FASEB JOURNAL
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2025
·Vol. 39
·期 20
·e71141
·
IF 4.2
Mingxing Sui,Shuying Wu,Qingqing Song,Siyao Chen,Yingli Lu
Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder with complex pathophysiology and limited therapeutic options. To elucidate potential biomarkers and molecular mechanisms underlying PCOS, we analyzed gene expression profiles in ovarian tissues from dehydroepiandrosterone (DHEA)-induced PCOS mice and control mice by conducting mRNA sequencing. Transcription factor forkhead box O6 (FOXO6) drew our focus, as it exhibited higher expression in PCOS ovarian tissues (fold change ≈1.71, p < 0.05). Functional validation revealed that FOXO6 knockdown alleviated ovarian dysfunction accompanied by attenuated mitochondrial damage and reduced apoptosis in the ovarian tissues of PCOS mice. Meanwhile, high expression of FOXO6 was also observed in dihydrotestosterone (DHT)-treated granulosa cells. Post-FOXO6 downregulation, DHT-induced apoptosis and mitochondrial dysfunction were suppressed. Notably, the RNA level of FOXO6 was upregulated by the methyltransferase METTL3, which inhibited the decay of FOXO6 RNA by increasing the m6A modification of FOXO6 RNA. The inhibitory effects of METTL3 knockdown on apoptosis and mitochondrial dysfunction in granulosa cells were weakened by FOXO6 overexpression. Furthermore, transcriptomic profiling of DHT-treated granulosa cells with or without FOXO6 overexpression was conducted. This analysis yielded 386 upregulated genes and 582 downregulated genes, among which thioredoxin-interacting protein (TXNIP) was prominently upregulated in FOXO6-overexpressing cells (fold change ≈4.5, p < 0.05). FOXO6 transcriptionally activated TXNIP by binding to its promoter, and TXNIP knockdown reversed the effects of FOXO6 overexpression. Collectively, our findings highlight the METTL3/FOXO6/TXNIP axis as a vital regulator of ovarian dysfunction in PCOS, offering novel insights for therapeutic intervention. Graphical To elucidate PCOS biomarkers and mechanisms, mRNA-sequencing of ovarian tissues from DHEA-induced PCOS and control mice identified highly expressed FOXO6 (FC ≈1.71, p < 0.05). FOXO6 knockdown alleviated PCOS ovarian dysfunction, mitochondrial damage, and apoptosis, and suppressed DHT-induced granulosa cell defects. METTL3 upregulated FOXO6 via m6A modification to inhibit its RNA decay. FOXO6 activated TXNIP transcription by binding its promoter. This highlights the METTL3/FOXO6/TXNIP axis as a key PCOS ovarian dysfunction regulator, offering new insights for PCOS therapy.
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FREE RADICAL BIOLOGY AND MEDICINE
·
2026
·
IF 8
Huanhuan Wang,Hanshu Zhao,Jiadi Gao,Sihan Liu,Yuanqi Xu,Xinyue Zhao,Shanshan Yang,Baozhi Gang,Zhongling Zhang
Vascular dementia (VaD) is a major cause of cognitive decline in the elderly, with chronic cerebral hypoperfusion (CCH) as its core pathogeny linked to neuroinflammation. Microglial M1 polarization drives CCH-related neuroinflammation, but its epigenetic regulation remains unclear. N6-methyladenosine (m6A) modification, centered on methyltransferase-like 14 (METTL14), is abundant in the brain, while CCAAT enhancer binding protein delta (CEBPD) is associated with central nervous system inflammation. This study explored METTL14’s role in microglial polarization and CCH pathology. In vitro , HMC3 cells induced by LPS/TNF-α (10 μg/mL, 50 ng/mL) showed upregulated METTL14 and CEBPD. METTL14 knockdown via short hairpin RNA inhibited the expression of M1 phenotypic markers (iNOS, CD86), reduced the release of pro-inflammatory factors (IL-1β, IL-6), and blocked NF-κB nuclear translocation, indicating that METTL14 silencing suppresses LPS/TNF-α-induced microglial M1 polarization and inflammatory response. In bilateral common carotid artery occlusion (BCCAo)-induced CCH rats, hippocampal METTL14/CEBPD was elevated. Adeno-associated virus-mediated METTL14 knockdown not only attenuated neuroinflammation and neuronal apoptosis in hippocampal CA1, but also significantly improved spatial learning memory and object recognition ability. Mechanistically, RIP-PCR and MeRIP-qPCR confirmed METTL14 enhances CEBPD mRNA stability via m6A modification. CEBPD overexpression reversed METTL14 knockdown’s effect, identifying it as a key downstream mediator. In conclusion, METTL14 knockdown impairs CEBPD mRNA stability via m6A, inhibits TLR4/MyD88/NF-κB pathway and microglial M1 polarization, alleviating CCH-related neuroinflammation and cognitive impairment, providing a potential epigenetic target for VaD.
