Biochemical and biophysical research communications最新文献_第8页

ALB suppresses epithelial-mesenchymal transition and glycolysis via SPARC regulation in metastatic clear cell renal cell carcinoma ALB通过SPARC调控抑制转移性透明细胞肾细胞癌的上皮-间质转化和糖酵解

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-21 DOI: 10.1016/j.bbrc.2026.153333

Wei Wang , Liuyang Shu , Sheng Xu , Xudong Jiang

Background

The most prevalent subtype of renal cell carcinoma is clear cell renal cell carcinoma (ccRCC). Approximately 20–30 % of ccRCC patients develop metastatic clear cell renal cell carcinoma (mccRCC), characterized by aggressive tumor behavior and resistance to conventional therapies. Identification of critical hub genes involved in mccRCC progression is essential for advancing clinical management.

Methods

Differentially expressed genes (DEGs) about ccRCC were identified by integrated analysis of four public datasets. Protein-protein interaction (PPI) network and topological analyses were executed to pinpoint hub genes. Functional assays, including quantitative real-time PCR, proliferation, Western blotting, transwell assays, and Seahorse metabolic flux analysis, were performed in ccRCC cell lines.

Results

Albumin (ALB) was recognized as a hub gene consistently downregulated in ccRCC and mccRCC cell lines. ALB expression proved a strong correlation with tumor stage, metastasis, and histological grade. Functional experiments demonstrated that ALB suppressed proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in primary and metastatic ccRCC. Mechanistically, ALB showed a negative association with SPARC, which could potentially influence EMT progression. Metabolomic and glycolytic flux analyses revealed that ALB overexpression reprogrammed glycolysis by reducing glycolytic intermediates, glucose uptake, and lactate production. Silencing ALB enhanced glycolysis and malignant phenotypes, which were reversed by glycolysis inhibition or SPARC knockdown.

Conclusion

ALB is associated with reduced proliferation, EMT, and glycolytic activity in mccRCC, potentially through its negative association with SPARC. This study provides novel insights into mccRCC pathogenesis and identifies ALB as a potential diagnostic biomarker and therapeutic target.

肾细胞癌中最常见的亚型是透明细胞肾细胞癌（ccRCC）。大约20 - 30%的ccRCC患者发展为转移性透明细胞肾细胞癌（mccRCC），其特点是肿瘤行为具有侵袭性，对常规治疗具有耐药性。鉴定参与mccRCC进展的关键枢纽基因对于推进临床管理至关重要。方法通过对4个公开数据集的综合分析，鉴定ccRCC的差异表达基因（DEGs）。通过蛋白-蛋白相互作用（PPI）网络和拓扑分析确定中心基因。在ccRCC细胞系中进行功能检测，包括实时荧光定量PCR、增殖、Western blotting、transwell检测和海马代谢通量分析。结果在ccRCC和mccRCC细胞系中，白蛋白（ALB）被认为是一个持续下调的枢纽基因。ALB表达与肿瘤分期、转移和组织学分级密切相关。功能实验表明，ALB抑制原发性和转移性ccRCC的增殖、迁移、侵袭和上皮-间质转化（EMT）。从机制上讲，ALB与SPARC呈负相关，这可能会影响EMT的进展。代谢组学和糖酵解通量分析显示，ALB过表达通过减少糖酵解中间体、葡萄糖摄取和乳酸生成来重编程糖酵解。沉默ALB可增强糖酵解和恶性表型，而糖酵解抑制或SPARC敲低可逆转这些表型。结论alb与mccRCC的增殖、EMT和糖酵解活性降低有关，可能与SPARC呈负相关。这项研究为mccRCC的发病机制提供了新的见解，并确定了ALB作为潜在的诊断生物标志物和治疗靶点。

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引用次数: 0

Live-cell atomic force microscopy nanoprofiling reveals protease-responsive membrane protein dynamics and cell-type-specific surface codes 活细胞原子力显微镜纳米谱揭示了蛋白酶响应膜蛋白动力学和细胞类型特异性表面代码

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-21 DOI: 10.1016/j.bbrc.2026.153338

