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The effectiveness of sequential afatinib and furmonertinib in an advanced lung adenocarcinoma with rare compound EGFR mutation (L833V/H835L).
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2025-01-24 DOI: 10.1097/CAD.0000000000001692
Yanqing Pan, Lingxin Yan, Yongyao Gu, Shaoxi Wang, Huiling Li, Pengli Yu, Quanfang Chen

Uncommon atypical mutations account for 10-15% of all epidermal growth factor receptor (EGFR) activating mutations in nonsmall-cell lung cancer (NSCLC). Tumors harboring rare EGFR mutations show highly heterogeneous responses to EGFR tyrosine kinase inhibitors (TKIs). There is insufficient clinical evidence for uncommon types of EGFR mutations, especially those with compound EGFR mutations. In addition, for those with uncommon compound EGFR mutations, few studies have focused on acquired resistance mechanisms and subsequent treatment strategies after disease progression on EGFR-TKIs. Here, a 66-year-old smoking male was diagnosed with lung adenocarcinoma accompanied by pleural metastasis. A rare L833V/H835L compound mutation in exon 21 of EGFR was detected in tumor biopsy by next-generation sequencing. Afatinib was used as first-line therapy and showed favorable efficacy. The patient continued afatinib treatment for a duration of 24 months. A new T790M mutation was detected with a rebiopsy after progression on afatinib. Then the patient received cryoablation therapy and a third-generation EGFR-TKI, furmonertinib. Our case suggests that a comprehensive screening for EGFR mutations should be conducted before and during treatment in clinical practice, and afatinib and furmonertinib could be first- and second-line treatment options in NSCLC patients harboring EGFR L833V/H835L mutations.

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引用次数: 0
circ_0006528 promotes nonsmall cell lung cancer progression by sponging miR-892a and regulating NRAS expression. circ_0006528通过海绵化miR-892a和调节NRAS表达促进非小细胞肺癌进展。
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2023-11-16 DOI: 10.1097/CAD.0000000000001439
Weixi Guo, Hongming Liu, Ming Zhong, Qinghua Qi, Yibin Li

Micro-RNAs play essential roles in developing and progressing nonsmall cell lung cancer (NSCLC) and drug resistance. Nevertheless, the functions and mechanisms are partly explored. Therefore, the present study analyzes the effect of circ_0006528 and the mechanism of regulation of NSCLC cell progression by sponging miR-892a to regulate neuroblastoma rat sarcoma viral oncogene (NRAS) expression. Initially, circ_0006528 is identified using divergent primers-based PCR and RNase R exonuclease treatments. After administration of the designed circ_0006528-specific siRNA, the RT-qPCR analysis is used to determine the interference efficiency of siRNA. At the same time, cell growth, invasion, and migration are assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), Transwell, and scratch assays in the NSCLC cell lines [secretory pathway Ca2+-ATPase isoform 1 (SPCA-1) and A549] in vitro, respectively. Further, miR-892a inhibitor is added to the cells for functional recovery assay. Finally, the xenograft mouse model is constructed to explore the effect of circ_0006528 on tumor growth in vivo . The RT-qPCR analysis in 66 pairs of NSCLC cancer and noncancerous tissues revealed that circ_0006528 is highly expressed in NSCLC patient tissues. The RNase R experiments revealed that HSA_circ_0006528 is unaffected by RNase R exonuclease. MTT assay showed that knockdown of hsa_circ_0006528 by siRNA significantly decreased cell proliferation and viability in A549 and SPCA-1 cells. The luciferase reporter assay showed direct binding of hsa_circ_0006528 to miR-892a, and miR-892a targets binding NRAS. In addition, the miR-892a inhibitor terminated the hsa_circ_0006528 siRNA, triggering inhibition of proliferation, invasion, and migration of NSCLC cells. In summary, the study revealed that the knockout of hsa_circ_0006528 downregulation of NRAS expression by sponging miR-892a inhibited NSCLC cell growth and invasion.

