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Cancer-associated fibroblast cell surface markers as potential biomarkers or therapeutic targets in lung cancer. 作为肺癌潜在生物标记物或治疗靶点的癌症相关成纤维细胞表面标记物。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-09-10 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.55
Samaneh Tokhanbigli, Mehra Haghi, Kamal Dua, Brian Gregory George Oliver

Cancer-associated fibroblasts (CAFs) are the vital constituent of the tumor microenvironment, and in communication with other cells, they contribute to tumor progression and metastasis. Fibroblasts are the proposed origin of CAFs, which are mediated by pro-inflammatory cytokines and the recruitment of immune cells akin to wound healing. Although various studies have identified different subpopulations of CAFs in lung cancer, the heterogeneity of CAFs, particularly in lung cancer, and their potential as a therapeutic target remain largely unknown. Notwithstanding CAFs were previously thought to have predominantly tumor-promoting features, their pro- or anti-tumorigenic properties may depend on various conditions and cell origins. The absence of distinct markers to identify CAF subpopulations presents obstacles to the successful therapeutic targeting and treatment of CAFs in cancer. Human clinical and animal studies targeting CAFs have shown that targeting CAFs exacerbates the disease progression, suggesting that subpopulations of CAFs may exert opposing functions in cancer progression. Therefore, it is essential to pinpoint specific markers capable of characterizing these subpopulations and revealing their mechanisms of function. The cell-specific surface markers of CAFs will serve as an initial step in investigating precise CAF subpopulations and their role in diagnosing and targeting therapy against cancer-promoting CAF subsets in lung cancer.

癌症相关成纤维细胞(CAFs)是肿瘤微环境的重要组成部分,它们与其他细胞相互作用,促进了肿瘤的发展和转移。成纤维细胞是 CAFs 的起源,它由促炎细胞因子和免疫细胞招募介导,类似于伤口愈合。尽管各种研究发现了肺癌中不同的 CAFs 亚群,但 CAFs 的异质性(尤其是在肺癌中)及其作为治疗靶点的潜力在很大程度上仍不为人所知。尽管 CAFs 以前被认为主要具有肿瘤促进特征,但它们的促或抗肿瘤特性可能取决于各种条件和细胞来源。由于缺乏识别 CAF 亚群的独特标记物,成功靶向和治疗癌症中的 CAFs 遇到了障碍。以 CAFs 为靶点的人体临床和动物研究表明,以 CAFs 为靶点会加剧疾病的进展,这表明 CAFs 亚群可能在癌症进展中发挥相反的功能。因此,必须找出能够描述这些亚群特征并揭示其功能机制的特异性标记物。CAFs的细胞特异性表面标记物将成为研究精确CAF亚群及其在诊断和针对肺癌促癌CAF亚群的治疗中的作用的第一步。
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引用次数: 0
Research progress on the role and mechanism of circular RNA in drug resistance of head and neck squamous cell carcinoma. 环状 RNA 在头颈部鳞状细胞癌耐药性中的作用和机制的研究进展。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-09-02 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.57
Hongli Zeng, Junshang Ge, Yi Meng, Qian Wang, Mei Yang, Zhaoyang Zeng, Wei Xiong, Xuyu Zu

Drug resistance in tumors constitutes a significant obstacle to tumor therapy. Head and neck squamous cell carcinoma (HNSCC) presents a major challenge due to its deep anatomical location, limited space, and complex structure. These factors complicate surgical procedures and hinder the effectiveness of chemoradiotherapy, leading to poor prognosis and reduced quality of life. However, there is hope in the form of circular RNAs (circRNAs), non-coding RNA molecules with a closed-loop structure that exhibits superior stability and resistance to degradation compared to linear RNAs. Recent advances in high-throughput sequencing and bioinformatics technology revealed that circRNAs participate in tumor proliferation, invasion, migration, and drug resistance. This review aims to summarize current research progress on the involvement of circRNAs in drug resistance of HNSCC and provide valuable insights for the prevention and mitigation of drug resistance in HNSCC.

