异常调控的长非编码 RNA (lncRNA) 在癌症中的功能强调了它们作为癌症治疗干预的潜在靶点的潜力。 LncRNA ASBEL 已被确定为癌基因，也是三阴性乳腺癌 (TNBC) 中 BTG3 肿瘤抑制基因的反义转录本。在此，基于生物活性透明质酸聚电解质 (CANP) 的多组分自组装聚电解质纳米复合物 (CANP) HA）和盐酸壳聚糖（CS）被设计和制备用于与antago3协同调节致癌lncRNA ASBEL，antago3是一种针对lncRNA ASBEL的寡核苷酸拮抗剂和疏水性姜黄素（Cur）共同递送，用于协同TNBC治疗。 Antago3 和 Cur 共掺 CANP 是通过非共价静电相互作用、氢键和疏水相互作用的一步组装策略实现的。此外，多组分组装的 CANP 还额外装饰有近红外荧光 (NIRF) Cy-5.5 染料 (FCANP)，用于同步 NIRF 成像和治疗监测性能。结果，MDA-MB-231细胞的增殖、迁移和侵袭被有效抑制，并且具有协调模式的FCANP诱导最高的凋亡率。在分子水平上，可以观察到lncRNA ASBEL/BTG3的有效调节以及Bcl-2和c-Met途径的同步调节。正如预期的那样，全身施用FCANP导致近红外荧光信号和Cur在体内有针对性地优先积累肿瘤组织。更有吸引力的是，系统性 FCANP 介导的协同调节 lncRNA ASBEL/BTG3 和 Cur 共同递送显着抑制了 MDA-MB-231 异种移植肿瘤的生长，抑制了转移并延长了生存率，且全身毒性可忽略不计。我们目前的研究代表了一种有效的方法，可以开发一种有前景的治疗诊断平台，以联合治疗模式对抗 TNBC。© 2023。作者。

Abnormally regulated long non-coding RNAs (lncRNAs) functions in cancer emphasize their potential to serve as potential targets for cancer therapeutic intervention. LncRNA ASBEL has been identified as oncogene and an anti-sense transcript of tumor-suppressor gene of BTG3 in triple-negative breast cancer (TNBC).Herein, multicomponent self-assembled polyelectrolyte nanocomplexes (CANPs) based on the polyelectrolytes of bioactive hyaluronic acid (HA) and chitosan hydrochloride (CS) were designed and prepared for the collaborative modulation of oncogenic lncRNA ASBEL with antago3, an oligonucleotide antagonist targeting lncRNA ASBEL and hydrophobic curcumin (Cur) co-delivery for synergetic TNBC therapy. Antago3 and Cur co-incorporated CANPs were achieved via a one-step assembling strategy with the cooperation of noncovalent electrostatic interactions, hydrogen-bonding, and hydrophobic interactions. Moreover, the multicomponent assembled CANPs were ulteriorly decorated with a near-infrared fluorescence (NIRF) Cy-5.5 dye (FCANPs) for synchronous NIRF imaging and therapy monitoring performance. Resultantly, MDA-MB-231 cells proliferation, migration, and invasion were efficiently inhibited, and the highest apoptosis ratio was induced by FCANPs with coordination patterns. At the molecular level, effective regulation of lncRNA ASBEL/BTG3 and synchronous regulation of Bcl-2 and c-Met pathways could be observed.As expected, systemic administration of FCANPs resulted in targeted and preferential accumulation of near-infrared fluorescence signal and Cur in the tumor tissue. More attractively, systemic FCANPs-mediated collaborative modulating lncRNA ASBEL/BTG3 and Cur co-delivery significantly suppressed the MDA-MB-231 xenograft tumor growth, inhibited metastasis and extended survival rate with negligible systemic toxicity. Our present study represented an effective approach to developing a promising theranostic platform for combating TNBC in a combined therapy pattern.© 2023. The Author(s).