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Insights into eye genetics and recent advances in ocular gene therapy 眼睛遗传学的见解和眼部基因治疗的最新进展。
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2025.102008
Viktória Szabó , Balázs Varsányi , Mirella Barboni , Ágnes Takács , Krisztina Knézy , Mária Judit Molnár , Zoltán Zsolt Nagy , Bence György , Carlo Rivolta
The rapid advancements in the field of genetics have significantly propelled the development of gene therapies, paving the way for innovative treatments of various hereditary disorders. This review focuses on the genetics of ophthalmologic conditions, highlighting the currently approved ophthalmic gene therapy and exploring emerging therapeutic strategies under development. Inherited retinal dystrophies represent a heterogeneous group of genetic disorders that manifest across a broad spectrum from infancy to late middle age. Key clinical features include nyctalopia (night blindness), constriction of the visual field, impairments in color perception, reduced central visual acuity, and rapid eye movements. Recent technological advancements, such as multimodal imaging, psychophysical assessments, and electrophysiological testing, have greatly enhanced our ability to understand disease progression and establish genotype-phenotype correlations.
Additionally, the integration of molecular diagnostics into clinical practice is revolutionizing patient stratification and the design of targeted interventions, underscoring the transformative potential of personalized medicine in ophthalmology. The review also covers the challenges and opportunities in developing gene therapies for other ophthalmic conditions, such as age-related macular degeneration and optic neuropathies. We discuss the viral and non-viral vector systems used in ocular gene therapy, highlighting their advantages and limitations. Additionally, we explore the potential of emerging technologies like CRISPR/Cas9 in treating genetic eye diseases. We briefly address the regulatory landscape, concerns, challenges, and future directions of gene therapy in ophthalmology. We emphasize the need for long-term safety and efficacy data as these innovative treatments move from bench to bedside.
遗传学领域的快速发展极大地推动了基因治疗的发展,为各种遗传疾病的创新治疗铺平了道路。本文综述了眼科疾病的遗传学,重点介绍了目前批准的眼科基因治疗方法,并探讨了正在开发的新兴治疗策略。遗传性视网膜营养不良症是一种异质性的遗传性疾病,从婴儿期到中年晚期都有。主要临床特征包括夜盲症(夜盲症)、视野狭窄、色彩感知障碍、中央视敏度降低和眼球快速运动。最近的技术进步,如多模态成像、心理物理评估和电生理测试,极大地提高了我们了解疾病进展和建立基因型-表型相关性的能力。此外,分子诊断与临床实践的结合正在彻底改变患者分层和有针对性干预的设计,强调了眼科个性化医疗的变革潜力。这篇综述还涵盖了其他眼科疾病,如年龄相关性黄斑变性和视神经病变的基因治疗的挑战和机遇。我们讨论了用于眼部基因治疗的病毒和非病毒载体系统,强调了它们的优点和局限性。此外,我们还探索了CRISPR/Cas9等新兴技术在治疗遗传性眼病方面的潜力。我们简要地介绍了眼科基因治疗的监管前景、关注、挑战和未来方向。我们强调,随着这些创新疗法从实验台走向临床,需要长期的安全性和有效性数据。
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引用次数: 0
Botox-A induced apoptosis and suppressed cell proliferation in fibroblasts pre-treated with breast cancer exosomes 肉毒杆菌a诱导乳腺癌外泌体预处理成纤维细胞凋亡和抑制细胞增殖。
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2024.102007
Hossein Sayaf , Niloufar Salimian , Mahnaz Mohammadi , Parisa Ahmadi , Amir Gholamzad , Sadegh Babashah , Maliheh Entezari , Najma Farahani , Maryam Montazeri , Mehrdad Hashemi

Background

breast cancer-associated fibroblast (CAF) is linked to metastasis and is poor for breast cancer prognosis. Since Clostridium Toxin A (Botox-A) had represented a cytotoxic effect on fibroblasts, this study aims to assess Botox-A cytotoxicity in both normal fibroblasts and exosome-induced CAFs.