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MOLECULAR CANCER RESEARCH
·
2026
·
IF 5.8
Han Tianci,Xie Junwei,Tong Wei,Zhang Liang
The poor prognosis of esophageal carcinoma (ESCA) highlights the need to identify novel targets for ESCA treatment. We found that inhibitor of differentiation 4 (ID4) was decreased in ESCA tumor tissues and its expression was associated with the survival of ESCA patients. However, the role of ID4 in ESCA remains unclear. Here, in this study, we found that overexpression of ID4 suppressed the cell proliferation of ESCA in vitro as well as tumor growth in vivo, whereas knockdown of ID4 presented the opposite trend. On the other hand, ESCA cells with overexpression of ID4 reduced macrophage migration and M2 polarization. However, significant increases in macrophage migration and M2 polarization were observed in cultures with ID4 silence. Interestingly, CCL2 was found to mediate the function of ID4 on macrophage polarization. Mechanistically, we identified for the first time that ID4 interacted physically with TCF4 to inactivate TCF4 transcriptional activity, which led to a decrease in CCL2 expression. Moreover, RNA binding protein cell cycle associated protein 1 (CAPRIN1) bound to ID4 mRNA and downregulated its stability, which may contribute to its low expression in ESCA. Taken together, these results support a novel hypothesis that ID4 downregulation may contribute to the development of ESCA by interacting with TCF4, resulting in abnormal proliferation of ESCA cells and tumor-associated macrophage infiltration. ID4 may contribute to the innovation of ESCA biotherapy.
Implications: ID4 inhibits ESCA through suppresses cancer cell proliferation and macrophage M2 polarization, and ID4 could be a potential prognostic marker for patients with ESCA.
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JOURNAL OF BIOLOGICAL CHEMISTRY
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2026
·
IF 4.1
Dongsheng Xing,Hongwei Cao,Yan Yang,Shengyang Liu,Hanbing Yu,Zhenyu Liu,Kunrong Wang,Xin Wei,Aihui Yan
Tristetraprolin (TTP), which encodes an RNA-binding protein, was identified as a biomarker in three types of IgE-driven allergic tissues. Remarkably, in the nasal mucosa of the ragweed pollen-induced AR mouse model, TTP mRNA levels were increased approximately threefold. TTP overexpression in AR mice alleviated nasal inflammation and epithelial barrier damage, accompanied by reduced frequency of nasal spray and nasal friction, eosinophils/neutrophils/macrophages/goblet cells infiltration, and Th2 cytokines interleukin (IL)-4, IL-5, and IL-13 secretion. The impact of TTP on the activation and differentiation of Th2 cells was assessed by utilizing naïve CD4 T cells isolated from mice. We found that TTP significantly suppressed Th2 activation and differentiation, as evidenced by the decreased levels of cytokines and the percentage of Th2. Transcriptomic profiling of CD4+ T cells (with/without TTP overexpression) was analyzed, and 14 down-regulated genes containing AU-rich elements (AREs) were obtained. The study concentrated on downregulated E3 ubiquitin ligase tripartite motif 18 (TRIM18) in TTP-overexpressed CD4+ T cells. Specifically, TTP protein bound to the ARE located at positions +3640 to +3644 (5’-UAUUU-3’) within the 3’UTR of mouse TRIM18, and this interaction reduces TRIM18 mRNA stability, a process that depends on the active-site residue Cys-139 within the second CCCH-type zinc finger motif of TTP. TRIM18 overexpression weakened the effects in CD4+ T cells induced by TTP overexpression. Collectively, TTP suppresses Th2 activation and differentiation in AR by modulating TRIM18 mRNA stability, highlighting their interaction as a critical pathway in allergic inflammation.
