IF 2.9 3区生物学

BMB Reports Pub Date : 2025-07-10

Yoonah R Oh, Min-Kyoo Shin

引用次数: 0

Contribution of histone deacetylases (HDACs) to the regulation of histone and non-histone proteins: implications for fibrotic diseases. 组蛋白去乙酰化酶（hdac）对组蛋白和非组蛋白调节的贡献：对纤维化疾病的影响

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-07-10

Sunyoung Jang, Nayun Choi, Jong Hoon Park, Kyung Hyun Yoo

{"title":"Contribution of histone deacetylases (HDACs) to the regulation of histone and non-histone proteins: implications for fibrotic diseases.","authors":"Sunyoung Jang, Nayun Choi, Jong Hoon Park, Kyung Hyun Yoo","doi":"","DOIUrl":"","url":null,"abstract":"Histone deacetylases (HDACs) are essential enzymes that play a pivotal role in the epigenetic regulation of gene expression by catalyzing the removal of acetyl groups from histone and non-histone proteins. This deacetylation is a crucial post-translational modification that influences several cellular processes, such as chromatin remodeling, transcriptional repression, and signal transduction. Recent studies have illuminated the significant involvement of HDACs in the pathogenesis of fibrotic diseases, conditions characterized by the excessive accumulation of extracellular matrix components leading to progressive organ dysfunction and failure. These diseases commonly affect the liver, kidney, heart, lung, and colon. The contribution of HDACs to fibrogenesis is multifaceted, involving the modulation of gene expression that governs inflammatory and fibrotic signaling pathways. Therefore, targeting HDACs with specific inhibitors has emerged as a promising therapeutic strategy to mitigate fibrosis in various organs. HDAC inhibitors (HDACi) can potentially reverse the aberrant gene expression profiles associated with fibrotic diseases by restoring acetylation levels, thus attenuating fibrotic responses. Several HDAC inhibitors, such as vorinostat, trichostatin A, and romidepsin, have shown efficacy in preclinical models of fibrosis, demonstrating their potential to suppress fibrogenic signaling pathways and reduce extracellular matrix deposition. In this review, we provide a comprehensive analysis of the current understanding of the roles of HDACs in the regulation of histone and non-histone proteins, and their implications for fibrotic diseases. We compare the molecular mechanisms by which different classes of HDACs contribute to fibrosis in various organs, and highlight the therapeutic potential of HDAC inhibition. This review underscores the importance of further research into HDAC-specific inhibitors as viable treatments for fibrotic diseases, aiming to develop targeted therapies that can effectively ameliorate fibrosis and improve patient outcomes.","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599328","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

Modulating CD226 and PD-(L)1 pathways improves CMV-specific CD8＋T cell responses in the absence of IL-2. 在缺乏IL-2的情况下，调节CD226和PD-(L)1通路可改善cmv特异性CD8+T细胞的应答。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-06-11

Hye-In Sim, Yunju Jo, Hyejin Ahn, Juyeon Hong, Hye-Bin Kim, Bohwan Yun, Haeun Son, Yeonjun Jeong, Jibaek Kim, Chan-Sik Park, Yoon Park, Hyung-Seung Jin

{"title":"Modulating CD226 and PD-(L)1 pathways improves CMV-specific CD8＋T cell responses in the absence of IL-2.","authors":"Hye-In Sim, Yunju Jo, Hyejin Ahn, Juyeon Hong, Hye-Bin Kim, Bohwan Yun, Haeun Son, Yeonjun Jeong, Jibaek Kim, Chan-Sik Park, Yoon Park, Hyung-Seung Jin","doi":"","DOIUrl":"","url":null,"abstract":"Glioblastoma (GBM) frequently expresses cytomegalovirus (CMV) antigens, making CMV-specific CD8＋T cells attractive candidates for adoptive immunotherapy due to their longevity and inherent tumor reactivity. However, these T cells encounter significant immunosuppressive challenges within the GBM microenvironment, including cytokine scarcity and checkpointmediated inhibition, which limit their proliferation and function. Here, we assessed strategies to overcome these limitations by modulating immune checkpoint pathways. Antigen stimulation combined with IL-2 robustly expanded high-avidity (tetramer-high) CMV-specific T cells with significant enrichment of CD62L＋ central memory (TCM) cells. In contrast, antigen stimulation alone modestly expanded tetramer-high cells with limited TCM enrichment. PD-L1 blockade in the absence of IL-2 favored expansion of tetramer-high CMV-specific CD8＋T cells, preserved CD62L expression, and enhanced CD226 expression. Furthermore, combining anti-PD-L1 blockade with an anti-CD226 agonist markedly enhanced proliferation, IFN-γ production, and TCM enrichment in both tetramer-high and tetramer-low populations, reaching levels comparable to IL-2-supported conditions. Together, these findings highlight that simultaneous modulation of PD-L1 and CD226 pathways can restore CMV-specific T cell function, offering a promising strategy to boost TCR-T efficacy in cytokine-deprived environments.","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265144","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

