International Journal of Biological Sciences最新文献_第4页

Therapeutic Activation of PPARα Inhibits Transformed Follicular Lymphoma Tumorigenesis via the FOXM1 Signaling Pathway. 治疗性激活PPARα通过FOXM1信号通路抑制转化性滤泡性淋巴瘤的发生

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.116437

Dongmei Qin, Hui Zhou, Jie Zhou, Chendi Xie, Shuman Jia, Xingxing Yu, Yan Hong, Li Zhang, Yueting Huang, Yong Zhou, Bing Xu, Jie Zha

{"title":"Therapeutic Activation of PPARα Inhibits Transformed Follicular Lymphoma Tumorigenesis via the FOXM1 Signaling Pathway.","authors":"Dongmei Qin, Hui Zhou, Jie Zhou, Chendi Xie, Shuman Jia, Xingxing Yu, Yan Hong, Li Zhang, Yueting Huang, Yong Zhou, Bing Xu, Jie Zha","doi":"10.7150/ijbs.116437","DOIUrl":"10.7150/ijbs.116437","url":null,"abstract":"Transformed follicular lymphoma (t-FL) is a subtype of follicular lymphoma (FL) characterized by aggressive behavior and poor treatment outcomes. Dysregulated glucose uptake and cell cycle disruption have been implicated in t-FL progression. Here, we found that PPARα is frequently low-expressed in transformed follicular lymphoma, and therapeutic activation of PPARα significantly represses the progression of t-FL in cell line-derived xenograft (CDX) and primary t-FL patient-derived xenograft (PDX) models in vivo. Mechanistically, activation of PPARα inhibits t-FL progression mainly through three different signaling pathways as follows: PPARα inhibits glycolysis in t-FL cells by blocking the HIF1α signaling pathway; activation of PPARα induces mitochondria-dependent apoptosis in t-FL cells by disrupting mitochondrial homeostasis; and PPARα transcriptionally inhibits FOXM1 expression, causing the downregulation of its downstream target genes and inducing cell cycle arrest in t-FL cells. Concurrently, knockdown of FOXM1 enhances the sensitivity of t-FL cells to chiglitazar, and overexpression of FOXM1 partially rescued the inhibitory effect of chiglitazar on t-FL cells, highlighting the involvement of the PPARα-FOXM1 axis in the antitumor effects of chiglitazar. These promising preclinical results support further clinical evaluation of chiglitazar as a potential therapeutic option for t-FL patients, providing a novel and effective treatment approach for this aggressive subtype of FL.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 12","pages":"5411-5427"},"PeriodicalIF":10.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435485/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

JPI-547, a Dual Inhibitor of PARP/Tankyrase, Shows Antitumor Activity Against Pancreatic Cancers with Homologous Recombination Repair Deficiency or Wnt-Addiction. PARP/ tankyase双抑制剂JPI-547对同源重组修复缺陷或wnt成瘾的胰腺癌具有抗肿瘤活性。

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.113726

Kyoung-Seok Oh, Ah-Rong Nam, Ju-Hee Bang, Yoojin Jeong, Sea Young Choo, Hyo Jung Kim, Su In Lee, Jae-Min Kim, Jeesun Yoon, Tae-Yong Kim, Do-Youn Oh