微rna在非小细胞肺癌(NSCLC)的发生发展和耐药过程中发挥着重要作用。然而,本文对其功能和机制进行了部分探讨。因此,本研究通过海绵miR-892a调控神经母细胞瘤大鼠肉瘤病毒癌基因(NRAS)表达,分析circ_0006528的作用及调控NSCLC细胞进展的机制。最初,circ_0006528是通过基于不同引物的PCR和RNase R外切酶处理鉴定的。在给予设计的circ_0006528特异性siRNA后,使用RT-qPCR分析来确定siRNA的干扰效率。同时,采用3-[4,5-二甲基噻唑-2-基]-2,5二苯基溴化四唑(MTT)、Transwell和scratch法分别在体外对NSCLC细胞系(分泌途径Ca2+- atp酶异型1 [SPCA-1]和A549)进行细胞生长、侵袭和迁移评估。进一步,将miR-892a抑制剂添加到细胞中进行功能恢复试验。最后,构建异种移植小鼠模型,探讨circ_0006528在体内对肿瘤生长的影响。通过对66对NSCLC癌组织和非癌组织的RT-qPCR分析,circ_0006528在NSCLC患者组织中高表达。RNase R实验显示HSA_circ_0006528不受RNase R外切酶的影响。MTT实验显示,siRNA敲低hsa_circ_0006528可显著降低A549和SPCA-1细胞的增殖和活力。荧光素酶报告基因检测显示hsa_circ_0006528与miR-892a直接结合,miR-892a靶向结合NRAS。此外,miR-892a抑制剂终止hsa_circ_0006528 siRNA,引发对NSCLC细胞增殖、侵袭和迁移的抑制。综上所述,本研究揭示了通过海绵miR-892a敲除hsa_circ_0006528下调NRAS表达可抑制NSCLC细胞的生长和侵袭。
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引用次数: 0
FSP1 expression as a predictor of platinum resistance and recurrence in epithelial ovarian cancer.
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2025-02-11 DOI: 10.1097/CAD.0000000000001676
Hang Xing, Hai-Ning Bi, Qi Yin, Ji Zhang, Xue Zhang, Yao-Jiao Li, Xue-Mei Gong, Ji-Fang Shi

The objective of this study is to assess the differential expression of ferroptosis suppressor protein 1 (FSP1) in relation to clinical features, platinum resistance, and recurrence in epithelial ovarian cancer (EOC). In addition, the potential significance of FSP1 in EOC as a predictor of platinum resistance and recurrence in EOC was explored. Patients with pathologically confirmed EOC who underwent surgical treatment were included in this analysis. Immunohistochemistry was employed to evaluate FSP1 expression in ovarian tissues, with quantitative analysis performed on the samples. Clinical data were collected during follow-up, and patients were categorized according to platinum resistance and recurrence criteria. Statistical analysis was conducted using SPSS version 27.0. A total of 40 tissue samples from patients with EOC were analyzed, along with 21 samples from benign ovarian tumors and 20 samples from normal ovarian tissues. The expression of FSP1 was significantly higher in the EOC group compared to both benign and normal tissue groups. Meanwhile, the expressions of FSP1 were higher in groups with clinically advanced stages, high-grade carcinoma, presence of cancerous ascites, lymph node metastasis, and in the clear cell EOC group, compared to those with clinically early stages, low-grade carcinoma, absence of cancerous ascites, no lymph node metastasis, and other pathological subtypes. A positive linear correlation was identified between FSP1 expression in EOC tissues and serum levels of CA125 and human epididymis protein 4 at the time of diagnosis. The elevated expression of FSP1 is positively correlated with serum CA125 and human epididymis protein 4 levels at the time of diagnosis, which is a risk factor for EOC drug resistance and recurrence. These findings suggest that FSP1 may serve as a valuable biomarker for predicting platinum resistance and recurrence in patients with EOC.