Material and method

the serum exosomes of 40 BC patients and 30 healthy individuals were isolated and lncRNA H19 (lnch19) levels were assessed by qRT-PCR method. After that, Breast Cancer (BC) exosomes co-cultured with Human foreskin fibroblasts (HFF) and qRT-PCR were applied to evaluate α-SMA, Vimentin, BCL-2, and BAX expression. Both Normal and malignant HFFs co-cultured with Botox-A, and Botox-A loaded exosome for 24 and 48 h and their apoptosis, Cell proliferation, and viability were monitored by MTT assay, Annexin V-FITC and PI staining and qRT-PCR for BCL-2, BAX, and cyclin D1 mRNAs.

Results

Serum exosomes of BC patients had significantly higher levels of lncRNA H19 than healthy individuals. MTT assay results showed Botox-A decreased vital Human foreskin fibroblasts in a dose-dependent manner. BC exosomes significantly increased α-SMA, Vimentin, and BCL-2 mRNA levels in Human foreskin fibroblasts, on the other hand, BAX decreased meaningfully. Co-culture of exosome-treated HFF cells with both Botox-A and Botox-A loaded exosomes significantly boosted BCL-2 mRNA levels, completely contrary to BAX and cyclid d1 expression. Meanwhile, flow cytometry results confirmed a high rate of apoptosis in malignant Human foreskin fibroblasts treated with Botox-A loaded exosome.

Conclusion

The findings of this study indicate that exosomal lncRNA H19 could be a diagnostic marker for Breast Cancer and these Breast cancer exosomes can induce malignant phenotype in fibroblasts and turn them into CAFs. Botox-A could be toxic for both normal fibroblasts and CAFs, inducing apoptosis and suppressing cell proliferation among them.
背景:乳腺癌相关成纤维细胞(CAF)与乳腺癌转移有关,对乳腺癌预后不良。由于肉毒杆菌毒素A (Botox-A)对成纤维细胞具有细胞毒性作用,本研究旨在评估肉毒杆菌A对正常成纤维细胞和外泌体诱导的CAFs的细胞毒性。材料与方法:分离40例BC患者和30例健康人的血清外泌体,采用qRT-PCR法检测lncRNA H19 (lnch19)水平。之后,采用人包皮成纤维细胞(HFF)与乳腺癌(BC)外泌体共培养,采用qRT-PCR检测α-SMA、Vimentin、BCL-2和BAX的表达。用MTT法、Annexin V-FITC和PI染色以及BCL-2、BAX和cyclin D1 mrna的qRT-PCR检测正常和恶性HFFs与Botox-A和负载Botox-A的外泌体共培养24和48小时,并监测其凋亡、细胞增殖和活力。结果:BC患者血清外泌体lncRNA H19水平明显高于健康人。MTT试验结果显示肉毒杆菌a以剂量依赖的方式降低人包皮成纤维细胞。BC外泌体显著提高人包皮成纤维细胞α-SMA、Vimentin和BCL-2 mRNA水平,BAX显著降低。外泌体处理的HFF细胞与装载Botox-A和Botox-A的外泌体共培养显著提高了BCL-2 mRNA水平,与BAX和cycle1的表达完全相反。同时,流式细胞术结果证实,负载Botox-A的外泌体对恶性包皮成纤维细胞有较高的凋亡率。结论:本研究结果提示外泌体lncRNA H19可作为乳腺癌的诊断标志物,这些乳腺癌外泌体可诱导成纤维细胞的恶性表型并将其转化为cas。肉毒杆菌a对正常成纤维细胞和CAFs均有毒性,诱导细胞凋亡,抑制细胞增殖。
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引用次数: 0
Targeting ferroptosis in gastrointestinal tumors: Interplay of iron-dependent cell death and autophagy 靶向胃肠道肿瘤铁下垂:铁依赖性细胞死亡和自噬的相互作用。
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2025.102013
Mohamad Hosein Safari , Payman Rahimzadeh , Elmira Alaei , Mina Alimohammadi , Negin Esfandiari , Salman Daneshi , Neda Malgard , Najma Farahani , Afshin Taheriazam , Mehrdad Hashemi
Ferroptosis is a regulated cell death mechanism distinct from apoptosis, autophagy, and necroptosis, marked by iron accumulation and lipid peroxidation. Since its identification in 2012, it has developed into a potential therapeutic target, especially concerning GI disorders like PC, HCC, GC, and CRC. This interest arises from the distinctive role of ferroptosis in the progression of diseases, presenting a new avenue for treatment where existing therapies fall short. Recent studies emphasize the promise of focusing on ferroptosis to fight GI cancers, showcasing its unique pathophysiological mechanisms compared to other types of cell death. By comprehending how ferroptosis aids in the onset and advancement of GI diseases, scientists aim to discover novel drug targets and treatment approaches. Investigating ferroptosis in gastrointestinal disorders reveals exciting possibilities for novel therapies, potentially revolutionizing cancer treatment and providing renewed hope for individuals affected by these tumors.
铁下垂是一种受调控的细胞死亡机制,不同于细胞凋亡、自噬和坏死下垂,其特征是铁积累和脂质过氧化。自2012年被发现以来,它已发展成为一种潜在的治疗靶点,特别是在PC、HCC、GC和CRC等胃肠道疾病中。这种兴趣源于铁下垂在疾病进展中的独特作用,为现有疗法不足的治疗提供了新的途径。最近的研究强调了关注铁下垂对抗胃肠道癌症的希望,展示了与其他类型的细胞死亡相比,其独特的病理生理机制。通过了解铁下垂如何帮助胃肠道疾病的发生和发展,科学家们的目标是发现新的药物靶点和治疗方法。研究胃肠道疾病中的铁下垂揭示了令人兴奋的新疗法的可能性,可能会彻底改变癌症治疗,并为受这些肿瘤影响的个体提供新的希望。
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引用次数: 0
High expression of ARPC1B promotes the proliferation and apoptosis of clear cell renal cell carcinoma cells, leading to a poor prognosis ARPC1B的高表达促进透明细胞肾细胞癌细胞的增殖和凋亡,导致预后不良。
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2025.102011
Hongbo Wang , Zhendong Liu , Yuelin Du , Xingbo Cheng , Shanjun Gao , Wenjia Liang , Qingyun Zhu , Zhengfa Jiang , Yanzheng Gao , Panfeng Shang