{"title":"JPI-547, a Dual Inhibitor of PARP/Tankyrase, Shows Antitumor Activity Against Pancreatic Cancers with Homologous Recombination Repair Deficiency or Wnt-Addiction.","authors":"Kyoung-Seok Oh, Ah-Rong Nam, Ju-Hee Bang, Yoojin Jeong, Sea Young Choo, Hyo Jung Kim, Su In Lee, Jae-Min Kim, Jeesun Yoon, Tae-Yong Kim, Do-Youn Oh","doi":"10.7150/ijbs.113726","DOIUrl":"10.7150/ijbs.113726","url":null,"abstract":"PARP inhibitors have demonstrated antitumor efficacy in solid tumors, including pancreatic ductal adenocarcinoma (PDAC) characterized by homologous recombination deficiency (HRD). The definition of HRD and other potential biomarkers should be further evaluated using PARP inhibitors. JPI-547 is a novel dual inhibitor targeting PARP1/2 and Tankyrase1/2. Herein, we demonstrate the potent antitumor activity of JPI-547 against BRCA2-/- PDAC cells. JPI-547 outperformed most PARP inhibitors, with a half-maximal inhibitory concentration approximately 10-fold lower than that of olaparib. JPI-547 efficiently trapped PARP1 on the chromatin, disrupted poly-ADP-ribosylation, induced G2/M phase arrest, and triggered apoptosis in PDAC cells. In addition to HRD, we identified Wnt addiction as a predictive factor for JPI-547 activity. PDAC cells reliant on Wnt signaling due to pathogenic RNF43 mutations showed increased susceptibility to JPI-547 without altering homologous recombination repair efficiency. JPI-547 disrupts the Wnt/β-catenin pathway in RNF43-mutated cells and inhibits the oncogenic YAP pathway, highlighting its multifaceted therapeutic potential in PDAC with HRD or Wnt-addiction.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 12","pages":"5460-5475"},"PeriodicalIF":10.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Mechanism of Ferroptosis and Its Role in Disease Development. 铁下垂的机制及其在疾病发展中的作用。

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.102859

Zhangruijian Ye, Bin Xie, Yongguang Tao, Desheng Xiao

引用次数: 0

E3 ligase MKRN2 destabilizes PPP2CA proteins to inactivate canonical Wnt pathway and mitigates tumorigenesis of clear cell renal cell carcinoma. E3连接酶MKRN2破坏PPP2CA蛋白的稳定性，使典型Wnt通路失活，减轻透明细胞肾细胞癌的肿瘤发生。

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.107130

Tiexi Yu, Weiquan Li, Xiangui Meng, Hongwei Yuan, Hailong Ruan, Wen Xiao, Xiaoping Zhang

{"title":"E3 ligase MKRN2 destabilizes PPP2CA proteins to inactivate canonical Wnt pathway and mitigates tumorigenesis of clear cell renal cell carcinoma.","authors":"Tiexi Yu, Weiquan Li, Xiangui Meng, Hongwei Yuan, Hailong Ruan, Wen Xiao, Xiaoping Zhang","doi":"10.7150/ijbs.107130","DOIUrl":"10.7150/ijbs.107130","url":null,"abstract":"Background: Emerging evidence suggests that Makorin Ring Finger Proteins (MKRNs) are dysregulated in various human malignancies. However, the clinical and biological significance of MKRN2 in clear cell renal cell carcinoma (ccRCC) has been minimally explored. In this study, we investigated the exceptional role of MKRN2 in ccRCC. Methods: MKRN2 expression in ccRCC was analyzed with clinical samples and The Cancer Genome Atlas (TCGA) database. The proliferation and migration of cancer cells were assessed by transwell, colony formation, and wound healing assays. Gene expression, DNA methylation, and protein expression and ubiquitination were assessed by real-time PCR, bisulfite sequencing PCR, and western blotting assay, respectively. Protein interactions were verified by co-immunoprecipitation and immunofluorescence assays. In vivo experiments identified MKRN2 was a potential tumor inhibitor in ccRCC. Results: Down-regulation of MKRN2 was observed in human ccRCC tissues in both public databases and our clinical samples, mechanistically linked with its promoter DNA hypermethylation. Conversely, overexpression of MKRN2 was associated with ccRCC inhibition and favorable clinical outcomes. MKRN2 interacted with Protein Phosphatase 2 Catalytic Subunit Alpha (PPP2CA) and promoted k48-linked ubiquitination at its K41 residue, leading to the proteasomal degradation of PPP2CA proteins. Consequently, MKRN2-mediated PPP2CA repression increased β-catenin phosphorylation and decreased its protein levels, causing the inactivation of Wnt signaling pathway and amplification of apoptosis in ccRCC cells. Conclusions: This study demonstrated that the E3 ligase activity of MKRN2 had a pivotal role in regulating the PPP2CA-β-catenin-Wnt pathway and granted MKRN2 as a candidate tumor suppressor in ccRCC.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 12","pages":"5361-5377"},"PeriodicalIF":10.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435490/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Increased CAPG inhibits ferroptosis to drive tumor proliferation and sorafenib resistance in hepatocellular carcinoma via the WDR74-p53-SLC7A11 pathway. 增加的CAPG抑制铁下垂，通过WDR74-p53-SLC7A11途径驱动肝癌肿瘤增殖和索拉非尼耐药。