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APOPTOSIS
·
2026
·Vol. 31
·期 2
·52
·
IF 8.1
Mao Dong,Sun Jufeng,Zhang Xiaowei,Wang Zhaoping,Zhang Yun
Colorectal cancer (CRC) is a malignant tumor originating from the epithelial cells of the colon and rectum. Interleukin enhancer binding factor 2 (ILF2), an emerging RNA-binding protein, has been implicated in the regulation of multiple cancer-related processes. However, its specific role in the pathogenesis and progression of CRC remains largely unexplored. In this study, we systematically investigated the functional role of ILF2 in CRC through multi-level experiments. ILF2 expression was first assessed in clinical CRC tissues via quantitative real-time PCR and western blot. Functional implications were further examined through gain-of-function and loss-of-function approaches. Cellular assays included CCK-8 proliferation, colony formation, Transwell migration/invasion, macrophage coculture, and flow cytometry for apoptosis, complemented by immunofluorescence staining. In vivo relevance was confirmed using xenograft models for tumor growth and metastasis. Mechanistically, Co-IP revealed a robust interaction between ILF2 and ILF3, while RIP, RNA pull-down and dual-luciferase reporter assays demonstrated direct binding of ILF3 to KLF16 mRNA, suggesting a novel regulatory axis in CRC progression. Our results demonstrated that both ILF2 mRNA and protein were significantly upregulated in colorectal cancer (CRC) tissues compared to matched peritumoral tissues. Functional assays revealed that ILF2 overexpression enhanced, whereas ILF2 knockdown suppressed, the proliferation, migration, and invasion capabilities of CRC cells in vitro. Additionally, ILF2 overexpression induced M0 macrophages to polarize toward an M2-like phenotype. Consistent with these findings, in vivo experiments indicated that ILF2 facilitated tumor growth and promoted liver metastasis in CRC. Our work suggests that ILF2 formed a complex with ILF3 to enhance the stability of KLF16 mRNA, thereby contributing to CRC progression through the regulation of KLF16. Graphical abstract A proposed working model of the ILF2/ILF3/KLF16/β-catenin axis in colorectal cancer progression. Hypothetical model illustrating that ILF2 binding to ILF3 stabilizes KLF16 mRNA, which in turn activates β-catenin signaling. This pathway ultimately promotes CRC cell proliferation, invasion, liver metastasis, and M2-type macrophage polarization.
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BIOCHEMICAL PHARMACOLOGY
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2026
·
IF 5.6
Mingxing Sui,Shuying Wu,Qingqing Song,Siyao Chen,Yingli Lu
Polycystic ovary syndrome (PCOS) is characterized by a constellation of symptoms, including menstrual cycle irregularities, hyperandrogenism, and polycystic ovarian morphology. Despite extensive research efforts, a thorough understanding of the underlying pathophysiology and effective treatment options for PCOS remain elusive. In this study, ovarian tissues from dehydroepiandrosterone (DHEA)-induced PCOS mice and control mice underwent mRNA sequencing. Through a comprehensive bioinformatics analysis, we systematically examined the sequencing data, and one cut homeobox 2 (Onecut2), a significantly downregulated gene in PCOS mice, was identified and selected as the primary research target. Our findings determined that the overexpression of Onecut2 efficiently alleviated pathological changes and reduced mitochondrial dysfunction in DHEA-induced PCOS mice. Additionally, Onecut2 was found to be expressed at a low level in human ovarian granulosa KGN cells treated with dihydrotestosterone (DHT). Gain-of-function and loss-of-function experiments uncovered that Onecut2 played a role in inhibiting apoptosis and mitochondrial damage in DHT-treated KGN cells. Dual-luciferase reporter assays demonstrated that Onecut2 overexpression activated the transcriptional activity of the sirtuin 3 (SIRT3) promoter, thereby controlling the function of granulosa cells. Mechanistic investigation revealed that the mRNA stability of Onecut2 was regulated by methyltransferase-like 3 (METTL3) via m6A modification. Collectively, this study demonstrates that Onecut2 exerts an inhibitory role in PCOS progression by transcriptionally regulating SIRT3 expression and that this regulation is influenced by METTL3-mediated m6A methylation.