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引用次数: 0
Berberine inhibits prostate cancer progression by inducing ferroptosis: evidence from network pharmacology. 小檗碱通过诱导铁下垂抑制前列腺癌进展:来自网络药理学的证据。
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2025-01-14 DOI: 10.1097/CAD.0000000000001691
Peiliang Zou, Shenghai Li, Qixiong He, Chixing Zheng

The uncertain ferroptosis-related role of berberine in prostate cancer was explored using network pharmacology methodology. Integration of ferroptosis targets in prostate cancer from the Genecard database and berberine targets from the Traditional Chinese Medicine Systems Pharmacology and SwissTargetPrediction databases revealed 17 common targets. Among these, 10 hub genes, including CCNB1 , CDK1 , AURKA , AR , CDC42 , ICAM1 , TYMS , NTRK1 , PTGS 2, and SCD , were identified. Enrichment analyses yielded 799 Gene Ontology terms and 23 Kyoto Encyclopedia of Genes and Genomes pathways associated with berberine-related targets. Molecular docking simulations indicated berberine's binding capacity to all hub genes. In-vitro studies on LNCaP and PC3 cells demonstrated berberine's inhibition of cell proliferation and significant downregulation of TYMS , CCNB1 , AURKA , CDK1 , and SCD in both cell lines. Berberine exhibited cell line-specific effects by reducing AR expression in LNCaP cells and suppressing ICAM1 in PC3 cells. Overall, berberine shows promise in inhibiting prostate cancer progression through modulation of ferroptosis-related genes, including TYMS , AR , CCNB1 , AURKA , CDK1 , ICAM1 , NTRK1 , SCD , and CDC42 .

利用网络药理学方法探讨了小檗碱在前列腺癌中与铁中毒相关的不确定作用。整合来自Genecard数据库的前列腺癌铁下垂靶点和来自中医系统药理学和SwissTargetPrediction数据库的小檗碱靶点,发现了17个共同靶点。其中,共鉴定出CCNB1、CDK1、AURKA、AR、CDC42、ICAM1、TYMS、NTRK1、PTGS2、SCD等10个枢纽基因。富集分析得到799个基因本体术语和23个与小檗碱相关靶点相关的京都基因和基因组百科全书路径。分子对接模拟显示了小檗碱与所有枢纽基因的结合能力。对LNCaP和PC3细胞的体外研究表明,小檗碱对两种细胞系的细胞增殖均有抑制作用,并显著下调TYMS、CCNB1、AURKA、CDK1和SCD。小檗碱通过降低LNCaP细胞中的AR表达和抑制PC3细胞中的ICAM1表现出细胞系特异性作用。总的来说,小檗碱通过调节铁致凋亡相关基因,包括TYMS、AR、CCNB1、AURKA、CDK1、ICAM1、NTRK1、SCD和CDC42,显示出抑制前列腺癌进展的希望。
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引用次数: 0
Clinical efficacy of pyrotinib combined with chemotherapy for neoadjuvant treatment in HER2-positive breast cancer: a single-center study. 吡罗替尼联合化疗新辅助治疗her2阳性乳腺癌的临床疗效:一项单中心研究
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2025-01-14 DOI: 10.1097/CAD.0000000000001690
Benkai Wei, Huanhuan Yan, Fan Li, Jun Shen

This study aimed to evaluate the efficacy of pyrotinib, an orally administered small molecule tyrosine kinase inhibitor, combined with neoadjuvant chemotherapy in treating patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer. Pyrotinib works by inhibiting the HER2 signaling pathway, thereby preventing tumor cell growth. This single-arm clinical trial aimed to assess the total pathological complete response (tpCR; ypT0/is and ypN0) rate as the primary endpoint. A total of 27 patients were enrolled, each receiving 4-8 cycles of pyrotinib in combination with neoadjuvant chemotherapy. Pyrotinib combined with neoadjuvant chemotherapy demonstrated notable antitumor activity in patients with HER2-positive breast cancer. Among 26 patients, the tpCR rate was 26% (7/26), while the breast pathological complete response rate was 30% (8/26), indicating complete inhibition of the primary tumor in some cases. Notably, patients with HR-negative breast cancer demonstrated a higher tpCR rate compared with those with HR-positive breast cancer. The treatment regimen was well-tolerated. Diarrhea was the most common adverse event, occurring in 92.3% of patients, with 46.2% experiencing grade 3 or higher diarrhea. No severe adverse events or treatment-related fatalities were reported.