Background

ARPC1B has been identified as a key regulator of malignant biological behavior in various tumors. However, its specific role in clear cell renal cell carcinoma (ccRCC) remains poorly understood. This study aims to evaluate the influence of ARPC1B on the prognosis and disease progression in ccRCC patients.

Methods

Multi-omics data and clinical information from public databases were analyzed to determine the associations between ARPC1B and prognosis, clinical features, immune microenvironment, and drug sensitivity in ccRCC. Co-expression and gene set enrichment analyses were conducted to elucidate the potential role of ARPC1B in ccRCC pathogenesis. Functional assays, including RT-qPCR, CCK8 assays, colony formation assays, immunofluorescence, immunohistochemistry, and xenograft tumor formation in nude mice, were performed to assess ARPC1B's impact on cell proliferation and apoptosis. Flow cytometry and Western blotting were further employed to investigate the underlying molecular mechanisms of ARPC1B in ccRCC.

Results

ARPC1B expression was significantly elevated in ccRCC and associated with an unfavorable prognosis. Both independent and meta-analyses confirmed that ARPC1B is an independent prognostic risk factor in ccRCC. Furthermore, ARPC1B expression significantly correlated with the immune microenvironment and drug sensitivity. In vitro, experiments demonstrated that ARPC1B knockdown suppressed ccRCC cell proliferation and induced apoptosis through the BAX-Bcl-2/c-caspase3/c-PARP axis, which was further validated by in vivo studies.