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MICROBIOLOGICAL RESEARCH
·
2026
·
IF 8.5
Juan Li,Lei Zhao,Mei Yang,Jingyu Hu,Haimin Li,Wei Yin,Yan Yan,Jinyan Gu,Jiyong Zhou
Pseudorabies virus (PRV) reprograms host inflammatory responses and epitranscriptomics, yet how these processes are connected remains unclear. Here, we report a JNK-WTAP-m⁶A-DUSP5 regulatory circuit that coordinates viral replication and inflammatory responses. PRV infection activated c-Jun N-terminal kinase (JNK), which phosphorylated wilms tumor-associated protein (WTAP) to drive its nuclear export and disrupt the activity of the m⁶A methyltransferase complex. Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and biochemical analyses revealed a global reduction of N6-methyladenosine (m⁶A) on host transcripts, particularly on proinflammatory cytokines, alongside widespread m⁶A modification sites on viral transcripts. Consequently, reduced m⁶A prolonged the half-lives of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-18 (IL-18) mRNAs, as well as viral transcripts, thereby synergistically promoting PRV replication. Inhibition of JNK activity or restoration of m⁶A modification suppressed PRV replication in vitro and in vivo . Moreover, the m⁶A hypomethylation stabilized dual-specificity phosphatase 5 (DUSP5) transcripts at early infection, transiently restraining JNK activation and forming a negative feedback loop. These findings demonstrate that PRV reprograms the m⁶A machinery via JNK-mediated WTAP phosphorylation and highlights RNA methylation restoration as a promising antiviral strategy.
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Journal for ImmunoTherapy of Cancer
·
2026
·Vol. 14
·期 8
·e015072
·
IF 11.7
Lu Liu,Shihao Qi,Liye Shao,Junyang Cai,Qingqing Zeng,Xu Jiang,Fang Ma,Weiwei Lin
Background The low response rate to immunotherapy in patients with lung adenocarcinoma is primarily due to tumor immune evasion. The tumor immunosuppressive microenvironment orchestrates this evasion, yet the underlying mechanisms remain elusive. Here we identify non-specific cytotoxic cell receptor protein 1 (NCCRP1) as a critical and previously uncharacterized regulator of this process. Methods We first analyzed publicly accessible patient-derived single-cell RNA sequencing and RNA sequencing data to investigate the expression of NCCRP1 in lung adenocarcinoma and its impact on the tumor immune microenvironment. Subsequently, the Nccrp1 gene was knocked out in mouse lung adenocarcinoma cells using CRISPR-Cas9. The effect of NCCRP1 deletion on tumor growth was then evaluated using subcutaneous transplantation models in both NSG and C57BL/6 mice. Single-cell RNA sequencing, flow cytometry and multiple targeted in vivo interventions were employed to assess the influence of NCCRP1 on the tumor immune microenvironment. To explore the underlying mechanisms by which NCCRP1 regulates the tumor immune microenvironment, we conducted co-immunoprecipitation, RNA pull-down, ubiquitination assay, mass spectrometry, isobaric tags for relative and absolute quantitation proteomics, dual-luciferase reporter gene assay, and ELISA. Results Loss of NCCRP1 inhibits lung tumor growth and prolongs survival in immunocompetent C57BL/6 mouse models. NCCRP1 deficiency upregulates CX3CL1 to recruit CX3CR1 + antitumoral macrophages. These macrophages subsequently secrete CXCL9 and CXCL10, enhancing the infiltration of CD8 + T cells and NK cells into the tumor microenvironment. Mechanistically, NCCRP1 and STAU1 competitively bind to NEDD4. NCCRP1 deficiency enhances the STAU1-NEDD4 interaction, promoting ubiquitination and proteasomal degradation of STAU1, thereby increasing CX3CL1 messenger RNA stability. Remarkably, ablating NCCRP1 synergized with anti-programmed cell death protein 1 or interferon-γ therapy, leading to complete tumor eradication. Conclusion Our findings highlight NCCRP1 targeting as a promising therapeutic strategy to reprogram the immunosuppressive microenvironment and overcome the “cold tumor” phenotype in lung adenocarcinoma.