肿瘤的耐药性是肿瘤治疗的一大障碍。头颈部鳞状细胞癌(HNSCC)因其解剖位置深、空间有限、结构复杂而成为一大难题。这些因素使手术过程复杂化,阻碍了化放疗的效果,导致预后不良和生活质量下降。然而,环状 RNA(circRNA)的出现让人们看到了希望。环状 RNA 是一种非编码 RNA 分子,具有闭环结构,与线性 RNA 相比,具有更高的稳定性和抗降解性。高通量测序和生物信息学技术的最新进展表明,circRNAs 参与了肿瘤的增殖、侵袭、迁移和耐药性。本综述旨在总结目前关于 circRNAs 参与 HNSCC 耐药性的研究进展,为预防和缓解 HNSCC 耐药性提供有价值的见解。
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引用次数: 0
The role of circRNAs and miRNAs in drug resistance and targeted therapy responses in breast cancer. circRNA 和 miRNA 在乳腺癌耐药性和靶向治疗反应中的作用。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-08-20 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.62
Meilan Zhang, Zhaokuan Zheng, Shouliang Wang, Ruihan Liu, Mengli Zhang, Zhiyun Guo, Hao Wang, Weige Tan

MicroRNAs (miRNAs) are small non-coding RNAs comprising 19-24 nucleotides that indirectly control gene expression. In contrast to other non-coding RNAs (ncRNAs), circular RNAs (circRNAs) are defined by their covalently closed loops, forming covalent bonds between the 3' and 5' ends. circRNAs regulate gene expression by interacting with miRNAs at transcriptional or post-transcriptional levels. Accordingly, circRNAs and miRNAs control many biological events related to cancer, including cell proliferation, metabolism, cell cycle, and apoptosis. Both circRNAs and miRNAs are involved in the pathogenesis of diseases, such as breast cancer. This review focuses on the latest discoveries on dysregulated circRNAs and miRNAs related to breast cancer, highlighting their potential as biomarkers for clinical diagnosis, prognosis, and chemotherapy response.

微小 RNA(miRNA)是由 19-24 个核苷酸组成的小型非编码 RNA,可间接控制基因表达。与其他非编码 RNA(ncRNA)不同,环状 RNA(circRNA)的定义是其共价闭合环,在 3' 端和 5' 端之间形成共价键。因此,circRNAs 和 miRNAs 控制着许多与癌症有关的生物事件,包括细胞增殖、新陈代谢、细胞周期和细胞凋亡。circRNAs 和 miRNAs 都与乳腺癌等疾病的发病机制有关。本综述重点介绍与乳腺癌相关的循环RNA和miRNA失调的最新发现,强调它们作为临床诊断、预后和化疗反应生物标志物的潜力。
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引用次数: 0
The uniqueness of ABCB5 as a full transporter ABCB5FL and a half-transporter-like ABCB5β. ABCB5 作为全转运体 ABCB5FL 和半转运体类 ABCB5β 的独特性。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-08-07 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.56
Louise Gerard, Jean-Pierre Gillet

The ABCB5 gene encodes several isoforms, including two transporters (i.e., ABCB5FL, ABCB5β) and several soluble proteins, such as ABCB5α which has been hypothesized to have a regulatory function. ABCB5FL is a full ABC transporter and is expressed in the testis and prostate, whereas ABCB5β is an atypical half-transporter with a ubiquitous expression pattern. ABCB5β has been shown to mark cancer stem cells in several cancer types. In addition, ABCB5β and ABCB5FL have been shown to play a role in tumorigenesis and multidrug resistance. However, ABCB5β shares its entire protein sequence with ABCB5FL, making them difficult to distinguish. It cannot be excluded that some biological effects described for one transporter may be mediated by the other isoform. Therefore, it is difficult to interpret the available data and some controversies remain regarding their function in cancer cells. In this review, we discuss the data collected on ABCB5 isoforms over the last 20 years and propose a common ground on which we can build further to unravel the pathophysiological roles of ABCB5 transporters.