Conclusion

ARPC1B overexpression is associated with poor prognosis, altered immune status, and drug sensitivity in ccRCC. Furthermore, ARPC1B promotes the malignant behavior of ccRCC cells and holds potential as a prognostic biomarker and therapeutic target for ccRCC.
背景:ARPC1B已被确定为多种肿瘤恶性生物学行为的关键调节因子。然而,其在透明细胞肾细胞癌(ccRCC)中的具体作用仍知之甚少。本研究旨在评估ARPC1B对ccRCC患者预后和疾病进展的影响。方法:分析多组学数据和公共数据库的临床信息,确定ARPC1B与ccRCC患者预后、临床特征、免疫微环境和药物敏感性的关系。通过共表达和基因集富集分析来阐明ARPC1B在ccRCC发病机制中的潜在作用。通过RT-qPCR、CCK8测定、集落形成测定、免疫荧光、免疫组织化学和裸鼠异种移植肿瘤形成等功能分析来评估ARPC1B对细胞增殖和凋亡的影响。通过流式细胞术和Western blotting进一步研究ARPC1B在ccRCC中的潜在分子机制。结果:ARPC1B在ccRCC中表达显著升高,且与不良预后相关。独立分析和荟萃分析均证实ARPC1B是ccRCC的独立预后危险因素。此外,ARPC1B表达与免疫微环境和药物敏感性显著相关。体外实验表明,ARPC1B敲低可通过BAX-Bcl-2/c-caspase3/c-PARP轴抑制ccRCC细胞增殖并诱导凋亡,体内实验进一步验证了这一结论。结论:ARPC1B过表达与ccRCC患者预后不良、免疫状态改变及药物敏感性相关。此外,ARPC1B促进ccRCC细胞的恶性行为,并具有作为ccRCC预后生物标志物和治疗靶点的潜力。
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引用次数: 0
Targeting the HLC-1, LC-2/ad, and PC-14 lung cancer cell lines by the silver nanoparticles green-formulated by Descurainia sophia leaf extract 以Descurainia sophia叶提取物绿色配制的银纳米粒子靶向HLC-1、LC-2/ad和PC-14肺癌细胞株。
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2024.102001
Jianjun Ge, Jianbo Wen, Mingjun Jiang, Kefeng Huang, Saichun Qi, Wei Huang, Linlin Tan
Descurainia sophia, as an an ethno-medicinal plant, contains antioxidant compounds that safeguard cellular integrity against various forms of damage and may play a role in cancer prevention. Antioxidant compounds present in this plant facilitate the body's production of new cells and diminish the risk of colon cancer. In recent years, silver nanoparticles synthesized through green methods using ethnomedicinal herbs have been employed in cancers treatment. We have conducted an investigation into silver nanoparticles that were synthesized through green chemistry principles, utilizing the Descurainia sophia leaves extract for lung carcinoma treatment. The efficacy of Ag NPs against prevalent lung cancer cells was assessed. The green-synthesized silver nanoparticles characterization was conducted utilizing X-ray diffraction (XRD), field emission scanning electron microscopy (FE-SEM), ultraviolet–visible spectroscopy (UV–Vis), energy-dispersive X-ray spectroscopy (EDX), and transmission electron microscopy (TEM). The findings from morphological analyses validate the nanoparticles spherical shape, which ranges in size from 20 to 60 nm. The IC50 values were determined to be 173, 125, and 109 μg/mL for HLC-1, LC-2/ad, and PC-14 cell lines, respectively. According to recent data, Ag NPs may be a useful option to support the treatment of lung cancer. Although the current study presents encouraging findings, further investigation is necessary to gain a deeper understanding of the mechanisms of action and potential side effects of silver nanoparticles on HUVEC cells.
摘要索非拉是一种民族药用植物,含有抗氧化成分,可保护细胞完整性免受各种形式的损伤,并可能在癌症预防中发挥作用。这种植物中含有的抗氧化化合物能促进身体产生新细胞,降低患结肠癌的风险。近年来,利用民族药材通过绿色方法合成的纳米银已被用于癌症治疗。我们研究了采用绿色化学原理合成的银纳米颗粒,利用鸢尾叶提取物治疗肺癌。评估了Ag NPs对流行肺癌细胞的作用。利用x射线衍射(XRD)、场发射扫描电子显微镜(FE-SEM)、紫外可见光谱(UV-Vis)、能量色散x射线光谱(EDX)和透射电子显微镜(TEM)对绿色合成的纳米银进行了表征。形态学分析的结果证实了纳米颗粒的球形,其尺寸范围从20到60纳米。HLC-1、LC-2/ad和PC-14细胞株的IC50值分别为173、125和109 μg/mL。根据最近的数据,Ag NPs可能是支持肺癌治疗的有用选择。虽然目前的研究结果令人鼓舞,但需要进一步的研究来更深入地了解银纳米颗粒对HUVEC细胞的作用机制和潜在的副作用。
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引用次数: 0
miR-375-3p predicts the severity of endometriosis and regulates cellular progression by targeting NOX4 miR-375-3p通过靶向NOX4预测子宫内膜异位症的严重程度并调节细胞进展。
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2024.101999
Junmei Wang , Jianling Li , Hua Han , Changhua Wang , Taiying Shi , Xueyun Yang