Xueyan Liu , Lin Liu

Cell membranes, as phospholipid-protein interfaces, regulate cellular recognition and communication. However, real-time nanoscale observation of native membrane proteins in live cells remains challenging. Here, we employed atomic force microscopy (AFM) to characterize the surface properties of live HeLa cells, and found that mild trypsin digestion reduced significantly surface roughness (Rq: ∼150 → 120 nm) and adhesion force (∼27 → 20 pN), whereas chemical fixation obscured these dynamic changes. Comparative AFM imaging across four cell lines revealed distinct topographies: MCF-7 cancer cells exhibited the highest surface roughness (Rq = 212 nm), versus smoother morphology of NIH-3T3 fibroblasts (Rq = 172 nm). These findings demonstrate that nanoscale surface morphology encodes cell identity, functional state, and malignancy, with increased roughness reflecting complex membrane protein organization. Live-cell AFM thus decodes membrane protein dynamics and cell-type-specific surface codes, offering a powerful platform for physiological studies and translational applications in biology, cancer research, neuroscience, and drug development.

细胞膜作为磷脂-蛋白界面，调节细胞识别和通讯。然而，活细胞中天然膜蛋白的实时纳米级观察仍然具有挑战性。在这里，我们使用原子力显微镜（AFM）来表征活HeLa细胞的表面特性，发现温和的胰蛋白酶消化显著降低了表面粗糙度（Rq: ~ 150→120 nm）和粘附力（~ 27→20 pN），而化学固定掩盖了这些动态变化。比较四种细胞系的AFM成像显示出不同的地形：MCF-7癌细胞表现出最高的表面粗糙度（Rq = 212 nm），而NIH-3T3成纤维细胞的表面粗糙度（Rq = 172 nm）更光滑。这些发现表明，纳米级表面形态编码细胞身份、功能状态和恶性，粗糙度增加反映了复杂的膜蛋白组织。因此，活细胞AFM解码膜蛋白动力学和细胞类型特异性表面密码，为生理研究和生物学、癌症研究、神经科学和药物开发中的转化应用提供了一个强大的平台。

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引用次数: 0

Corrigendum to “Effect of L-theanine on the hippocampus, cerebral cortex and cerebellum of doxorubicin-treated rats” [Biochem. Biophys. Res. Commun.797 (2026) 153216] “l -茶氨酸对阿霉素治疗大鼠海马、大脑皮层和小脑的影响”的更正[生物化学]。Biophys。[Res. com .797(2026) 153216]。

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-21 DOI: 10.1016/j.bbrc.2026.153314

Birgül Kural , Sevil Kör , Meltem Arıkan Malkoç , Hilal Öztürk , Tenzile Beyza Durmuş , Esin Yuluğ , Selcen Aydın-Abidin , İsmail Abidin , Asım Örem

引用次数: 0

The role of the TLR2 gene in regulating proliferation of rabbit dermal papilla cells TLR2基因在兔真皮乳头细胞增殖调控中的作用

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-21 DOI: 10.1016/j.bbrc.2026.153323

Yu Zhou , Bohao Zhao , Shaoning Sun , Xiaoman Han , Yongqi Yu , Jinbao Li , Yang Chen , Xinsheng Wu

Hair follicle (HF) morphogenesis, growth, and regeneration are fundamentally governed by reciprocal interactions between the epidermal and dermal compartments of the skin, with dermal papilla cells (DPCs) serving as a central regulatory element in this process. Here, the functional role of Toll-like receptor 2 (TLR2) in the control of DPC proliferation was investigated. The coding sequence (CDS) of the rabbit TLR2 gene was successfully cloned and subjected to preliminary bioinformatics analyses to characterize its predicted structural and functional features. Gain- and loss-of-function experiments demonstrated that modulation of TLR2 expression significantly altered the transcription of HF growth- and development-associated genes, including BCL2, CCND1, CTNNB1, FGF2, and TGFβ. Functional assays, including CCK-8 proliferation analysis, EdU incorporation, and immunostaining for proliferating cell nuclear antigen (PCNA), consistently showed that TLR2 overexpression markedly enhanced DPC proliferation, whereas TLR2 knockdown exerted a pronounced inhibitory effect. These results provide mechanistic insight into the role of TLR2 in regulating DPC proliferation and offer a theoretical basis for further investigations into its contribution to hair follicle biology.

