GEPIA2 and HPA databases. The CCK-8 assay and colony formation assay demonstrated that eugenol significantly inhibited the proliferation of hepatocellular carcinoma cells. Western blot analysis confirmed that eugenol upregulated MT-ND1 while downregulating the expression of targets such as AKT1, NDUFB7, and NDUFS3. Furthermore, it was found that eugenol could influence the expression of the AKT1 target through the AKT/p70 S6K pathway. This study provides new insights into the potential mechanisms of eugenol in liver cancer and offers novel perspectives for network-based liver cancer research.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"177-189"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943245","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}

{"title":"Paeoniflorin sensitizes imatinib mesylate-resistant chronic myeloid leukemia cells via the inhibition of Cyr61 production.","authors":"Yanfang Song, Li Luo, Zhen Lin, Taigang Zhang, Zhaozhong Li, Yinping Cao, Xianjin Zhu","doi":"10.1097/CAD.0000000000001681","DOIUrl":"10.1097/CAD.0000000000001681","url":null,"abstract":"<p><p>Imatinib mesylate (IM) is a first-line therapy for chronic myeloid leukemia (CML) and exhibits good therapeutic effects, but not in all patients with CML owing to drug resistance. Our previous study showed that Cyr61 plays a key role in IM resistance in CML cells. Paeoniflorin (PF) is a bioactive compound isolated from the traditional Chinese medicine Paeonia lactiflora Pall that displays anticancer activity. Little is, however, known regarding the role of PF in IM-resistant CML cells. This study aimed to evaluate whether PF could decrease Cyr61 production and improve IM-resistant CML cell sensitivity to IM and to investigate the underlying mechanisms. CML cell lines (K562 and KCL22) and IM-resistant cell lines (K562G and KCL22R) were used as CML study models. Cyr61 expression was assessed in both parental and IM-resistant CML cells by western blotting, real-time quantitative PCR , and ELISA. Lentiviral vectors were used to induce the knockdown of Cyr61 expression, followed by a comprehensive evaluation of cell proliferation and apoptosis. The results showed that PF decreased the production of Cyr61 in the presence of IM by inhibiting extracellular regulated protein kinases 1/2 activation. PF significantly decreased the IC50 value of IM and increased IM-induced apoptosis of IM-resistant CML cells. Importantly, PF also improved the sensitivity of CML cells to bosutinib and dasatinib via inhibition of Cyr61 production. In conclusion, we report for the first time that PF may effectively improve the sensitivity of IM-resistant CML cells to IM, bosutinib, and dasatinib, at least in part, by subsequently downregulating Cyr61.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"190-198"},"PeriodicalIF":1.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943244","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}

{"title":"Occult epidermal growth factor receptor-mutant lung adenocarcinoma complicated by prostatic metastasis: a case report.","authors":"Fan Yang, Xing Zhao, Hua Xie, Yajie Zhu, Yi Wang, Jin Zhou","doi":"10.1097/CAD.0000000000001710","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001710","url":null,"abstract":"<p><p>Herein, we report a case of occult epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma complicated by prostatic metastasis. A 75-year-old male with >30 years of smoking history presented with lower back pain as the initial symptom. Respiratory symptoms, including cough and sputum production, were absent. PET-computed tomography revealed the presence of bone and prostatic metastases, without any lung abnormalities. Biopsies of the space-occupying bone and metastatic lesions suggested that the metastases originated from primary lung adenocarcinoma. Genetic testing indicated EGFR 21L858R(+). The patient had an abnormal serum carcinoembryonic antigen level but a normal prostate-specific antigen level. Following a multidisciplinary discussion, a diagnosis of occult primary lung adenocarcinoma complicated by bone and prostatic metastases (TxN0M1b, Stage IVB) was considered. Following targeted therapy with oral osimertinib, the patient achieved a partial response, with alleviation of pain symptoms alleviated and normalization of carcinoembryonic antigen levels. In the absence of tissue biopsy, such cases can often be misdiagnosed as prostate cancer complicated by multiple bone metastases. Hence, the present case highlights the importance of comprehensive diagnostic testing, including tissue biopsy, to accurately identify the underlying cause of metastatic disease.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536553","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}