Background

Due to the complex pathogenesis of endometriosis, its early screening and development prediction are still challenging problems in the clinic.

Objectives

This study evaluated the significance of miR-375-3p in endometriosis onset, progression, and recurrence, aiming to identify a novel biomarker for disease diagnosis and prognosis.

Materials and methods

The study enrolled 100 patients with endometriosis and 80 healthy females. The serum miR-375-3p levels were compared between the two groups, and its diagnostic significance and predictive value were assessed by ROC and Cox regression analyses. The effect of miR-375-3p on endometriosis cell growth and motility was evaluated by CCK8 and Transwell assays.

Results

Endometriosis patients showed a lower serum miR-375-3p level relative to healthy females, and more severe the disease condition, lower the miR-375-3p in endometrial tissues is. Reducing serum miR-375-3p could discriminate endometriosis patients sensitively and specifically. Additionally, miR-375-3p was identified as a predictor for the recurrence of endometriosis together with stage, lesion size, and the levels of related hormones. In endometriosis cells, miR-375-3p was demonstrated to target NOX4 and negatively regulated its expression. Overexpressing miR-375-3p significantly suppressed cell proliferation, migration, and invasion, which was reversed by NOX4.

Conclusion

Decreasing miR-375-3p served as a biomarker for endometriosis onset, development, and recurrence. miR-375-3p regulated endometriosis cell growth and motility via negatively modulating NOX4.
背景:由于子宫内膜异位症的发病机制复杂,其早期筛查和发展预测仍是临床上的难题:由于子宫内膜异位症的发病机制复杂,其早期筛查和发展预测仍是临床上的难题:本研究评估了miR-375-3p在子宫内膜异位症发病、进展和复发中的意义,旨在为疾病诊断和预后确定一种新的生物标志物:研究对象包括100名子宫内膜异位症患者和80名健康女性。比较两组患者的血清 miR-375-3p 水平,并通过 ROC 和 Cox 回归分析评估其诊断意义和预测价值。通过CCK8和Transwell试验评估了miR-375-3p对子宫内膜异位症细胞生长和活力的影响:结果:与健康女性相比,子宫内膜异位症患者的血清 miR-375-3p 水平较低;病情越严重,子宫内膜组织中的 miR-375-3p 水平越低。降低血清中的 miR-375-3p 可以灵敏、特异地鉴别子宫内膜异位症患者。此外,miR-375-3p 与子宫内膜异位症的分期、病灶大小和相关激素水平一起被认为是子宫内膜异位症复发的预测因子。在子宫内膜异位症细胞中,miR-375-3p 被证明靶向 NOX4 并负向调节其表达。过表达 miR-375-3p 能显著抑制细胞增殖、迁移和侵袭,而 NOX4 能逆转这种抑制作用:miR-375-3p通过负向调节NOX4来调控子宫内膜异位症细胞的生长和运动。
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引用次数: 0
miR-28–3p suppresses gastric cancer growth and EMT-driven metastasis by targeting the ARF6/Hedgehog axis miR-28-3p通过靶向ARF6/Hedgehog轴抑制胃癌生长和emt驱动的转移。
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2025.102010
Hua Ji , Sicheng Liu , Libo Yang , Yunhua Wu , Huanqing Zhang , Xueqing Liu , Linhai Li , Lihua Li
Gastric cancer (GC), among the most prevalent malignant tumors globally, demonstrates a rapid metastasis rate leading to high mortality. While microRNAs (miRNAs) have been recognized as critical regulators of tumor progression, the specific role of miR-28–3p in GC remains unclear. In this study, we demonstrate that miR-28–3p acts as a tumor suppressor by inhibiting GC cell proliferation and EMT-driven migration in vitro, as well as tumor growth and metastasis in vivo. Mechanistically, miR-28–3p directly targets ADP ribosylation factor 6 (ARF6), a small GTPase identified as an oncogene in