ABCB5 基因编码多种异构体,包括两种转运体(即 ABCB5FL 和 ABCB5β)和几种可溶性蛋白,如 ABCB5α,据推测它具有调节功能。ABCB5FL 是一种完全 ABC 转运体,在睾丸和前列腺中表达,而 ABCB5β 是一种非典型半转运体,其表达模式无处不在。研究表明,ABCB5β可标记几种癌症类型中的癌症干细胞。此外,ABCB5β和ABCB5FL还被证明在肿瘤发生和多药耐药性中发挥作用。然而,ABCB5β与ABCB5FL共享整个蛋白质序列,因此很难将它们区分开来。不能排除一种转运体的某些生物效应可能是由另一种异构体介导的。因此,很难解释现有的数据,关于它们在癌细胞中的功能仍存在一些争议。在这篇综述中,我们讨论了过去 20 年中收集到的有关 ABCB5 异构体的数据,并提出了一个共同点,在此基础上我们可以进一步揭示 ABCB5 转运体的病理生理作用。
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引用次数: 0
Unraveling the complexity of drug resistance mechanisms to SINE, T cell-engaging therapies and CELMoDs in multiple myeloma: a comprehensive review. 揭示多发性骨髓瘤中SINE、T细胞激活疗法和CELMoDs耐药机制的复杂性:综述。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-06-26 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.39
Jacqueline Schütt, Kerstin Brinkert, Andrzej Plis, Tino Schenk, Annamaria Brioli

Despite significant advances in the understanding of multiple myeloma (MM) biology and the development of novel treatment strategies in the last two decades, MM is still an incurable disease. Novel drugs with alternative mechanisms of action, such as selective inhibitors of nuclear export (SINE), modulators of the ubiquitin pathway [cereblon E3 ligase modulatory drugs (CELMoDs)], and T cell redirecting (TCR) therapy, have led to significant improvement in patient outcomes. However, resistance still emerges, posing a major problem for the treatment of myeloma patients. This review summarizes current data on treatment with SINE, TCR therapy, and CELMoDs and explores their mechanism of resistance. Understanding these resistance mechanisms is critical for developing strategies to overcome treatment failure and improve therapeutic outcomes.

尽管在过去二十年里,人们对多发性骨髓瘤(MM)生物学的认识和新型治疗策略的开发取得了重大进展,但MM仍然是一种无法治愈的疾病。具有替代作用机制的新型药物,如核输出选择性抑制剂(SINE)、泛素通路调节剂[脑龙E3连接酶调节药物(CELMoDs)]和T细胞重定向(TCR)疗法,已使患者的预后得到显著改善。然而,耐药性依然存在,给骨髓瘤患者的治疗带来了重大问题。本综述总结了目前有关SINE、TCR疗法和CELMoDs治疗的数据,并探讨了它们的耐药机制。了解这些耐药机制对于制定克服治疗失败和改善治疗效果的策略至关重要。
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引用次数: 0
Inhibition of glutaminolysis alone and in combination with HDAC inhibitor has anti-myeloma therapeutic effects. 单独或与 HDAC 抑制剂联合抑制谷氨酰胺分解具有抗骨髓瘤治疗效果。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-06-24 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.35
Seiichi Okabe, Yuko Tanaka, Mitsuru Moriyama, Akihiko Gotoh