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.111419

Bing Quan, Fan Yao, Wenfeng Liu, Bei Tang, Miao Li, Shenxin Lu, Jinghuan Li, Rongxin Chen, Zhenggang Ren, Xin Yin

{"title":"Increased CAPG inhibits ferroptosis to drive tumor proliferation and sorafenib resistance in hepatocellular carcinoma via the WDR74-p53-SLC7A11 pathway.","authors":"Bing Quan, Fan Yao, Wenfeng Liu, Bei Tang, Miao Li, Shenxin Lu, Jinghuan Li, Rongxin Chen, Zhenggang Ren, Xin Yin","doi":"10.7150/ijbs.111419","DOIUrl":"10.7150/ijbs.111419","url":null,"abstract":"Hepatocellular carcinoma (HCC) presents a global therapeutic challenge owing to its aggressive tumor progression and limited treatment options. Therefore, identifying novel therapeutic targets is urgently needed. In this study, we identified CAPG as a top candidate gene that is upregulated in HCC tissues and predicts poor clinical prognosis, based on proteomic sequencing, public database analysis, and immunohistochemistry. The biological role of CAPG in HCC tumorigenesis was investigated using cell lines, xenograft models, and pulmonary metastasis models. We found that CAPG depletion inhibited tumor proliferation and metastasis both in vivo and in vitro. Functional assays were also performed to assess the effects of CAPG on sorafenib-induced ferroptosis. Colony formation assays, IC50 assays, qPCR, and Western blot analyses were conducted to examine the relationship between CAPG expression and sorafenib treatment. Notably, CAPG was upregulated following sorafenib exposure and contributed to sorafenib resistance. RNA sequencing, ChIP sequencing, co-immunoprecipitation, and ubiquitination assays were further employed to elucidate the molecular mechanisms involving CAPG. Mechanistically, CAPG promoted gene expression by inducing WDR74 transcription, which modulated the interaction between p53 and MDM2, resulting in p53 degradation. Our findings demonstrate that CAPG drives tumor proliferation and sorafenib resistance by inhibiting ferroptosis, suggesting that CAPG may serve as a promising target in HCC.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 12","pages":"5476-5495"},"PeriodicalIF":10.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

CLDN6 induces chemoresistance through protective autophagy in breast cancer. CLDN6通过保护性自噬诱导乳腺癌化疗耐药。