GC. We reveal that ARF6 is significantly upregulated in GC and activates the GLI1/2-dependent Hedgehog signaling pathway, promoting tumor growth and EMT. Notably, ARF6 knockdown mitigates the pro-tumor effects caused by miR-28–3p deficiency, while combined ARF6 inhibition and Hedgehog pathway suppression exhibit synergistic anti-tumor effects. This study establishes the miR-28-3p-ARF6-Hedgehog signaling axis as a critical regulatory pathway in GC progression. Our findings provide novel insights into GC pathogenesis and highlight the therapeutic potential of targeting this axis for innovative treatment strategies.
胃癌(GC)是全球最常见的恶性肿瘤之一,其转移率快,死亡率高。虽然microRNAs (miRNAs)已被认为是肿瘤进展的关键调节因子,但miR-28-3p在胃癌中的具体作用尚不清楚。在本研究中,我们证明了miR-28-3p在体外通过抑制GC细胞增殖和emt驱动的迁移以及体内肿瘤生长和转移来发挥肿瘤抑制作用。在机制上,miR-28-3p直接靶向ADP核糖化因子6 (ARF6),这是一种小的GTPase,在GC中被认为是一种致癌基因。我们发现ARF6在GC中显著上调,激活gli1 /2依赖性Hedgehog信号通路,促进肿瘤生长和EMT。值得注意的是,ARF6敲低可减轻miR-28-3p缺失引起的促肿瘤作用,而ARF6抑制与Hedgehog途径抑制联合作用则具有协同抗肿瘤作用。本研究确定miR-28-3p-ARF6-Hedgehog信号轴是GC进展的关键调控途径。我们的研究结果为GC的发病机制提供了新的见解,并强调了针对这一轴的创新治疗策略的治疗潜力。
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引用次数: 0
Circulating miR-574–5p shows diagnostic and prognostic significance and regulates oxygen-glucose deprivation (OGD)-induced inflammatory activation of microglia by targeting ATP2B2
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-01 DOI: 10.1016/j.mcp.2025.102016
Xia Yin , Chunlei Zhang

Background

Early screening is critical for the prevention of ischemic stroke. miR-574–5p was considered a promising biomarker for ischemic stroke but lacks direct confirmation. This study evaluated miR-574–5p in discriminating ischemic stroke and predicting the severity and prognosis of patients, aiming to provide novel insights into the clinical prevention of ischemic stroke.

Methods

The clinical significance of miR-574–5p was evaluated in 103 ischemic stroke patients with 87 healthy individuals as control. The potential of serum miR-574–5p in the diagnosis and prognosis of ischemic stroke was assessed by ROC and logistic regression analyses. In vitro, oxygen-glucose deprivation (OGD)-induced microglia was established. The regulation of inflammation, oxidative stress, and proliferation of microglia by miR-574–5p were assessed by cell transfection. The downstream targets of miR-574–5p were predicted from public databases, and the targeting relationship was evaluated by luciferase reporter assay.

Results

Reducing serum miR-574–5p was observed in ischemic stroke patients relative to healthy individuals, which discriminated ischemic stroke patients. Serum miR-574–5p was negatively correlated with the NIHSS score of ischemic stroke patients and was identified as a risk factor for patients’ adverse prognosis. In OGD-induced microglia, overexpressing miR-574–5p could alleviate OGD-induced inflammation and oxidative stress and promote cell growth. Among predicted targets, ATP2B2 was upregulated in ischemic stroke and showed a negative correlation with miR-574–5p. miR-574–5p negatively regulated ATP2B2 in OGD-induced microglia, and the overexpression of ATP2B2 reversed the protective effect of miR-574–5p.