Aim: This study aimed to investigate drug candidates and their efficacy in treating refractory multiple myeloma (MM) despite significant therapeutic advances and the introduction of novel agents. Our study focused on how myeloma cells mediate the metabolic pathways essential for survival. Therefore, we examined the role of glutaminolysis in this process. Methods: We investigated the role of glutaminolysis in myeloma cell growth. In addition, we analyzed the ability of CB-839 (telaglenastat), a glutaminase (GLS) inhibitor, to suppress myeloma cell proliferation and enhance the sensitivity to histone deacetylase (HDAC) inhibitors. Results: Glutamate deprivation significantly reduced MM cell proliferation. We observed an upregulation of GLS1 expression in MM cell lines compared to that in normal controls. CB-839 inhibits MM cell proliferation in a dose-dependent manner, resulting in enhanced cytotoxicity. Additionally, intracellular α-ketoglutarate and nicotinamide adenine dinucleotide phosphate levels decreased after CB-839 administration. Combining panobinostat with CB-839 resulted in enhanced cytotoxicity and increased caspase 3/7 activity. Cells transfected with GLS shRNA exhibited reduced cell viability and elevated sub-G1 phase according to cell cycle analysis results. Compared to control cells, these cells also showed increased sensitivity to panobinostat. Conclusion: Glutaminolysis contributes to the viability of MM cells, and the GLS inhibitor CB-839 has been proven to be an effective treatment for enhancing the cytotoxic effect of HDAC inhibition. These results are clinically relevant and suggest that CB-839 is a potential therapeutic candidate for patients with MM.

目的:本研究旨在调查候选药物及其在治疗难治性多发性骨髓瘤(MM)方面的疗效,尽管在治疗方面取得了重大进展并引入了新型药物。我们的研究重点是骨髓瘤细胞如何介导生存所必需的代谢途径。因此,我们研究了谷氨酰胺溶解在这一过程中的作用。研究方法我们研究了谷氨酰胺分解在骨髓瘤细胞生长中的作用。此外,我们还分析了谷氨酰胺酶(GLS)抑制剂 CB-839(替拉格纳司他)抑制骨髓瘤细胞增殖并提高其对组蛋白去乙酰化酶(HDAC)抑制剂敏感性的能力。研究结果谷氨酸剥夺能明显减少骨髓瘤细胞的增殖。与正常对照组相比,我们在 MM 细胞系中观察到 GLS1 表达上调。CB-839 以剂量依赖的方式抑制 MM 细胞增殖,从而增强细胞毒性。此外,服用 CB-839 后,细胞内的α-酮戊二酸和烟酰胺腺嘌呤二核苷酸磷酸酯水平下降。将帕诺比诺司他(panobinostat)与 CB-839 结合使用可增强细胞毒性并提高 caspase 3/7 活性。细胞周期分析结果显示,转染 GLS shRNA 的细胞存活率降低,亚 G1 期升高。与对照细胞相比,这些细胞对泛比诺司他的敏感性也有所提高。结论谷氨酰胺溶解有助于提高 MM 细胞的活力,而 GLS 抑制剂 CB-839 已被证明是增强 HDAC 抑制的细胞毒性效果的有效治疗方法。这些结果与临床相关,表明 CB-839 是 MM 患者的潜在候选治疗药物。
{"title":"Inhibition of glutaminolysis alone and in combination with HDAC inhibitor has anti-myeloma therapeutic effects.","authors":"Seiichi Okabe, Yuko Tanaka, Mitsuru Moriyama, Akihiko Gotoh","doi":"10.20517/cdr.2024.35","DOIUrl":"https://doi.org/10.20517/cdr.2024.35","url":null,"abstract":"<p><p><b>Aim:</b> This study aimed to investigate drug candidates and their efficacy in treating refractory multiple myeloma (MM) despite significant therapeutic advances and the introduction of novel agents. Our study focused on how myeloma cells mediate the metabolic pathways essential for survival. Therefore, we examined the role of glutaminolysis in this process. <b>Methods:</b> We investigated the role of glutaminolysis in myeloma cell growth. In addition, we analyzed the ability of CB-839 (telaglenastat), a glutaminase (GLS) inhibitor, to suppress myeloma cell proliferation and enhance the sensitivity to histone deacetylase (HDAC) inhibitors. <b>Results:</b> Glutamate deprivation significantly reduced MM cell proliferation. We observed an upregulation of GLS1 expression in MM cell lines compared to that in normal controls. CB-839 inhibits MM cell proliferation in a dose-dependent manner, resulting in enhanced cytotoxicity. Additionally, intracellular α-ketoglutarate and nicotinamide adenine dinucleotide phosphate levels decreased after CB-839 administration. Combining panobinostat with CB-839 resulted in enhanced cytotoxicity and increased caspase 3/7 activity. Cells transfected with GLS shRNA exhibited reduced cell viability and elevated sub-G1 phase according to cell cycle analysis results. Compared to control cells, these cells also showed increased sensitivity to panobinostat. <b>Conclusion:</b> Glutaminolysis contributes to the viability of MM cells, and the GLS inhibitor CB-839 has been proven to be an effective treatment for enhancing the cytotoxic effect of HDAC inhibition. These results are clinically relevant and suggest that CB-839 is a potential therapeutic candidate for patients with MM.</p>","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":"7 ","pages":"25"},"PeriodicalIF":4.6,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Recent advanced lipid-based nanomedicines for overcoming cancer resistance. 用于克服癌症抗药性的最新先进脂基纳米药物。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-06-21 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.19
Piroonrat Dechbumroong, Runjing Hu, Wisawat Keaswejjareansuk, Katawut Namdee, Xing-Jie Liang

