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Emerging roles of small extracellular vesicles in metabolic reprogramming and drug resistance in cancers. 细胞外小泡在癌症代谢重编程和抗药性中的新作用。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-09-27 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.81
Jingcun Shi, Ying Shen, Jianjun Zhang

Studies of carcinogenic metabolism have shown that cancer cells have significant metabolic adaptability and that their metabolic dynamics undergo extensive reprogramming, which is a fundamental feature of cancer. The Warburg effect describes the preference of cancer cells for glycolysis over oxidative phosphorylation (OXPHOS), even under aerobic conditions. However, metabolic reprogramming in cancer cells involves not only glycolysis but also changes in lipid and amino acid metabolism. The mechanisms of these metabolic shifts are critical for the discovery of novel cancer therapeutic targets. Despite advances in the field of oncology, chemotherapy resistance, including multidrug resistance, remains a challenge. Research has revealed a correlation between metabolic reprogramming and anticancer drug resistance, but the underlying complex mechanisms are not fully understood. In addition, small extracellular vesicles (sEVs) may play a role in expanding metabolic reprogramming and promoting the development of drug resistance by mediating intercellular communication. The aim of this review is to assess the metabolic reprogramming processes that intersect with resistance to anticancer therapy, with particular attention given to the changes in glycolysis, lipid metabolism, and amino acid metabolism that accompany this phenomenon. In addition, the role of sEVs in disseminating metabolic reprogramming and promoting the development of drug-resistant phenotypes will be critically evaluated.

对致癌新陈代谢的研究表明,癌细胞具有很强的新陈代谢适应能力,其新陈代谢动态会发生广泛的重编程,这是癌症的一个基本特征。沃伯格效应描述了癌细胞对糖酵解的偏好,而不是氧化磷酸化(OXPHOS),即使在有氧条件下也是如此。然而,癌细胞的代谢重编程不仅涉及糖酵解,还包括脂质和氨基酸代谢的变化。这些代谢转变的机制对于发现新型癌症治疗靶点至关重要。尽管肿瘤学领域取得了进展,但化疗耐药性(包括多药耐药性)仍是一项挑战。研究发现,代谢重编程与抗癌药物耐药性之间存在相关性,但其背后的复杂机制尚未完全明了。此外,细胞外小泡(sEVs)可能通过介导细胞间通讯,在扩大代谢重编程和促进耐药性发展方面发挥作用。本综述旨在评估与抗癌治疗耐药性交织在一起的代谢重编程过程,尤其关注伴随这一现象出现的糖酵解、脂质代谢和氨基酸代谢的变化。此外,还将严格评估 sEV 在传播代谢重编程和促进耐药表型发展方面的作用。
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引用次数: 0
Competing endogenous RNAs (ceRNAs) and drug resistance to cancer therapy. 竞争性内源性 RNA(ceRNA)与癌症治疗的耐药性。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-09-25 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.66
Kenneth K W To, Hang Zhang, William C Cho

Competing endogenous RNAs (ceRNAs) are transcripts that possess highly similar microRNA response elements (MREs). microRNAs (miRNAs) are short, endogenous, single-stranded non-coding RNAs (ncRNAs) that can repress gene expression by binding to MREs on the 3' untranslated regions (UTRs) of the target mRNA transcripts to suppress gene expression by promoting mRNA degradation and/or inhibiting protein translation. mRNA transcripts, circular RNAs (circRNAs), long non-coding RNAs (lncRNAs), and transcribed pseudogenes could share similar MREs, and they can compete for the same pool of miRNAs. These ceRNAs may affect the level of one another by competing for their shared miRNAs. This interplay between different RNAs constitutes a ceRNA network, which regulates many important biological processes. Cancer drug resistance is a major factor leading to treatment failure in patients receiving chemotherapy. It can be acquired through genetic, epigenetic, and various tumor microenvironment mechanisms. The involvement of ceRNA crosstalk and its disruption in chemotherapy resistance is attracting attention in the cancer research community. This review presents an updated summary of the latest research on ceRNA dysregulation causing drug resistance across different cancer types and chemotherapeutic drug classes. Interestingly, accumulating evidence suggests that ceRNAs may be used as prognostic biomarkers to predict clinical response to cancer chemotherapy. Nevertheless, detailed experimental investigations of the putative ceRNA networks generated by computational algorithms are needed to support their translation for therapeutic and prognostic applications.