Conclusion

miR-574–5p acted as a biomarker for ischemic stroke and mediated neuroinflammation via targeting ATP2B2.
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引用次数: 0
The Role of APOA1-AS in Colorectal Cancer: Investigating Its Association with Malignant Biological Behaviors. APOA1-AS 在结直肠癌中的作用:研究其与恶性生物学行为的关系
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-01-29 DOI: 10.1016/j.mcp.2025.102017
Gang Liu, Qin Zhao, Yan Li, Dongmei Zhu, Hong Peng

Purpose: Colorectal cancer (CRC) is a common malignant tumor associated with high morbidity and mortality. Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression. This study aimed to explore the role of lncRNA APOA1-AS in colorectal cancer and elucidate its underlying mechanisms.

Methods: Clinical samples were collected, and high-throughput sequencing was performed to identify differentially expressed lncRNAs in colorectal cancer. Among these, the key lncRNA APOA1-AS was selected for further investigation. The expression of APOA1-AS in colorectal cancer tissues and cells was evaluated. The effects of APOA1-AS on cell proliferation, migration, invasion, and apoptosis were assessed through knockdown and overexpression of APOA1-AS in SW620 and RKO cells. Additionally, the relationship between APOA1-AS and the malignant biological behaviors of colorectal cancer cells was also investigated. Furthermore, the involvement of APOA1-AS in glucose metabolism reprogramming and the cGMP-PKG signaling pathway was analyzed.

Results: A total of 2,985 differentially expressed lncRNAs were identified in colorectal cancer, including APOA1-AS, which showed the most significant upregulation. APOA1-AS expression was significantly higher in colorectal cancer tissues compared to normal tissues. Overexpression of APOA1-AS promoted cell proliferation, migration, and invasion while inhibiting apoptosis in SW620 and RKO cells. Furthermore, APOA1-AS was found to regulate glucose metabolism reprogramming, enhance tumor malignant biological behaviors and facilitate tumor cell drug resistance through the cGMP-PKG signaling pathway.

Conclusion: Our study demonstrates that APOA1-AS is a potential key regulator in colorectal cancer development and progression. It functions via glucose metabolism reprogramming and the cGMP-PKG signaling pathway, offering a novel therapeutic target for colorectal cancer.

{"title":"The Role of APOA1-AS in Colorectal Cancer: Investigating Its Association with Malignant Biological Behaviors.","authors":"Gang Liu, Qin Zhao, Yan Li, Dongmei Zhu, Hong Peng","doi":"10.1016/j.mcp.2025.102017","DOIUrl":"https://doi.org/10.1016/j.mcp.2025.102017","url":null,"abstract":"<p><strong>Purpose: </strong>Colorectal cancer (CRC) is a common malignant tumor associated with high morbidity and mortality. Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression. This study aimed to explore the role of lncRNA APOA1-AS in colorectal cancer and elucidate its underlying mechanisms.</p><p><strong>Methods: </strong>Clinical samples were collected, and high-throughput sequencing was performed to identify differentially expressed lncRNAs in colorectal cancer. Among these, the key lncRNA APOA1-AS was selected for further investigation. The expression of APOA1-AS in colorectal cancer tissues and cells was evaluated. The effects of APOA1-AS on cell proliferation, migration, invasion, and apoptosis were assessed through knockdown and overexpression of APOA1-AS in SW620 and RKO cells. Additionally, the relationship between APOA1-AS and the malignant biological behaviors of colorectal cancer cells was also investigated. Furthermore, the involvement of APOA1-AS in glucose metabolism reprogramming and the cGMP-PKG signaling pathway was analyzed.</p><p><strong>Results: </strong>A total of 2,985 differentially expressed lncRNAs were identified in colorectal cancer, including APOA1-AS, which showed the most significant upregulation. APOA1-AS expression was significantly higher in colorectal cancer tissues compared to normal tissues. Overexpression of APOA1-AS promoted cell proliferation, migration, and invasion while inhibiting apoptosis in SW620 and RKO cells. Furthermore, APOA1-AS was found to regulate glucose metabolism reprogramming, enhance tumor malignant biological behaviors and facilitate tumor cell drug resistance through the cGMP-PKG signaling pathway.</p><p><strong>Conclusion: </strong>Our study demonstrates that APOA1-AS is a potential key regulator in colorectal cancer development and progression. It functions via glucose metabolism reprogramming and the cGMP-PKG signaling pathway, offering a novel therapeutic target for colorectal cancer.</p>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":" ","pages":"102017"},"PeriodicalIF":2.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Clinical significance analysis of microRNA-199a-3p in gingival crevicular fluid for patients with chronic periodontitis.
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-01-25 DOI: 10.1016/j.mcp.2025.102015
Kaixuan Yan, Yu Zheng, Jing Liu, Shuo Li, Wei Si