本研究旨在评估口服小分子酪氨酸激酶抑制剂pyrotinib联合新辅助化疗治疗人表皮生长因子受体2 (HER2)阳性乳腺癌患者的疗效。Pyrotinib通过抑制HER2信号通路起作用,从而阻止肿瘤细胞生长。这项单臂临床试验旨在评估总病理完全缓解(tpCR;ypT0/is和ypN0)率作为主要终点。共有27例患者入组,每位患者接受4-8个周期的吡罗替尼联合新辅助化疗。吡咯替尼联合新辅助化疗在her2阳性乳腺癌患者中显示出显著的抗肿瘤活性。26例患者中,tpCR率为26%(7/26),乳腺病理完全缓解率为30%(8/26),部分患者原发肿瘤得到完全抑制。值得注意的是,hr阴性乳腺癌患者的tpCR率高于hr阳性乳腺癌患者。治疗方案耐受性良好。腹泻是最常见的不良事件,发生在92.3%的患者中,46.2%的患者出现3级或更高级别的腹泻。无严重不良事件或治疗相关死亡报告。
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引用次数: 0
Preclinical evidence that fibroblast growth factor receptor pathway inhibition by BGJ398 enhances small cell lung cancer response to chemotherapy. 临床前证据表明BGJ398抑制成纤维细胞生长因子受体通路可增强小细胞肺癌对化疗的反应。
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2025-01-17 DOI: 10.1097/CAD.0000000000001683
Yingying Shen, Yan Jiang, Junyao Wu, Chenyu Wang, Jiao Bo Kun Huang, Jie Liu, Sen Chen

Small cell lung cancer (SCLC) is a highly aggressive form of lung cancer with limited therapeutic options and poor prognosis. In this study, we explored the therapeutic potential of BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, alone and in combination with standard chemotherapy (cisplatin and paclitaxel) in SCLC. High-throughput screening of kinase inhibitors was performed on three SCLC cell lines (NCI-H446, NCI-H69, and NCI-H182), identifying BGJ398 as one of the most potent and selective inhibitors. BGJ398 demonstrated significant synergy with cisplatin and paclitaxel in vitro , as indicated by combination index values below 1. In vivo , combination treatments significantly inhibited tumor growth and extended survival in SCLC xenograft models compared to monotherapies. Notably, the combination of BGJ398 with cisplatin exhibited the most pronounced tumor suppression and survival benefits. Immunohistochemistry analysis confirmed that BGJ398 effectively inhibited FGFR signaling pathways, reducing levels of phosphorylated FGFR, protein kinase B, signal transducer and activator of transcription 3, and extracellular signal-regulated kinase. These findings suggest that BGJ398, particularly in combination with chemotherapy, holds significant promise as a treatment strategy for SCLC, providing enhanced anti-tumor efficacy and improved survival outcomes.