竞争性内源性 RNA(ceRNA)是指具有高度相似的 microRNA 响应元件(MRE)的转录本。microRNA(miRNA)是短的内源性单链非编码 RNA(ncRNA),可通过与目标 mRNA 转录本 3' 非翻译区(UTR)上的 MRE 结合抑制基因表达,从而通过促进 mRNA 降解和/或抑制蛋白质翻译来抑制基因表达。mRNA 转录本、环状 RNA(circRNA)、长非编码 RNA(lncRNA)和转录假基因可能共享相似的 MREs,它们可以竞争同一个 miRNA 池。这些 ceRNA 可通过竞争共享的 miRNA 而影响彼此的水平。不同 RNA 之间的这种相互作用构成了一个 ceRNA 网络,它调控着许多重要的生物过程。癌症耐药性是导致化疗患者治疗失败的一个主要因素。耐药性可通过遗传、表观遗传和各种肿瘤微环境机制获得。ceRNA串联及其在化疗耐药性中的作用正引起癌症研究界的关注。本综述对不同癌症类型和化疗药物类别中导致耐药性的 ceRNA 失调的最新研究进行了总结。有趣的是,越来越多的证据表明,ceRNA 可作为预后生物标志物来预测癌症化疗的临床反应。不过,还需要对计算算法生成的假定 ceRNA 网络进行详细的实验研究,以支持其在治疗和预后方面的应用。
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引用次数: 0
Screening of photosensitizers-ATP binding cassette (ABC) transporter interactions in vitro. 在体外筛选光敏剂-ATP 结合盒 (ABC) 转运体之间的相互作用。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-09-21 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.50
Shruti Vig, Payal Srivastava, Idrisa Rahman, Renee Jaranson, Anika Dasgupta, Robert Perttilä, Petteri Uusimaa, Huang-Chiao Huang

Aim: ATP-binding cassette (ABC) transporters are proteins responsible for the efflux of drug molecules from cancer cells, reducing the efficacy of anti-cancer treatments. This study assesses the susceptibility of a panel of clinically used photosensitizers to be transported by ABC transporters in vitro. Methods: The involvement of P-glycoprotein (P-gp/ABCB1), breast cancer resistance protein (BCRP/ABCG2), and multidrug resistance-associated protein 1 (MRP1/ABCC1) in the transport of 7 clinically utilized photosensitizers [benzoporphyrin derivative (BPD), temoporfin, redaporfin, talaporfin sodium, rose bengal, methylene blue, and indocyanine green] were investigated using human breast cancer cell lines following well-established protocols. Briefly, parental MCF-7 cells and sublines that overexpress P-gp (MCF-7 TX400), ABCG2 (MCF-7 MX100), or MRP1 (MCF-7/VP) were treated with photosensitizers with and without ABC transporter inhibitors. Intracellular levels of photosensitizers were measured using extraction method and flow cytometry to determine whether the ABC transporters are associated with efflux or uptake of photosensitizers. Results: The ABCG2 inhibitor (fumitremorgin C) and P-gp inhibitor (valspodar) effectively blocked the transport mediated by ABCG2 and P-gp of rose bengal and BPD. Redaporfin showed increased accumulation in the presence of valspodar with flow cytometry. Interestingly, MCF-7/VP cells were found to have reduced intracellular accumulation of rose bengal, which was restored with MRP1 inhibitor (MK571). The cell viability assay showed photodynamic therapy (PDT) resistance with Redaporfin in P-gp-overexpressing cells, BPD in ABCG2- and P-gp-overexpressing cells, and with Rose bengal in ABCG2-, P-gp- and MRP1-overexpressing cells, respectively. However, no change in intracellular retention was observed for other photosensitizers. Conclusion: In summary, our study provided new knowledge that temoporfin, talaporfin sodium, methylene blue, and indocyanine green are not substrates of ABCG2, P-gp, or MRP1. Redaporfin is a substrate for P-gp. BPD is a known substrate of ABCG2 and P-gp. Rose bengal is a substrate of ABCG2, P-gp, and MRP1. The results presented here indicate ABC transporter substrate status as a possible cause for cellular resistance to photodynamic therapy with rose bengal, redaporfin, and BPD.