Identification of optimal adenine and cytosine base editors for genome editing in Arabidopsis and soybean. 拟南芥和大豆基因组编辑最佳腺嘌呤和胞嘧啶碱基编辑器的鉴定。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-06-11

Yeong Yeop Jeong, Jun Hee Han, Jihyeon Yu, Sangsu Bae, Pil Joon Seo

引用次数: 0

Diagnosis and therapeutic targeting of quiescent cancer cells: road to conquer cancer recurrence. 静止癌细胞的诊断与治疗靶向：攻克癌症复发之路。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-06-11

Moon Jong Kim

{"title":"Diagnosis and therapeutic targeting of quiescent cancer cells: road to conquer cancer recurrence.","authors":"Moon Jong Kim","doi":"","DOIUrl":"","url":null,"abstract":"Quiescent cancer cells (QCCs) are considered an origin of cancer recurrence and present an ongoing challenge in cancer treatment. Following anti-cancer therapy, non-proliferating, therapy-resistant QCCs have been detected as subsets of residual cancer cells within patients. Clinicians and researchers widely believe that these minimal residual QCCs can eventually regain proliferative activity, acting as \"seeds\" for cancer recurrence. Despite the significance of QCCs, tracing and analyzing these microscopic residual cells in vivo models and patients remains extremely challenging, limiting our understanding. Consequently, reliable biomarkers for QCCs and the mechanisms underlying their 'reversible' reactivation are still poorly understood. This knowledge gap has hindered the development of diagnostics and targeted therapies for QCCs. The absence of diagnostic tools for QCCs also complicates predicting cancer relapse and determining the optimal duration of anti-cancer treatment. Moreover, without strategies to eradicate QCCs, preventing cancer recurrence remains elusive. This review aims to provide an overview of the current understanding of QCCs and related diagnostic efforts in both basic and clinical research. Additionally, potential strategies for the targeted elimination of QCCs are explored. Focused research and clinical attention to diagnosing and eradicating residual QCCs are essential for preventing cancer recurrence and ultimately conquering this deadly disease.","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265207","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

Auranofin, an antirheumatic drug, shows anticancer stem cell potential via suppression of the Stat3 signal. 抗风湿药物金嘌呤通过抑制Stat3信号显示出抗癌干细胞的潜能。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-06-11

Seung-Yeon Ko, Yuna Kim, Jin Sun Chung, Young Bin Kim, Su-Lim Kim, Dong-Sun Lee, Kyung-Hee Chun, Hack Sun Choi

{"title":"Auranofin, an antirheumatic drug, shows anticancer stem cell potential via suppression of the Stat3 signal.","authors":"Seung-Yeon Ko, Yuna Kim, Jin Sun Chung, Young Bin Kim, Su-Lim Kim, Dong-Sun Lee, Kyung-Hee Chun, Hack Sun Choi","doi":"","DOIUrl":"","url":null,"abstract":"Accumulating data have shown that targeting breast cancer stem cells (CSCs) is an auspicious way for anticancer therapies. This study demonstrated that the antirheumatic drug auranofin is a potent CSC inhibitor with anti-CSC action on breast cancer. This research focused on investigating the effect of auranofin on breast cancer and CSCs and its cellular mechanism. Mammosphere formation, colony formation, levels of CD44high/CD24low, and aldehyde dehydrogenase 1 expression in the cells were evaluated after auranofin treatment. The anti-CSC properties of auranofin were further examined by gel shift assay and cytokine detection. Auranofin suppressed cell growth, colony formation, migration, and mammosphere formation and triggered apoptosis in breast cancer. Auranofin decreased the CD44high/CD24low- and aldehyde dehydrogenaseexpressed subpopulations, as well as the Stat3-DNA interaction and phosphorylated Stat3 level. Auranofin also decreased the extracellular levels of interleukin-8 (IL-8) in the mammosphere media. Auranofin suppressed the Stat3/IL-8 signal and killed CSCs; therefore, it may be a potential target for CSCs.","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265206","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