小细胞肺癌(SCLC)是一种高度侵袭性的肺癌,治疗选择有限,预后差。在这项研究中,我们探索了BGJ398的治疗潜力,BGJ398是一种选择性成纤维细胞生长因子受体(FGFR)抑制剂,单独或联合标准化疗(顺铂和紫杉醇)治疗SCLC。在三种SCLC细胞系(NCI-H446, NCI-H69和NCI-H182)上进行了激酶抑制剂的高通量筛选,确定BGJ398是最有效和选择性的抑制剂之一。BGJ398与顺铂、紫杉醇体外协同作用显著,联合指数低于1。在体内,与单一治疗相比,联合治疗显著抑制SCLC异种移植模型的肿瘤生长并延长生存期。值得注意的是,BGJ398与顺铂联合使用显示出最明显的肿瘤抑制和生存益处。免疫组织化学分析证实,BGJ398有效抑制FGFR信号通路,降低磷酸化FGFR、蛋白激酶B、信号传导和转录激活因子3以及细胞外信号调节激酶的水平。这些发现表明,BGJ398,特别是联合化疗,作为SCLC的治疗策略具有重要的前景,提供增强的抗肿瘤疗效和改善的生存结果。
{"title":"Preclinical evidence that fibroblast growth factor receptor pathway inhibition by BGJ398 enhances small cell lung cancer response to chemotherapy.","authors":"Yingying Shen, Yan Jiang, Junyao Wu, Chenyu Wang, Jiao Bo Kun Huang, Jie Liu, Sen Chen","doi":"10.1097/CAD.0000000000001683","DOIUrl":"10.1097/CAD.0000000000001683","url":null,"abstract":"<p><p>Small cell lung cancer (SCLC) is a highly aggressive form of lung cancer with limited therapeutic options and poor prognosis. In this study, we explored the therapeutic potential of BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, alone and in combination with standard chemotherapy (cisplatin and paclitaxel) in SCLC. High-throughput screening of kinase inhibitors was performed on three SCLC cell lines (NCI-H446, NCI-H69, and NCI-H182), identifying BGJ398 as one of the most potent and selective inhibitors. BGJ398 demonstrated significant synergy with cisplatin and paclitaxel in vitro , as indicated by combination index values below 1. In vivo , combination treatments significantly inhibited tumor growth and extended survival in SCLC xenograft models compared to monotherapies. Notably, the combination of BGJ398 with cisplatin exhibited the most pronounced tumor suppression and survival benefits. Immunohistochemistry analysis confirmed that BGJ398 effectively inhibited FGFR signaling pathways, reducing levels of phosphorylated FGFR, protein kinase B, signal transducer and activator of transcription 3, and extracellular signal-regulated kinase. These findings suggest that BGJ398, particularly in combination with chemotherapy, holds significant promise as a treatment strategy for SCLC, providing enhanced anti-tumor efficacy and improved survival outcomes.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"290-296"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998840","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
Dual inhibition of TYK2 and PD-L1 boosts immune response in triple negative breast cancer. 双重抑制JAK3和PD-L1增强三阴性乳腺癌的免疫应答。
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2025-01-17 DOI: 10.1097/CAD.0000000000001685
Huali Xiang, Binfeng Tu, Xin Feng, Linjing Chen, Yajuan Huang

Recent studies have shown that Janus Kinase inhibitors can enhance the tumor therapeutic effect of immune checkpoint inhibitors. However, it remains to be studied whether TYK2 selective inhibitors can enhance the therapeutic effect of small molecule PD-L1 inhibitors in triple-negative breast cancer (TNBC). We verified the efficacy of the combination of the selective TYK2 inhibitor Deucravacitinib and the small molecule inhibitor of PD-L1, INCB086550, in two TNBC animal models: a syngeneic mouse model (4T1 with humanized PD-L1) and a peripheral blood mononuclear cell (PBMC)-humanized model (MDA-MB-231). Following that, we explored the regulation of immune cell activity in tumors by the combined treatment using flow cytometry. Finally, we validated the expression of genes related to the regulated immune cells through reverse transcription-PCR. Both animal models demonstrated that the addition of a TYK2 inhibitor to a PD-L1 inhibitor significantly enhanced the antitumor capabilities of mice with good safety profiles. The combined therapy significantly elevated the counts of T, B, and natural killer cells while concurrently diminishing myeloid-derived suppressor cells in the syngeneic model. Similarly, in the PBMC-humanized model, this therapy markedly augmented progenitor-like and proliferative precursor-like CD8 T cells, while effectively diminishing exhausted and terminally differentiated CD8 T cell populations. This enhanced antitumor effect is associated with the modulation of antitumor immune-related gene expression by the combined therapy. The combination of TYK2 inhibitors and immune checkpoint inhibitors is a potentially effective strategy for treating TNBC.