The increasing prevalence of cancer drug resistance not only critically limits the efficiency of traditional therapies but also causes relapses or recurrences of cancer. Consequently, there remains an urgent need to address the intricate landscape of drug resistance beyond traditional cancer therapies. Recently, nanotechnology has played an important role in the field of various drug delivery systems for the treatment of cancer, especially therapy-resistant cancer. Among advanced nanomedicine technologies, lipid-based nanomaterials have emerged as effective drug carriers for cancer treatment, significantly improving therapeutic effects. Due to their biocompatibility, simplicity of preparation, and potential for functionalization, lipid-based nanomaterials are considered powerful competitors for resistant cancer. In this review, an overview of lipid-based nanomaterials for addressing cancer resistance is discussed. We summarize the recent progress in overcoming drug resistance in cancer by these lipid-based nanomaterials, and highlight their potential in future applications to reverse cancer resistance.

癌症耐药性的日益普遍不仅严重限制了传统疗法的效率,还会导致癌症复发或复发。因此,在传统癌症疗法之外,仍然迫切需要解决错综复杂的耐药性问题。最近,纳米技术在治疗癌症,尤其是耐药性癌症的各种给药系统领域发挥了重要作用。在先进的纳米医学技术中,脂基纳米材料已成为治疗癌症的有效药物载体,可显著提高治疗效果。由于脂基纳米材料具有生物相容性、制备简单、功能化潜力大等特点,被认为是抗药性癌症的有力竞争者。在这篇综述中,我们将概述用于解决癌症抗药性的脂基纳米材料。我们总结了这些脂基纳米材料在克服癌症耐药性方面的最新进展,并强调了它们在未来应用于逆转癌症耐药性方面的潜力。
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引用次数: 0
Emerging role of MYB transcription factors in cancer drug resistance. MYB 转录因子在癌症抗药性中的新作用。
Q1 ONCOLOGY Pub Date : 2024-04-30 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2023.158
Bernhard Biersack, Michael Höpfner

Decades ago, the viral myeloblastosis oncogene v-myb was identified as a gene responsible for the development of avian leukemia. However, the relevance of MYB proteins for human cancer diseases, in particular for solid tumors, remained basically unrecognized for a very long time. The human family of MYB transcription factors comprises MYB (c-MYB), MYBL2 (b-MYB), and MYBL1 (a-MYB), which are overexpressed in several cancers and are associated with cancer progression and resistance to anticancer drugs. In addition to overexpression, the presence of activated MYB-fusion proteins as tumor drivers was described in certain cancers. The identification of anticancer drug resistance mediated by MYB proteins and their underlying mechanisms are of great importance in understanding failures of current therapies and establishing new and more efficient therapy regimens. In addition, new drug candidates targeting MYB transcription factor activity and signaling have emerged as a promising class of potential anticancer therapeutics that could tackle MYB-dependent drug-resistant cancers in a more selective way. This review describes the correlation of MYB transcription factors with the formation and persistence of cancer resistance to various approved and investigational anticancer drugs.