Diesel exhaust particles disrupt blood-retina barrier integrity via TLR2 and TLR4 activation. 柴油废气颗粒通过激活TLR2和TLR4破坏血视网膜屏障的完整性。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-06-11

Ji Young Kim, Eun Young Lee, Jin-Hee Kim, Eoi Jong Seo, Sang-Yong Eom, Je Hoon Seo

{"title":"Diesel exhaust particles disrupt blood-retina barrier integrity via TLR2 and TLR4 activation.","authors":"Ji Young Kim, Eun Young Lee, Jin-Hee Kim, Eoi Jong Seo, Sang-Yong Eom, Je Hoon Seo","doi":"","DOIUrl":"","url":null,"abstract":"Diesel exhaust particles (DEPs), a major component of air pollution, are well-known to induce inflammation and vascular dysfunction. However, the molecular mechanisms linking DEP exposure to the disruption of the blood-retina barrier (BRB) remain poorly understood. Toll-like receptors (TLRs), particularly TLR2 and TLR4, play critical roles in inflammatory signaling and may contribute to DEP-induced retinal endothelial dysfunction. This study investigates the involvement of TLR2 and TLR4 in mediating DEP-induced disruption of the BRB and evaluates the protective effects of TLR inhibition using both in vitro and in vivo experiments. U937 human macrophages were exposed to DEPs of ultrafine size (＜0.2 μm), and the mRNA expression of TNF-α and IL-1β was quantified. Conditioned media from DEP-exposed U937 cultures were then used to treat human retinal endothelial cells (HRECs). DEP exposure significantly increased TNF-α and IL-1β mRNA expression in U937 macrophages. Conditioned media from DEP-exposed U937 macrophages reduced claudin-5 and ZO-1 expression in HRECs, resulting in increased BRB permeability. Inhibition of TLR2 and TLR4 using C29 and TAK242, respectively, significantly attenuated TNF-α and IL-1β mRNA expression in DEP-exposed U937 macrophages and preserved BRB integrity by maintaining claudin-5 and ZO-1 expression in HRECs. In the mouse model, DEP exposure caused a marked reduction in claudin-5 and ZO-1 levels in retinal vessels, whereas treatment with C29 and TAK242 mitigated the loss of these tight junction proteins. This study demonstrates that DEPs induce inflammation and BRB dysfunction through TLR2 and TLR4 activation, leading to increased vascular permeability and potential retinal damage. Furthermore, TLR2 and TLR4 inhibition may be a promising therapeutic strategy to protect retinal health from air pollution-induced damage.","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265208","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

SERPINA3 as a modulator of skin cell functionality in human dermal fibroblasts. SERPINA3在人真皮成纤维细胞中作为皮肤细胞功能的调节剂。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-06-01

Young Du Choi, Young Un Kim, HyunJoon Gi, Do-Wan Kim, Sang Bae Lee, KyeongJin Kim

{"title":"SERPINA3 as a modulator of skin cell functionality in human dermal fibroblasts.","authors":"Young Du Choi, Young Un Kim, HyunJoon Gi, Do-Wan Kim, Sang Bae Lee, KyeongJin Kim","doi":"","DOIUrl":"","url":null,"abstract":"Skin aging is a complex biological process driven by intrinsic and extrinsic factors, leading to a progressive structural and functional decline. The balance between extracellular matrix (ECM) degradation and synthesis is critical for maintaining skin homeostasis, with collagen loss and reduced cell proliferation contributing to age-related deterioration. Serpin Family A Member 3 (SERPINA3), a serine protease inhibitor, has been implicated in inflammation and tissue remodeling. However, its role in skin aging remains largely unexplored. In this study, we examined the expression and function of SERPINA3 in human skin cells. RNA-seq analysis revealed that SERPINA3 expression is significantly downregulated in aged human dermal fibroblasts and was further diminished under oxidative stress. Functional assays demonstrated that SERPINA3 promotes cell proliferation, accelerates wound healing, and activates key signaling pathways such as ERK and AKT. These findings suggest that SERPINA3 may serve as a protective factor against skin aging by supporting ECM integrity and enhancing cellular regeneration. These results provide novel insights into the molecular functions of SERPINA3 and highlight its potential as a therapeutic target for age-related skin deterioration. [BMB Reports 2025; 58(6): 264-268].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"264-268"},"PeriodicalIF":2.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12207443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exercise induces Mettl14 in iWAT but regulates browning and metabolism independently of Mettl14. 运动诱导iWAT中的Mettl14，但独立于Mettl14调节褐变和代谢。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-06-01