Objective: The aim was to investigate the clinical performance of microRNA-199a-3p (miR-199a-3p) in patients with chronic periodontitis.

Methods: 91 patients with chronic periodontitis and 78 healthy individuals were enrolled for the research subjects. MiR-199a-3p expression was detected using real-time quantitative PCR (RT-qPCR) assay. Pearson correlation analysis was used for the relevance of miR-199a-3p with inflammatory mediators. Receiver operating characteristic (ROC) and logistic regression were conducted for the evaluation of the diagnostic performance and risk factors of chronic periodontitis. Bioinformatics analysis was utilized for miR-199a-3p-related genes.

Results: MiR-199a-3p was distinctly decreased in gingival crevicular fluid from patients with chronic periodontitis. The area under the curve (AUC) was 0.978 to discriminate chronic periodontitis patients from healthy individuals. The negative correlation was observed between miR-199a-3p and inflammatory factors. Logistic regression showed that miR-199a-3p was an independently protective factor for the occurrence of chronic periodontitis. Bioinformatics analysis revealed that the predictive regulated genes of miR-199a-3p mainly concentrated in inflammatory-associated signaling pathways.

Conclusion: MiR-199a-3p was attenuated in patients with chronic periodontitis and an underlying diagnostic biomarker for the disease.

{"title":"Clinical significance analysis of microRNA-199a-3p in gingival crevicular fluid for patients with chronic periodontitis.","authors":"Kaixuan Yan, Yu Zheng, Jing Liu, Shuo Li, Wei Si","doi":"10.1016/j.mcp.2025.102015","DOIUrl":"https://doi.org/10.1016/j.mcp.2025.102015","url":null,"abstract":"<p><strong>Objective: </strong>The aim was to investigate the clinical performance of microRNA-199a-3p (miR-199a-3p) in patients with chronic periodontitis.</p><p><strong>Methods: </strong>91 patients with chronic periodontitis and 78 healthy individuals were enrolled for the research subjects. MiR-199a-3p expression was detected using real-time quantitative PCR (RT-qPCR) assay. Pearson correlation analysis was used for the relevance of miR-199a-3p with inflammatory mediators. Receiver operating characteristic (ROC) and logistic regression were conducted for the evaluation of the diagnostic performance and risk factors of chronic periodontitis. Bioinformatics analysis was utilized for miR-199a-3p-related genes.</p><p><strong>Results: </strong>MiR-199a-3p was distinctly decreased in gingival crevicular fluid from patients with chronic periodontitis. The area under the curve (AUC) was 0.978 to discriminate chronic periodontitis patients from healthy individuals. The negative correlation was observed between miR-199a-3p and inflammatory factors. Logistic regression showed that miR-199a-3p was an independently protective factor for the occurrence of chronic periodontitis. Bioinformatics analysis revealed that the predictive regulated genes of miR-199a-3p mainly concentrated in inflammatory-associated signaling pathways.</p><p><strong>Conclusion: </strong>MiR-199a-3p was attenuated in patients with chronic periodontitis and an underlying diagnostic biomarker for the disease.</p>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":" ","pages":"102015"},"PeriodicalIF":2.3,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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Molecular and Cellular Probes
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