毛囊（HF）的形态发生、生长和再生从根本上是由皮肤表皮和真皮间室之间的相互作用所控制的，真皮乳头细胞（DPCs）在这一过程中起着中心调节作用。本研究探讨toll样受体2 （TLR2）在控制DPC增殖中的功能作用。成功克隆了兔TLR2基因的编码序列（CDS），并进行了初步的生物信息学分析，以表征其预测的结构和功能特征。功能增益和功能丧失实验表明，TLR2表达的调节显著改变了HF生长和发育相关基因的转录，包括BCL2、CCND1、CTNNB1、FGF2和TGFβ。功能分析，包括CCK-8增殖分析、EdU掺入和增殖细胞核抗原（PCNA）的免疫染色，一致表明TLR2过表达显著增强DPC增殖，而TLR2敲低具有明显的抑制作用。这些结果为TLR2在调控DPC增殖中的作用提供了机制认识，并为进一步研究其在毛囊生物学中的作用提供了理论基础。

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引用次数: 0

DLST mediates the malignant progression of osteosarcoma cells by regulating the p38 MAPK signaling pathway DLST通过调节p38 MAPK信号通路介导骨肉瘤细胞的恶性进展

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-21 DOI: 10.1016/j.bbrc.2026.153341

Chong Guo , Kaiqiong Liao , Kai Xu , Jiongfeng Zhang , Guanglong Chen , Xiaohui Luo , Jun Yang , Zhengzai Dai , Xiao-Bin Lv , Feifei Zhang , Zhiping Zhang

Background

This research investigates the function of dihydrolipoic acid succinyltransferase (DLST) in the initiation and progression of osteosarcoma.

Methods

Cellular functions were assessed using CCK-8, colony formation, scratch assays, transwell assays, and flow cytometry. The expression of relevant genes at both mRNA and protein levels was detected using quantitative real-time PCR (qRT-PCR) and Western blotting techniques. The regulatory mechanism of DLST was analyzed through RNA-sequencing. Finally, tumor growth in vivo was evaluated using established animal models.

Results

DLST was highly expressed in osteosarcoma. Knockdown of DLST limited the proliferative, migratory, invasive, and anti-apoptotic abilities of osteosarcoma cells. RNA-seq was employed to analyze its mechanism, which showed that DLST can influence the p38 MAPK signaling pathway. Functional validation further showed that the p38 MAPK signaling pathway inhibitor was able to reverse the malignant functional changes in osteosarcoma cells that had been caused by DLST knockdown. Finally, in in vivo experiments, knocking down the DLST gene in the osteosarcoma animal model slowed down tumor growth.

Conclusion

In this study, we found that DLST promotes the proliferation, migration, invasion, anti-apoptosis of osteosarcoma cells, as well as tumor growth, regulated through the p38 MAPK signaling pathway. These results could offer novel and valuable perspectives for the clinical management of osteosarcoma.

本研究探讨了二氢硫辛酸琥珀基转移酶（DLST）在骨肉瘤发生和发展中的作用。方法采用CCK-8、菌落形成、划痕法、transwell法和流式细胞术检测细胞功能。采用实时荧光定量PCR （qRT-PCR）和Western blotting技术检测相关基因在mRNA和蛋白水平上的表达。通过rna测序分析DLST的调控机制。最后，利用已建立的动物模型评估肿瘤在体内的生长情况。结果dlst在骨肉瘤中高表达。DLST的下调限制了骨肉瘤细胞的增殖、迁移、侵袭和抗凋亡能力。通过RNA-seq分析其作用机制，发现DLST可以影响p38 MAPK信号通路。功能验证进一步表明，p38 MAPK信号通路抑制剂能够逆转由DLST敲低引起的骨肉瘤细胞的恶性功能变化。最后，在体内实验中，敲除骨肉瘤动物模型中的DLST基因可以减缓肿瘤的生长。结论本研究发现DLST通过p38 MAPK信号通路调控，促进骨肉瘤细胞增殖、迁移、侵袭、抗凋亡及肿瘤生长。这些结果可以为骨肉瘤的临床治疗提供新的和有价值的观点。

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引用次数: 0

Neuropeptide INS-14 modulates apoptotic cell clearance in Caenorhabditis elegans 神经肽INS-14调节秀丽隐杆线虫凋亡细胞的清除

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-21 DOI: 10.1016/j.bbrc.2026.153337