目的:ATP 结合盒(ABC)转运体是一种蛋白质,负责将药物分子从癌细胞中排出,从而降低抗癌治疗的疗效。本研究评估了一组临床使用的光敏剂在体外被 ABC 转运体转运的敏感性。方法:采用人乳腺癌细胞系,按照成熟的方案研究了 P-糖蛋白(P-gp/ABCB1)、乳腺癌抗性蛋白(BCRP/ABCG2)和多药耐药性相关蛋白 1(MRP1/ABCC1)参与 7 种临床常用光敏剂[苯并卟啉衍生物(BPD)、替莫卟吩、瑞达泊芬、他拉泊芬钠、玫瑰红、亚甲蓝和吲哚菁绿]转运的情况。简而言之,亲代 MCF-7 细胞和过表达 P-gp(MCF-7 TX400)、ABCG2(MCF-7 MX100)或 MRP1(MCF-7/VP)的亚系细胞在使用或不使用 ABC 转运体抑制剂的情况下用光敏剂处理。使用萃取法和流式细胞术测量细胞内光敏剂的水平,以确定 ABC 转运体是否与光敏剂的外流或吸收有关。结果ABCG2抑制剂(fumitremorgin C)和P-gp抑制剂(valspodar)能有效阻断玫瑰红和BPD在ABCG2和P-gp介导下的转运。流式细胞术显示,在 valspodar 的存在下,Redaporfin 的积累增加。有趣的是,MCF-7/VP 细胞发现玫瑰红素在细胞内的蓄积减少了,而使用 MRP1 抑制剂(MK571)后又恢复了。细胞活力测定显示,P-gp 基因过表达细胞对 Redaporfin 的光动力疗法(PDT)耐药,ABCG2-和 P-gp 基因过表达细胞对 BPD 的光动力疗法耐药,ABCG2-、P-gp-和 MRP1 基因过表达细胞对玫瑰红的光动力疗法耐药。然而,其他光敏剂在细胞内的保留时间没有变化。结论总之,我们的研究提供了新的知识,即替莫泊芬、他拉泊芬钠、亚甲基蓝和吲哚菁绿不是 ABCG2、P-gp 或 MRP1 的底物。雷达波芬是 P-gp 的底物。BPD 是 ABCG2 和 P-gp 的已知底物。玫瑰红是 ABCG2、P-gp 和 MRP1 的底物。本文的研究结果表明,ABC 转运体底物状态可能是导致细胞对玫瑰红、redaporfin 和 BPD 光动力疗法产生耐药性的原因之一。
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引用次数: 0
Intercellular transfer of multidrug resistance mediated by extracellular vesicles. 由细胞外囊泡介导的多药耐药性细胞间转移。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-09-21 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.84
Anxiang Yang, Hui Sun, Xiaokun Wang

Multidrug resistance (MDR) poses a formidable obstacle in cancer treatment, enabling cancer cells to evade the cytotoxic effects of chemotherapeutic drugs through various mechanisms. These mechanisms include intrinsic resistance, which is present prior to treatment, and acquired resistance, which develops after exposure to chemotherapy agents. Small membrane-bound vesicles, known as extracellular vesicles (EVs), are crucial in intercellular signaling as they transport bioactive molecules that can modify the characteristics and functions of recipient cells. Recent research highlights EVs as pivotal players in fostering drug resistance. This review focuses on the intercellular transfer of MDR from donor cells to susceptible recipient cells through specific cargo in EVs, such as ATP-binding cassette (ABC) transporter proteins, nucleic acids, and other regulatory factors. Additionally, the features of intercellular communication mediated by EVs are also discussed. Gaining insight into these mechanisms is essential for developing strategies to counteract resistance and improve the effectiveness of cancer treatments.

多药耐药性(MDR)是癌症治疗中的一个巨大障碍,它使癌细胞能够通过各种机制逃避化疗药物的细胞毒性作用。这些机制包括治疗前就存在的内在耐药性和接触化疗药物后产生的获得性耐药性。被称为细胞外囊泡(EVs)的膜结合小囊泡在细胞间信号传递中至关重要,因为它们运输的生物活性分子可以改变受体细胞的特性和功能。最近的研究强调,EVs 是产生耐药性的关键因素。本综述重点探讨了 MDR 通过 EV 中的特定货物(如 ATP 结合盒 (ABC) 转运蛋白、核酸和其他调节因子)从供体细胞向易感受体细胞的细胞间转移。此外,还讨论了由 EVs 介导的细胞间通信的特点。深入了解这些机制对于开发抗药性策略和提高癌症治疗效果至关重要。
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引用次数: 0
Non-coding RNA and drug resistance in head and neck cancer. 头颈癌中的非编码 RNA 和耐药性。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-09-20 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.59
Yulong Zhang, Yingming Peng, Bingqin Lin, Shuai Yang, Feiqiang Deng, Xuan Yang, An Li, Wanyi Xia, Chenxi Gao, Shaona Lei, Wei Liao, Qi Zeng