最近的研究表明,Janus激酶抑制剂可以增强免疫检查点抑制剂的肿瘤治疗效果。然而,TYK2选择性抑制剂是否能增强小分子PD-L1抑制剂在三阴性乳腺癌(TNBC)中的治疗效果仍有待研究。我们在两种TNBC动物模型中验证了选择性TYK2抑制剂Deucravacitinib与PD-L1小分子抑制剂INCB086550联合治疗的疗效:一种是同基因小鼠模型(4T1与人源化PD-L1),另一种是外周血单核细胞(PBMC)人源化模型(MDA-MB-231)。随后,我们利用流式细胞术探讨了联合治疗对肿瘤免疫细胞活性的调节作用。最后,我们通过逆转录- pcr验证了调控免疫细胞相关基因的表达。两种动物模型均表明,在PD-L1抑制剂中添加TYK2抑制剂可显著增强小鼠的抗肿瘤能力,且具有良好的安全性。在同基因模型中,联合治疗显著提高T、B和自然杀伤细胞的计数,同时减少髓源性抑制细胞。同样,在pmc人源化模型中,该疗法显著增强了祖细胞样和增殖前体细胞样CD8 T细胞,同时有效地减少了耗尽和终末分化的CD8 T细胞群。这种增强的抗肿瘤效果与联合治疗对抗肿瘤免疫相关基因表达的调节有关。TYK2抑制剂和免疫检查点抑制剂联合使用是治疗TNBC的潜在有效策略。
{"title":"Dual inhibition of TYK2 and PD-L1 boosts immune response in triple negative breast cancer.","authors":"Huali Xiang, Binfeng Tu, Xin Feng, Linjing Chen, Yajuan Huang","doi":"10.1097/CAD.0000000000001685","DOIUrl":"10.1097/CAD.0000000000001685","url":null,"abstract":"<p><p>Recent studies have shown that Janus Kinase inhibitors can enhance the tumor therapeutic effect of immune checkpoint inhibitors. However, it remains to be studied whether TYK2 selective inhibitors can enhance the therapeutic effect of small molecule PD-L1 inhibitors in triple-negative breast cancer (TNBC). We verified the efficacy of the combination of the selective TYK2 inhibitor Deucravacitinib and the small molecule inhibitor of PD-L1, INCB086550, in two TNBC animal models: a syngeneic mouse model (4T1 with humanized PD-L1) and a peripheral blood mononuclear cell (PBMC)-humanized model (MDA-MB-231). Following that, we explored the regulation of immune cell activity in tumors by the combined treatment using flow cytometry. Finally, we validated the expression of genes related to the regulated immune cells through reverse transcription-PCR. Both animal models demonstrated that the addition of a TYK2 inhibitor to a PD-L1 inhibitor significantly enhanced the antitumor capabilities of mice with good safety profiles. The combined therapy significantly elevated the counts of T, B, and natural killer cells while concurrently diminishing myeloid-derived suppressor cells in the syngeneic model. Similarly, in the PBMC-humanized model, this therapy markedly augmented progenitor-like and proliferative precursor-like CD8 T cells, while effectively diminishing exhausted and terminally differentiated CD8 T cell populations. This enhanced antitumor effect is associated with the modulation of antitumor immune-related gene expression by the combined therapy. The combination of TYK2 inhibitors and immune checkpoint inhibitors is a potentially effective strategy for treating TNBC.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"280-289"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943243","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
Antibiotic-derived approaches in cancer therapy: effectiveness of ikarugamycin in hexokinase-2 inhibition, tissue factor modulation, and metabolic regulation in breast cancer.
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2025-01-30 DOI: 10.1097/CAD.0000000000001689
Serra Vildan Akgul Obeidin, Masite Sehadet Senol, Zeynep Dogru Koseoglu, Feyza Bayramoglu, Sevgi Disli, Turkan Yigitbasi, Neslin Emekli