Hye Jin Kim, Je Kyung Seong

{"title":"Exercise induces Mettl14 in iWAT but regulates browning and metabolism independently of Mettl14.","authors":"Hye Jin Kim, Je Kyung Seong","doi":"","DOIUrl":"","url":null,"abstract":"Exercise is a key driver of metabolic enhancement, and the impact of exercise on methyltransferase-like14 protein (Mettl14)-mediated N6-methyladenosine (m6A) modification remains unexplored. This study investigates the role of Mettl14 in inguinal white adipose tissue (iWAT) concerning exercise-induced metabolic improvement and its underlying mechanisms. We examined voluntary wheel-running exercise in C57BL/6N mice and Mettl14 heterozygous knockout (HET) mice models. We assessed metabolic phenotyping and molecular responses through body composition analysis, blood profiles, indirect calorimetry, real-time PCR, immunoblotting, and immunohistology. m6A levels were significantly elevated in the iWAT of trained mice, a result of increased Mettl14 expression. Additionally, higher Mettl14 levels induced by exercise were positively associated with browning markers in iWAT. Mettl14 HET led to increased weight gain and fat accumulation in a mechanism dependent on m6A levels. Furthermore, HET mice demonstrated notable reductions in oxygen consumption and energy expenditure at baseline. m6A levels were notably reduced in the iWAT of exercise-induced HET mice, yet the associated metabolic impairment was significantly mitigated. Exercise substantially correlates with enhanced browning and metabolic improvements by modulating m6A levels through Mettl14 expression in iWAT. However, this pathway does not critically regulate exercise-induced browning and the enhancement of whole-body metabolism. [BMB Reports 2025; 58(6): 269-275].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"269-275"},"PeriodicalIF":2.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12207442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

High-resolution detection of RPS24 microexon variations reveals novel splicing patterns in response to KRAS-targeted therapy in lung adenocarcinoma. 高分辨率检测RPS24微外显子变异揭示了kras靶向治疗肺腺癌的新剪接模式。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-06-01

Dahye Nam, Bin Tian, Jiyeon Park, Yeun-Jun Chung

{"title":"High-resolution detection of RPS24 microexon variations reveals novel splicing patterns in response to KRAS-targeted therapy in lung adenocarcinoma.","authors":"Dahye Nam, Bin Tian, Jiyeon Park, Yeun-Jun Chung","doi":"","DOIUrl":"","url":null,"abstract":"Alternative splicing (AS) dysregulation is increasingly recognized as a critical factor in cancer progression and drug response. However, precisely detecting and characterizing complex splicing events, particularly those involving microexons, remains technically challenging. Ribosomal Protein 24 (RPS24), which contains three microexons (3, 18, and 22 bp), serves as an ideal model for studying complex AS regulation in cancer. We developed a high-resolution detection method for RPS24 microexon variations and investigate their relationship with KRAS proto-oncogene, GTPase (KRAS) inhibition in lung adenocarcinoma (LUAD) to identify potential biomarkers for KRAS-targeted inhibitors. We established an integrated methodological approach combining RNA-seq analysis with fragment analysis to detect RPS24 AS patterns. Using this method, we analyzed RPS24 AS across a panel of lung cancer cell lines and examined AS changes in KRAS-mutant cell lines following treatment with KRAS inhibitors. Our method successfully characterized distinct RPS24 AS isoform compositions across lung cancer cell lines, demonstrating high accuracy in detecting 3 bp variations. In KRASmutant cell lines, we observed a consistent upregulation of the 3 bp-containing isoform following KRAS inhibition, indicating a specific correlation with treatment response. This study provides a robust methodology for analyzing complex AS events and supports the RPS24 3 bp-containing isoform as a potential biomarker for KRAS inhibitor response in LUAD. These findings offer new insights into the molecular mechanisms of KRAS inhibitor therapy and strategies for monitoring treatment response. [BMB Reports 2025; 58(6): 244-249].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"244-249"},"PeriodicalIF":2.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12207440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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