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.116340

Huinan Qu, Qiu Jin, Mingzi Zhang, Da Qi, Minghao Sun, Yuan Dong, Chengshi Quan

{"title":"CLDN6 induces chemoresistance through protective autophagy in breast cancer.","authors":"Huinan Qu, Qiu Jin, Mingzi Zhang, Da Qi, Minghao Sun, Yuan Dong, Chengshi Quan","doi":"10.7150/ijbs.116340","DOIUrl":"10.7150/ijbs.116340","url":null,"abstract":"Protective autophagy, a defensive response of cancer cells to chemotherapeutic stress, plays a critical role in the development of chemoresistance. Our previous research has demonstrated that the tight junction protein Claudin-6 (CLDN6) can induce autophagy and chemoresistance respectively. However, it remains unclear whether CLDN6 triggers protective autophagy under chemotherapeutic conditions. In this study, we focused on the role and mechanism of CLDN6 in inducing protective autophagy and promoting chemoresistance in breast cancer. We found that CLDN6 promoted chemoresistance by inducing protective autophagy in response to adriamycin (ADM) and paclitaxel (PTX). Mechanistically, CLDN6 interacted with LKB1 through its PDZ-binding motif, leading to the activation of AMPK/ULK1 signaling and subsequent promotion of protective autophagy. Notably, we discovered that chemotherapy increased CLDN6 expression through the reactive oxygen species (ROS)/GATA4 axis. Our results suggest that CLDN6 plays a pivotal role in breast cancer chemoresistance through protective autophagy, highlighting its potential as a therapeutic target to improve treatment outcomes of breast cancer patients.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 12","pages":"5444-5459"},"PeriodicalIF":10.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Altered Heme and Redox Homeostasis Underpin Late-onset Alzheimer's Disease. 改变血红素和氧化还原稳态支持晚发型阿尔茨海默病。

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.116204

Adedamola Saidi Soladogun, Chantal Vidal, Maria Del Carmen Chacon Castro, Heng Du, Li Zhang

{"title":"Altered Heme and Redox Homeostasis Underpin Late-onset Alzheimer's Disease.","authors":"Adedamola Saidi Soladogun, Chantal Vidal, Maria Del Carmen Chacon Castro, Heng Du, Li Zhang","doi":"10.7150/ijbs.116204","DOIUrl":"10.7150/ijbs.116204","url":null,"abstract":"Early-onset Alzheimer's disease (EOAD) is associated with highly penetrant mutations in genes such as PSEN2, whereas the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD) is the APOE4 allele. Despite intense research efforts, how neuronal dysfunction is initiated in LOAD cases and how the initiating events for EOAD and LOAD differ remain to be clarified. Using biochemical measurements of energy metabolism, heme and redox homeostasis, in combination with RNA-Sequencing analysis, we characterized biochemical and transcriptome differences in neurons differentiated from human EOAD and LOAD iPSC-derived neural stem cells, relative to their respective control neurons. Strikingly, we found that LOAD neurons, not EOAD neurons, are defective in heme and redox homeostasis. The levels of multiple proteins and enzymes involved in heme synthesis, degradation, and oxidative phosphorylation are preferentially decreased in LOAD neurons, not EOAD neurons. Likewise, heme transport is decreased in LOAD neurons. ROS generation is strongly increased in LOAD neurons, not EOAD neurons. Further, many genes involved in heme and redox homeostasis, as well as cellular energy generation, are downregulated in LOAD neurons, not EOAD neurons. Together, these results strongly suggest that altered heme and redox homeostasis in LOAD neurons underlie the initiation of neurological deficits.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 12","pages":"5393-5410"},"PeriodicalIF":10.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Mitochondrial RNA in Inflammation. 炎症中的线粒体RNA。