We aimed to explore the role of ikarugamycin (IKA) in breast cancer, its connection with hexokinase-2 (HK-2) repression, and tissue factor (TF). This study sought to extend the role of HK-2 as a TF activator in a comprehensive analysis of these interactions from the enzyme, gene, and protein levels. The investigation was performed with MDA-MB-231 and MCF-7 breast cancer lines. The oxidative stress index (OSI), lactate production, and HK activity were assessed using colorimetric assays. Western blot and quantitative PCR analyses were performed to determine HK-2 and TF expressions. Prothrombin time Tests additionally assessed the effect of IKA therapy on TF activation. Three over four significantly downregulated genes were identified after a specific analysis of the IKA's effect on HK-2 and TF in breast cancer cell lines. In the IKA treatment group, lactate production was markedly reduced ( P  < 0.05) and hexokinase activity was found to be reduced in all groups ( P  < 0.05, <0.01). Paclitaxel cytotoxicity independently causes lower OSI in all IKA-treated groups as compared to controls even though OSI is elevated in IKA groups compared to control. Molecular analysis results demonstrated significantly downregulated HK-2 and TF expressions at the protein level ( P  < 0.05, P  < 0.01). Partial thromboplastin time results also showed that IKA-treated cells had longer TF activation duration. A potential indirect association of HK-2 inhibition and TF regulation in breast cancer cells is put forward in this study by presenting IKA's bioactivation of breast cancer in all gene, protein, and enzyme levels.

{"title":"Antibiotic-derived approaches in cancer therapy: effectiveness of ikarugamycin in hexokinase-2 inhibition, tissue factor modulation, and metabolic regulation in breast cancer.","authors":"Serra Vildan Akgul Obeidin, Masite Sehadet Senol, Zeynep Dogru Koseoglu, Feyza Bayramoglu, Sevgi Disli, Turkan Yigitbasi, Neslin Emekli","doi":"10.1097/CAD.0000000000001689","DOIUrl":"10.1097/CAD.0000000000001689","url":null,"abstract":"<p><p>We aimed to explore the role of ikarugamycin (IKA) in breast cancer, its connection with hexokinase-2 (HK-2) repression, and tissue factor (TF). This study sought to extend the role of HK-2 as a TF activator in a comprehensive analysis of these interactions from the enzyme, gene, and protein levels. The investigation was performed with MDA-MB-231 and MCF-7 breast cancer lines. The oxidative stress index (OSI), lactate production, and HK activity were assessed using colorimetric assays. Western blot and quantitative PCR analyses were performed to determine HK-2 and TF expressions. Prothrombin time Tests additionally assessed the effect of IKA therapy on TF activation. Three over four significantly downregulated genes were identified after a specific analysis of the IKA's effect on HK-2 and TF in breast cancer cell lines. In the IKA treatment group, lactate production was markedly reduced ( P  < 0.05) and hexokinase activity was found to be reduced in all groups ( P  < 0.05, <0.01). Paclitaxel cytotoxicity independently causes lower OSI in all IKA-treated groups as compared to controls even though OSI is elevated in IKA groups compared to control. Molecular analysis results demonstrated significantly downregulated HK-2 and TF expressions at the protein level ( P  < 0.05, P  < 0.01). Partial thromboplastin time results also showed that IKA-treated cells had longer TF activation duration. A potential indirect association of HK-2 inhibition and TF regulation in breast cancer cells is put forward in this study by presenting IKA's bioactivation of breast cancer in all gene, protein, and enzyme levels.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"328-337"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063174","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
HER2 regulates autophagy and promotes migration in gastric cancer cells through the cGAS-STING pathway. HER2 通过 cGAS-STING 通路调节自噬并促进胃癌细胞的迁移。
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2025-01-28 DOI: 10.1097/CAD.0000000000001680
Panping Liang, Zedong Li, Zhengwen Chen, Zehua Chen, Fengjun He, Tao Jin, Yuwei Cao, Kun Yang