{"title":"Low-dose anlotinib plus immune checkpoint inhibitors offers better efficacy and safety in advanced non-small cell lung cancer treatment.","authors":"Tingfei Tan, Siyu Yuan, Weiwei Chu, Jiemei Jiang, Meiling Chen, Quan Xia, Junping Wang","doi":"10.1097/CAD.0000000000001701","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001701","url":null,"abstract":"<p><p>The combination of anlotinib with immune checkpoint inhibitors (ICIs) has become a common treatment modality in clinical practice. However, the optimal dose of anlotinib to use remains unclear. We collected patients with advanced non-small cell lung cancer (NSCLC) who received programmed cell death-1 blockade combined with different dose of anlotinib as second-line or later line therapy. Subsequently, the efficacy and safety of the combination therapy as well as subgroup analyses of different doses of anlotinib were analyzed. Cox regression was performed to analyze significant factors correlated with progression-free survival (PFS) and overall survival (OS). A total of 50 eligible patients with NSCLC who received anlotinib combined with ICIs therapy were included, of which 27 received low-dose anlotinib (8 mg), and 23 were administered high-dose anlotinib (12 mg). The median PFS (mPFS) and the median OS (mOS) for all patients were 8.3 months [95% confidence interval (CI): 6.3-10.3] and 17.6 months (95% CI: 16.5-18.7), respectively. Subgroup analyses showed that patients treated with 8 mg of anlotinib plus ICIs had significantly longer mPFS than those treated with 12 mg of anlotinib plus ICIs (8.7 vs 6.7 months, P  = 0.016). The overall incidence of adverse events was 68.0%, and the most common adverse events of all grades were hypertension. Meanwhile, the incidence of adverse events was higher for 12 mg of anlotinib plus ICIs than that of 8 mg of anlotinib plus ICIs (82.6 vs 55.6%, P  = 0.041). Low-dose anlotinib in combination with ICIs for advanced NSCLC may be an effective and well-tolerated option.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481994","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}

{"title":"BTK inhibitors enhance NKG2D ligand expression by regulating IL-10/STAT3 pathway in activated non-GCB diffuse large B-cell lymphoma cells.","authors":"Zhu-Xia Jia, Bi-Tao Xiao, Jin Li, Xiao-Hui Cai, Wei Qin, Min Zhou, Xu-Zhang Lu","doi":"10.1097/CAD.0000000000001696","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001696","url":null,"abstract":"<p><p>The aim of this study is to explore the role of the IL-10/STAT3 pathway in the upregulation of natural killer group 2, member D (NKG2D) ligands (MICA and ULBP2) induced by Bruton's tyrosine kinase (BTK) inhibitors in non-germinal center B-cell-like diffuse large B-cell lymphoma cells. The expression levels of NKG2D ligands and the IL-10/STAT3 pathway in SUDHL4, U2932, and OCI-LY3 cells were analyzed using western blotting. After stimulation of the B-cell receptor signaling pathway with IgM antibodies, the expression levels of NKG2D ligands, as well as IL-10 and phosphorylated STAT3 (p-STAT3) were significantly reduced. In contrast, treatment with ibrutinib produced effects opposite to those induced by IgM antibodies. Additionally, treatment of U2932 and OCI-LY3 cells with the STAT3 inhibitor (STAT3-IN-1) led to an increase in NKG2D ligand expression and a decrease in IL-10 levels. When IL-10 neutralizing antibodies were introduced, p-STAT3 levels decreased, and NKG2D ligand expression increased. Similar outcomes were observed when the BTK inhibitors ACP-196 and BGB-3111 were administered. Our findings suggest that the IL-10/STAT3 pathway plays a key role in the upregulation of NKG2D ligands induced by BTK inhibitors in U2932 and OCI-LY3 cells.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539947","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}