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.119841

Jian Chen, Chen You, Haibo Xie, Qixing Zhu

{"title":"Mitochondrial RNA in Inflammation.","authors":"Jian Chen, Chen You, Haibo Xie, Qixing Zhu","doi":"10.7150/ijbs.119841","DOIUrl":"10.7150/ijbs.119841","url":null,"abstract":"Mitochondria are dynamic organelles integral to cellular energy metabolism and homeostasis. Beyond their traditional roles, a growing body of evidence underscores the importance of mitochondria as pivotal regulators of innate immune signaling pathways. Recently, mitochondrial RNA (mtRNA) has been identified as a novel modulator of inflammatory responses. mtRNA is detected by intracellular pattern recognition receptors (PRRs), which subsequently activate the mitochondrial antiviral-signaling protein (MAVS) and the interferon regulatory factor 3 (IRF3)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling axis, as well as inflammasome pathways. This activation leads to the production of type I interferons and pro-inflammatory cytokines. Furthermore, mtRNA facilitates the propagation of inflammatory signals through exosome-mediated intercellular transfer. Among the various forms of mtRNA, mitochondrial double-stranded RNA (mt-dsRNA) is particularly prone to activating inflammatory responses due to its distinctive double-helical structure. The aberrant accumulation of mt-dsRNA is strongly linked autoimmune diseases, degenerative disease, Liver Disease, kidney disease, cancers, cardiovascular diseases, and respiratory ailments. This review proposes innovative therapeutic strategies aimed at degrading pathological mtRNA or interrupting inflammatory pathways by targeting critical regulatory nodes in mtRNA metabolism and its downstream inflammatory processes.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 12","pages":"5378-5392"},"PeriodicalIF":10.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast. Dectin-1通过促进巨噬细胞浸润和向肌成纤维细胞转化在慢性肾脏疾病中的致病作用

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-16 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.119129

Lingling Shen, Jingyi Li, Anqi Zhang, Sijing Yan, Wenxin Sha, Yucheng Wang, Shi Feng, Cuili Wang, Zhimin Chen, Hongfeng Huang, Bingjue Li, Pingping Ren, Suhan Zhou, Siqi Wu, Yanli Wang, Zhouji Shen, Song Rong, Hermann Haller, Hong Jiang, Jianghua Chen

{"title":"Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast.","authors":"Lingling Shen, Jingyi Li, Anqi Zhang, Sijing Yan, Wenxin Sha, Yucheng Wang, Shi Feng, Cuili Wang, Zhimin Chen, Hongfeng Huang, Bingjue Li, Pingping Ren, Suhan Zhou, Siqi Wu, Yanli Wang, Zhouji Shen, Song Rong, Hermann Haller, Hong Jiang, Jianghua Chen","doi":"10.7150/ijbs.119129","DOIUrl":"10.7150/ijbs.119129","url":null,"abstract":"Dectin-1, a pattern recognition receptor predominantly expressed on myeloid cells, is required for maintaining immune homeostasis. However, the role of Dectin-1 in chronic kidney disease (CKD) remains unknown. Here we reported that Dectin-1 was markedly upregulated in the fibrotic kidneys of CKD patients, primarily in macrophages, and its expression correlated with fibrosis severity and renal dysfunction. Genetic deletion of Dectin-1 attenuated renal fibrosis induced by unilateral ureteral obstruction (UUO) or ischemia-reperfusion (IR), a finding confirmed in bone marrow chimeric mice. Macrophage-specific Dectin-1 deletion similarly protected against renal fibrosis, demonstrating its cell-autonomous role. Mechanistically, Dectin-1 promoted macrophage infiltration via Syk/NF-κB/CCL2-CCR2 axis, while facilitating macrophage-to-myofibroblast transition (MMT) by activating TGF-β/Smad signaling. Pre-clinically, pharmacological inhibition of Dectin-1 with Laminarin significantly reduced renal fibrosis in UUO and IR models, highlighting its therapeutic potential for CKD.","PeriodicalId":13762,"journal":{"name":"International Journal of Biological Sciences","volume":"21 12","pages":"5287-5304"},"PeriodicalIF":10.0,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Comment on "IGF2BP3 promotes the proliferation and cisplatin resistance of bladder cancer by enhancing the mRNA stability of CDK6 in an m⁶A dependent manner". 点评“IGF2BP3通过增强CDK6 mRNA的稳定性，以m6A依赖的方式促进膀胱癌的增殖和顺铂耐药”

IF 1 2区生物学

International Journal of Biological Sciences Pub Date : 2025-08-16 eCollection Date: 2025-01-01 DOI: 10.7150/ijbs.120024

Yongzheng Han, Chengming Li, Guangzhen Wu

引用次数: 0