In gastric cancer, the relationship between human epidermal growth factor receptor 2 (HER2), the cyclic GMP-AMP synthase-stimulator of the interferon genes (cGAS-STING) pathway, and autophagy remains unclear. This study examines whether HER2 regulates autophagy in gastric cancer cells via the cGAS-STING signaling pathway, influencing key processes such as cell proliferation and migration. Understanding this relationship could uncover new molecular targets for diagnosis and treatment. Through lentiviral transfection, cell counting kit-8 assays, colony formation, transwell migration, scratch assays, and siRNA, we found that HER2 overexpression suppresses the cGAS-STING pathway, inhibits autophagy, and enhances the migratory ability of gastric cancer cells. In contrast, HER2 knockdown activates the cGAS-STING pathway, promotes autophagy, and reduces cell migration. We further observed that the inhibition of autophagy using chloroquine (CQ) increases the migration ability of HER2-overexpressing cells. Moreover, interfering with STING expression reversed the migration defects caused by HER2 knockdown, underscoring the critical role of the cGAS-STING pathway in HER2-regulated cell migration. We also revealed that high STING expression in gastric cancer is significantly associated with poor prognosis. STING expression was identified as an independent prognostic factor for survival (hazard ratio, 1.942; 95% confidence interval, 1.06-3.54; P  = 0.031). These results highlight the importance of HER2-driven regulation of autophagy through the cGAS-STING pathway in gastric cancer progression and its potential as a therapeutic target.

{"title":"HER2 regulates autophagy and promotes migration in gastric cancer cells through the cGAS-STING pathway.","authors":"Panping Liang, Zedong Li, Zhengwen Chen, Zehua Chen, Fengjun He, Tao Jin, Yuwei Cao, Kun Yang","doi":"10.1097/CAD.0000000000001680","DOIUrl":"10.1097/CAD.0000000000001680","url":null,"abstract":"<p><p>In gastric cancer, the relationship between human epidermal growth factor receptor 2 (HER2), the cyclic GMP-AMP synthase-stimulator of the interferon genes (cGAS-STING) pathway, and autophagy remains unclear. This study examines whether HER2 regulates autophagy in gastric cancer cells via the cGAS-STING signaling pathway, influencing key processes such as cell proliferation and migration. Understanding this relationship could uncover new molecular targets for diagnosis and treatment. Through lentiviral transfection, cell counting kit-8 assays, colony formation, transwell migration, scratch assays, and siRNA, we found that HER2 overexpression suppresses the cGAS-STING pathway, inhibits autophagy, and enhances the migratory ability of gastric cancer cells. In contrast, HER2 knockdown activates the cGAS-STING pathway, promotes autophagy, and reduces cell migration. We further observed that the inhibition of autophagy using chloroquine (CQ) increases the migration ability of HER2-overexpressing cells. Moreover, interfering with STING expression reversed the migration defects caused by HER2 knockdown, underscoring the critical role of the cGAS-STING pathway in HER2-regulated cell migration. We also revealed that high STING expression in gastric cancer is significantly associated with poor prognosis. STING expression was identified as an independent prognostic factor for survival (hazard ratio, 1.942; 95% confidence interval, 1.06-3.54; P  = 0.031). These results highlight the importance of HER2-driven regulation of autophagy through the cGAS-STING pathway in gastric cancer progression and its potential as a therapeutic target.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"306-318"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045264","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
Identification and validation of mitochondria-related LncRNA signatures as a novel prognostic model for glioma.
IF 1.8 4区 医学 Q3 ONCOLOGY Pub Date : 2025-04-01 Epub Date: 2025-01-14 DOI: 10.1097/CAD.0000000000001677
Kaihan Deng, Wei Zhao, Lin Dai, Zixuan Jing, Lixin Ma

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.

{"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":"<p><p>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.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":"36 4","pages":"297-305"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143575682","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
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Anti-Cancer Drugs
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