Yunmin Xie , Lu Chen , Fuqiao Liu, Qian Zheng, Lei Yuan, Hui Xiao, Hui Wang

Apoptosis, a principal form of programmed cell death, is integral to animal development. Neuropeptides, which are crucial signaling molecules in the nervous system, play roles in various physiological and behavioral processes. Until now, there has been no evidence of neuropeptides being involved in the clearance of apoptotic cells. Consequently, utilizing Caenorhabditis elegans—an exemplary model organism for investigating apoptosis and its regulatory mechanisms—we performed a comprehensive functional screening of neuropeptide genes via RNA interference (RNAi) technology to identify pivotal neuropeptide genes involved in apoptosis and apoptotic cell clearance. C. elegans possesses 113 neuropeptide genes. Our screening identified 9 neuropeptide genes as preliminary regulators of apoptosis, with 2 neuropeptide genes specifically involved in apoptotic cell clearance. Among these, the neuropeptide gene ins-14 exhibited the most significant regulatory phenotype. Further mechanistic investigations revealed that, during the late stage of apoptotic cell clearance, disruptions in ins-14 function markedly affect the recruitment efficiency of the key protein LAAT-1 to phagosomes and disrupt the normal acidification process within phagosomes. Moreover, we found that ins-14 modulated laat-1 expression at the transcriptional level. This study is the first to elucidate the regulatory role of neuropeptides in apoptotic cell clearance in C. elegans, offering novel experimental evidence for a more profound understanding of neuropeptide-mediated apoptotic regulatory networks.

细胞凋亡是细胞程序性死亡的主要形式，是动物发育过程中不可或缺的一部分。神经肽是神经系统中重要的信号分子，在各种生理和行为过程中发挥重要作用。到目前为止，还没有证据表明神经肽参与凋亡细胞的清除。因此，我们利用秀丽隐杆线虫——研究细胞凋亡及其调控机制的典型模式生物——通过RNA干扰（RNAi）技术对神经肽基因进行了全面的功能筛选，以确定参与细胞凋亡和凋亡细胞清除的关键神经肽基因。秀丽隐杆线虫具有113个神经肽基因。我们的筛选确定了9个神经肽基因作为细胞凋亡的初步调节因子，其中2个神经肽基因特异性参与凋亡细胞清除。其中，神经肽基因in -14表现出最显著的调控表型。进一步的机制研究表明，在凋亡细胞清除的后期，in -14功能的破坏显著影响关键蛋白LAAT-1向吞噬体的招募效率，并破坏吞噬体内正常的酸化过程。此外，我们发现in -14在转录水平上调节laat-1的表达。本研究首次阐明了神经肽在秀丽隐杆线虫凋亡细胞清除中的调节作用，为更深入地了解神经肽介导的凋亡调节网络提供了新的实验证据。

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引用次数: 0

Nonsteroidal mineralocorticoid receptor antagonist finerenone ameliorates cardiac hypertrophy with increasing glucocorticoid signaling sensitivity 非甾体矿物皮质激素受体拮抗剂细烯酮通过增加糖皮质激素信号敏感性改善心脏肥厚

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-21 DOI: 10.1016/j.bbrc.2026.153332

Kei Morikawa , Yuichiro Arima , Takumi Nagakura , Yuqing Xu , Akira Fujiyama , Miho Kataoka , Shinsuke Hanatani , Yasushi Matsuzawa , Yasuhiro Izumiya , Eiichiro Yamamoto , Kenichi Tsujita

Background

Nonsteroidal mineralocorticoid receptor antagonists (MRAs) have emerged as promising therapies for cardiovascular disease. Finerenone, a highly selective nonsteroidal MRA, has shown efficacy in slowing the progression of heart failure with mildly reduced or preserved ejection fraction, as demonstrated in the FINEARTS-HF trial. However, its mechanisms of action, particularly in heart failure with preserved ejection fraction (HFpEF), remain poorly understood.

Methods

We established a murine model of HFpEF characterized by obesity, metabolic dysfunction-associated fatty liver disease, type 2 diabetes, and hypertension-induced cardiac hypertrophy. This was induced through long-term administration of a high-fat, high-fructose diet combined with NG-nitro-l-arginine methyl ester (l-NAME). Finerenone was administered during the early stage of myocardial remodeling, coinciding with the first histological evidence of cardiac hypertrophy. Cardiac function and structure were evaluated using transthoracic echocardiography, 24-h ambulatory blood pressure monitoring, and histological analysis. To investigate cardiomyocyte-specific transcriptional changes, we performed RNA sequencing on isolated cardiomyocyte nuclei.