几十年前,病毒性骨髓母细胞病致癌基因 v-myb 被确定为禽类白血病的致病基因。然而,MYB 蛋白与人类癌症疾病,尤其是实体瘤的相关性在很长一段时间内基本上仍未被认识到。人类 MYB 转录因子家族包括 MYB(c-MYB)、MYBL2(b-MYB)和 MYBL1(a-MYB)。除过表达外,某些癌症中还出现了作为肿瘤驱动因素的活化 MYB 融合蛋白。确定由 MYB 蛋白介导的抗癌药物耐药性及其内在机制,对于了解当前疗法的失败以及建立更有效的新疗法具有重要意义。此外,以 MYB 转录因子活性和信号转导为靶点的候选新药已成为一类前景广阔的潜在抗癌疗法,可以更有选择性地解决依赖 MYB 的耐药癌症问题。本综述介绍了 MYB 转录因子与癌症耐药性的形成和持续存在的相关性,以及各种已批准和正在研究的抗癌药物的耐药性。
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引用次数: 0
HER3-targeted therapy: the mechanism of drug resistance and the development of anticancer drugs. HER3靶向疗法:耐药机制与抗癌药物的开发。
Q1 ONCOLOGY Pub Date : 2024-04-29 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.11
Huilan Zeng, Wei Wang, Lin Zhang, Zhenghong Lin

Human epidermal growth factor receptor 3 (HER3), which is part of the HER family, is aberrantly expressed in various human cancers. Since HER3 only has weak tyrosine kinase activity, when HER3 ligand neuregulin 1 (NRG1) or neuregulin 2 (NRG2) appears, activated HER3 contributes to cancer development and drug resistance by forming heterodimers with other receptors, mainly including epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2). Inhibition of HER3 and its downstream signaling, including PI3K/AKT, MEK/MAPK, JAK/STAT, and Src kinase, is believed to be necessary to conquer drug resistance and improve treatment efficiency. Until now, despite multiple anti-HER3 antibodies undergoing preclinical and clinical studies, none of the HER3-targeted therapies are licensed for utilization in clinical cancer treatment because of their safety and efficacy. Therefore, the development of HER3-targeted drugs possessing safety, tolerability, and sensitivity is crucial for clinical cancer treatment. This review summarizes the progress of the mechanism of HER3 in drug resistance, the HER3-targeted therapies that are conducted in preclinical and clinical trials, and some emerging molecules that could be used as future designed drugs for HER3, aiming to provide insights for future research and development of anticancer drugs targeting HER3.

人类表皮生长因子受体 3(HER3)属于 HER 家族,在各种人类癌症中异常表达。由于 HER3 只具有微弱的酪氨酸激酶活性,当 HER3 配体神经胶质蛋白 1(NRG1)或神经胶质蛋白 2(NRG2)出现时,活化的 HER3 会与其他受体(主要包括表皮生长因子受体(EGFR)和人表皮生长因子受体 2(HER2))形成异二聚体,从而导致癌症发展和耐药性。抑制 HER3 及其下游信号转导,包括 PI3K/AKT、MEK/MAPK、JAK/STAT 和 Src 激酶,被认为是克服耐药性和提高治疗效率的必要条件。迄今为止,尽管有多种抗 HER3 抗体正在进行临床前和临床研究,但由于其安全性和有效性问题,还没有一种 HER3 靶向疗法被授权用于临床癌症治疗。因此,开发具有安全性、耐受性和敏感性的 HER3 靶向药物对于临床癌症治疗至关重要。本综述总结了HER3耐药机制的研究进展、已开展临床前和临床试验的HER3靶向疗法,以及一些可作为未来HER3设计药物的新兴分子,旨在为未来靶向HER3的抗癌药物研发提供启示。
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引用次数: 0
Dysregulation of calcium homeostasis in cancer and its role in chemoresistance. 癌症中的钙平衡失调及其在化疗抗药性中的作用。
Q1 ONCOLOGY Pub Date : 2024-03-15 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2023.145
Neema Kumari, Narasimha Pullaguri, Subha Narayan Rath, Ashish Bajaj, Vikas Sahu, Kranti Kiran Reddy Ealla