Head and neck cancer (HNC) is ranked as the sixth most common malignant tumor, and the overall survival rate with current treatment options remains concerning, primarily due to drug resistance that develops following antitumor therapy. Recent studies indicate that non-coding RNAs play a crucial role in drug resistance among HNC patients. This article systematically reviews the current research landscape, explores novel targets and treatment strategies related to non-coding RNAs and HNC resistance, raises some unresolved issues, and discusses five promising research directions in this field: ferroptosis, nanomedicine, exosomes, proteolysis-targeting chimeras (PROTACs), and artificial intelligence. We hope that our work will contribute to advancing research on overcoming HNC resistance through the regulation of non-coding RNAs.

头颈癌(HNC)被列为第六大常见恶性肿瘤,目前的治疗方案的总体生存率仍然令人担忧,这主要是由于抗肿瘤治疗后产生的耐药性。最近的研究表明,非编码 RNA 在 HNC 患者的耐药性中起着至关重要的作用。本文系统回顾了当前的研究现状,探讨了与非编码 RNA 和 HNC 耐药性相关的新靶点和治疗策略,提出了一些尚未解决的问题,并讨论了该领域五个前景广阔的研究方向:铁肽化、纳米药物、外泌体、蛋白酶靶向嵌合体 (PROTAC) 和人工智能。我们希望我们的工作将有助于推动通过调控非编码 RNA 克服 HNC 抗性的研究。
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引用次数: 0
Current applications of tumor local ablation (TLA) combined with immune checkpoint inhibitors in breast cancer treatment. 肿瘤局部消融(TLA)联合免疫检查点抑制剂在乳腺癌治疗中的应用现状。
IF 4.6 Q1 ONCOLOGY Pub Date : 2024-09-13 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2024.77
Lingpeng Tang, Dandan Wang, Ting Hu, Xiaoying Lin, Songsong Wu

Breast cancer is one of the most common cancers in women globally, posing significant challenges to treatment because of the diverse and complex pathological and molecular subtypes. The emergence of immune checkpoint inhibitors (ICIs) has revolutionized the treatment of breast cancer, particularly for triple-negative breast cancer (TNBC), significantly improving patient outcomes. However, the overall tumor response rate remains suboptimal due to drug resistance to ICIs. This resistance is primarily due to the immune-suppressive tumor microenvironment (TME), tumor cells' ability to evade immune surveillance, and other complex immune regulatory mechanisms. To address these challenges, clinical researchers are actively exploring combinatorial therapeutic strategies with ICIs. Tumor local ablation (TLA) technology is anticipated to overcome resistance to ICIs and enhance therapeutic efficacy by ablating tumor tissue, releasing tumor antigens, remodeling the TME, and stimulating local and systemic immune responses. Combination therapy with TLA and ICIs has demonstrated promising results in preclinical breast cancer studies, underscoring the feasibility and importance of addressing drug resistance mechanisms in breast cancer. This provides novel strategies for breast cancer treatment and is expected to drive further advancements in the field.

乳腺癌是全球妇女最常见的癌症之一,由于其病理和分子亚型的多样性和复杂性,给治疗带来了巨大挑战。免疫检查点抑制剂(ICIs)的出现彻底改变了乳腺癌的治疗,尤其是三阴性乳腺癌(TNBC)的治疗,显著改善了患者的预后。然而,由于对 ICIs 的耐药性,总体肿瘤反应率仍不理想。这种耐药性主要是由于免疫抑制性肿瘤微环境(TME)、肿瘤细胞逃避免疫监视的能力以及其他复杂的免疫调节机制造成的。为了应对这些挑战,临床研究人员正在积极探索 ICIs 的组合治疗策略。肿瘤局部消融(TLA)技术有望通过消融肿瘤组织、释放肿瘤抗原、重塑 TME 以及刺激局部和全身免疫反应来克服 ICIs 的抗药性并提高疗效。在乳腺癌临床前研究中,TLA 与 ICIs 的联合疗法取得了令人鼓舞的结果,突出了解决乳腺癌耐药机制的可行性和重要性。这为乳腺癌治疗提供了新策略,有望推动该领域的进一步发展。
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引用次数: 0
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
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