Results

Fifteen weeks of combined metabolic and hypertensive stress resulted in obesity, glucose intolerance, hypertension, reduced exercise capacity, and myocardial hypertrophy. Finerenone, administered during the final two weeks, significantly attenuated myocardial hypertrophy without affecting systemic blood pressure. Cardiomyocyte-specific transcriptomic analysis revealed downregulation of hypertrophic gene expression and upregulation of glucocorticoid receptor (GR)-responsive genes.

Conclusions

Finerenone alleviates early-stage cardiac hypertrophy in a murine HFpEF model driven by metabolic and hemodynamic stress. Its cardioprotective effects appear to be independent of systemic blood pressure reduction and may involve modulation of GR signaling pathways in cardiomyocytes.

背景：非甾体矿物皮质激素受体拮抗剂（MRAs）已成为治疗心血管疾病的有希望的治疗方法。Finerenone是一种高度选择性的非甾体MRA， FINEARTS-HF试验表明，Finerenone在减缓心力衰竭进展并轻度降低或保留射血分数方面有效。然而，其作用机制，特别是在保留射血分数的心力衰竭（HFpEF）中，仍然知之甚少。方法建立以肥胖、代谢功能障碍相关脂肪性肝病、2型糖尿病和高血压性心肌肥厚为特征的HFpEF小鼠模型。这是通过长期服用高脂肪、高果糖饮食和ng-硝基-l-精氨酸甲酯（l-NAME）诱导的。在心肌重构早期给予芬尼酮，与心肌肥厚的第一个组织学证据一致。采用经胸超声心动图、24小时动态血压监测和组织学分析评估心功能和结构。为了研究心肌细胞特异性转录变化，我们对分离的心肌细胞核进行了RNA测序。结果15周的代谢和高血压联合应激导致肥胖、葡萄糖耐受不良、高血压、运动能力下降和心肌肥大。在最后两周给予芬尼酮，显著减轻心肌肥厚而不影响全身血压。心肌细胞特异性转录组学分析显示，肥厚基因表达下调，糖皮质激素受体（GR）应答基因上调。结论芬烯酮可减轻代谢和血流动力学应激引起的小鼠HFpEF模型早期心肌肥厚。它的心脏保护作用似乎与全身血压降低无关，可能涉及心肌细胞中GR信号通路的调节。

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引用次数: 0

Localization of Asgard archaeal ESCRT proteins to eukaryotic cellular structures Asgard古细菌ESCRT蛋白在真核细胞结构中的定位

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-20 DOI: 10.1016/j.bbrc.2026.153301

Kishore Babu Naripogu , Yee Han Tee , Yosuke Senju , Alexander Bershadsky , Robert C. Robinson

The emergence of internal membrane systems was a defining step in eukaryogenesis, but how pre-eukaryotic proteins were adapted to these novel compartments and structures remains unclear. Asgard archaea, the closest known prokaryotic relatives of eukaryotes, encode homologs of ESCRT (Endosomal Sorting Complex Required for Transport) proteins, which mediate membrane remodeling in eukaryotic cells, processes ranging from endosomal sorting to cytokinetic abscission. Here, we show that ESCRT-II and ESCRT-III homologs, VSP4 and ubiquitin from the Asgard achaeon Promethearchaeum syntrophicum (MK-D1) are recruited to discrete structures when expressed in human cells. These archaeal proteins localize to canonical eukaryotic ESCRT recruitment sites, midbodies and centrosomes, structures which are absent from MK-D1. This localization reflects conserved molecular interactions that predate the emergence of eukaryotic internal membranes and other eukaryotic cellular structures. These findings support a model in which protein machines were repurposed to support cellular complexity during eukaryogenesis, allowing the integration of ancestral ESCRT molecular functions and networks in to novel cellular architectures.