Globally, cancer, as a major public health concern, poses a severe threat to people's well-being. Advanced and specialized therapies can now cure the majority of people with early-stage cancer. However, emerging resistance to traditional and novel chemotherapeutic drugs remains a serious issue in clinical medicine. Chemoresistance often leads to cancer recurrence, metastasis, and increased mortality, accounting for 90% of chemotherapy failures. Thus, it is important to understand the molecular mechanisms of chemoresistance and find novel therapeutic approaches for cancer treatment. Among the several factors responsible for chemoresistance, calcium (Ca2+) dysregulation plays a significant role in cancer progression and chemoresistance. Therefore, targeting this derailed Ca2+ signalling for cancer therapy has become an emerging research area. Of note, the Ca2+ signal and its proteins are a multifaceted and potent tool by which cells achieve specific outcomes. Depending on cell survival needs, Ca2+ is either upregulated or downregulated in both chemosensitive and chemoresistant cancer cells. Consequently, the appropriate treatment should be selected based on Ca2+ signalling dysregulation. This review discusses the role of Ca2+ in cancer cells and the targeting of Ca2+ channels, pumps, and exchangers. Furthermore, we have emphasised the role of Ca2+ in chemoresistance and therapeutic strategies. In conclusion, targeting Ca2+ signalling is a multifaceted process. Methods such as site-specific drug delivery, target-based drug-designing, and targeting two or more Ca2+ proteins simultaneously may be explored; however, further clinical studies are essential to validate Ca2+ blockers' anti-cancer efficacy.

在全球范围内,癌症作为一种主要的公共健康问题,对人们的福祉构成了严重威胁。目前,先进的专业疗法可以治愈大多数早期癌症患者。然而,对传统和新型化疗药物产生的抗药性仍然是临床医学的一个严重问题。耐药性往往导致癌症复发、转移和死亡率上升,占化疗失败的 90%。因此,了解化疗耐药性的分子机制并找到新的癌症治疗方法非常重要。在导致化疗耐药性的几个因素中,钙(Ca2+)失调在癌症进展和化疗耐药性中起着重要作用。因此,针对这种脱轨的 Ca2+ 信号进行癌症治疗已成为一个新兴的研究领域。值得注意的是,Ca2+ 信号及其蛋白质是一种多方面的有效工具,细胞可通过它获得特定的结果。根据细胞生存的需要,Ca2+ 在化疗敏感和化疗耐药癌细胞中都会上调或下调。因此,应根据 Ca2+ 信号失调情况选择适当的治疗方法。本综述讨论了 Ca2+ 在癌细胞中的作用以及 Ca2+ 通道、泵和交换器的靶向作用。此外,我们还强调了 Ca2+ 在化疗耐药性和治疗策略中的作用。总之,靶向 Ca2+ 信号是一个多方面的过程。可探索的方法包括:特定部位给药、基于靶点的药物设计以及同时靶向两种或两种以上 Ca2+ 蛋白质;然而,进一步的临床研究对于验证 Ca2+ 阻滞剂的抗癌疗效至关重要。
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引用次数: 0
期刊
癌症耐药(英文)
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