内部膜系统的出现是真核发生的决定性步骤，但真核前蛋白质如何适应这些新的隔室和结构尚不清楚。阿斯加德古菌是已知与真核生物最接近的原核亲缘生物，它们编码ESCRT（运输所需的内体分选复合体）蛋白的同源物，该蛋白介导真核细胞的膜重塑，包括从内体分选到细胞动力学脱落的过程。在这里，我们发现来自Asgard achaeon Promethearchaeum syntrophicum （MK-D1）的ESCRT-II和ESCRT-III同源物、VSP4和泛素在人细胞中表达时被招募到离散结构中。这些古细菌蛋白定位于典型的真核ESCRT招募位点、中间体和中心体，这些结构在MK-D1中是不存在的。这种定位反映了在真核内膜和其他真核细胞结构出现之前保守的分子相互作用。这些发现支持了一个模型，在这个模型中，蛋白质机器被重新用于支持真核发生过程中的细胞复杂性，允许将祖先的ESCRT分子功能和网络整合到新的细胞结构中。

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引用次数: 0

MPC1 deficiency promotes melanoma progression via Wnt/β-catenin signaling MPC1缺乏通过Wnt/β-catenin信号通路促进黑色素瘤进展

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-20 DOI: 10.1016/j.bbrc.2026.153310

Qing Zhu , Mao Zhao , Weinan Guo , Huina Wang

Melanoma represents the most aggressive and lethal form of skin cancer with high metastatic potential and elucidating the mechanisms underlying its progression is essential for developing effective therapies. The mitochondrial pyruvate carrier 1 (MPC1) is critical in linking glycolysis and oxidative phosphorylation, which has also been implicated in the pathogenesis of various cancers, yet its role in melanoma progression remains poorly understood. In this study, we found that MPC1 was markedly downregulated in both melanoma cell lines and tissues compared to control, and the alteration was more prominent in metastatic stage. Functional studies revealed that MPC1 deficiency enhanced melanoma cell proliferation, migration, and invasion in vitro and augmented melanoma metastasis in vivo. Mechanistically, RNA sequencing and subsequent functional study have demonstrated that MPC1 suppressed the activation of Wnt/β-catenin pathway by regulating DKK3, a key Wnt antagonist. Furthermore, pharmacologic inhibition of Wnt/β-catenin abrogated the pro-tumorigenic effects of MPC1 knockdown both in vitro and in vivo. Collectively, these data demonstrated that MPC1 deficiency promotes melanoma progression via Wnt/β-catenin signaling that is associated with DKK3 regulation. Targeting MPC1-Wnt/β-catenin axis may represent a novel therapeutic strategy for advanced melanoma treatment.

黑色素瘤是具有高转移潜力的最具侵袭性和致死性的皮肤癌，阐明其发展的机制对于开发有效的治疗方法至关重要。线粒体丙酮酸载体1 （MPC1）是连接糖酵解和氧化磷酸化的关键，这也与各种癌症的发病机制有关，但其在黑色素瘤进展中的作用仍知之甚少。在本研究中，我们发现与对照组相比，MPC1在黑色素瘤细胞系和组织中均明显下调，且在转移期改变更为突出。功能研究表明，MPC1缺失增强了黑色素瘤细胞在体外的增殖、迁移和侵袭，并增强了黑色素瘤在体内的转移。在机制上，RNA测序和随后的功能研究表明MPC1通过调节关键的Wnt拮抗剂DKK3抑制Wnt/β-catenin通路的激活。此外，Wnt/β-catenin的药理学抑制在体外和体内均消除了MPC1敲除的促肿瘤作用。总的来说，这些数据表明MPC1缺乏通过与DKK3调节相关的Wnt/β-catenin信号通路促进黑色素瘤的进展。靶向MPC1-Wnt/β-catenin轴可能是晚期黑色素瘤治疗的一种新的治疗策略。

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引用次数: 0

Corrigendum to “NMN synbiotics intervention modulates gut microbiota and metabolism in APP/PS1 Alzheimer's disease mouse models” [Biochem. Biophys. Res. Commun. 726 (2024) 150–274] “NMN合生干预调节APP/PS1阿尔茨海默病小鼠模型中的肠道微生物群和代谢”[生物化学]的勘误表。Biophys。《共同法典》，第726（2024）条[150-274]。

IF 2.2 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2026-01-20 DOI: 10.1016/j.bbrc.2026.153298

Jianing Zhang , Xiaodong Zhao , Huilian Xu , Xiaoyong Liu , Yan He , Xiaojun Tan , Jinsong Gu

引用次数: 0