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JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
·
2026
·
IF 3.5
Xiaoran Sun,Yifan Chen,Kunyi Liu,Yi Si,Mingda Xuan,Rui Zhang,Jiao Jiao,Ting Liu,Shuangshuang Han,Jia Wang,Weifang Yu
Objective Gastric cancer remains a major global health burden. This study aimed to investigate the biological function, clinical significance, and underlying molecular mechanism of the RNA-binding protein YTHDF3 in gastric cancer (GC) progression. Methods YTHDF3 expression was analyzed using public databases (TCGA, GEO), clinical GC specimens (IHC, RT-qPCR), and GC cell lines. Functional roles were assessed through in vitro proliferation, migration, invasion, and apoptosis assays following YTHDF3 knockdown or overexpression, and via an in vivo subcutaneous tumor model. Mechanistic insights were gained through RNA sequencing, RIP-qPCR, dual-luciferase reporter assay, co-immunofluorescence, rescue experiments, and western blotting to identify downstream targets and signaling pathways. Results YTHDF3 was significantly upregulated in GC tissues, correlating with lymph node metastasis and advanced TNM stage. In vitro, YTHDF3 knockdown inhibited GC cell proliferation, migration, and invasion while promoting apoptosis, whereas its overexpression had the opposite effects. In vivo, YTHDF3 knockdown suppressed tumor growth. Mechanistically, YTHDF3 directly bound to and stabilized NEK7 mRNA. NEK7 was highly expressed in GC and crucial for YTHDF3-mediated oncogenic effects. Furthermore, YTHDF3 promoted GC progression by activating the Wnt/β-catenin signaling pathway via NEK7, which was validated using a pathway inhibitor (IWR-1-endo). Conclusion This study identifies the YTHDF3/NEK7 axis as a key regulator of GC progression via activation of the Wnt/β-catenin pathway. YTHDF3 represents a potential prognostic biomarker and a promising therapeutic target for GC. Graphical YTHDF3 binds to and stabilizes NEK7 mRNA in an m6A-dependent manner, thereby activating the Wnt/β-catenin signaling pathway and promoting gastric cancer progression. This study identifies the YTHDF3/NEK7 axis as a potential prognostic biomarker and therapeutic target in gastric cancer.
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MEDICAL ONCOLOGY
·
2025
·Vol. 42
·期 8
·1-13
·
IF 3.5
Cai Zhiren,Xie Yanqi,Li Luyao,Zheng Yuhang,Zhou Xianghui,Zhou Guanghua,Wang Ganping,Zeng Xin
Bladder cancer is a major health concern, and understanding its molecular mechanisms is essential for developing effective therapies. TET3, a DNA hydroxymethylase, has been linked to tumor progression, but its role in bladder cancer remains unclear. We analyzed single-cell RNA sequencing data and identified TET3 as a key regulator in tumor-promoting cells using scissor analysis. Functional experiments were performed to evaluate the effects of TET3 knockdown on cell proliferation, migration, and gene expression. In vivo tumor growth assays and histological analyses were conducted to assess the role of TET3 in tumor progression. Additionally, we assessed the impact of TET3 on stemness-associated gene expression and performed sphere formation assays to evaluate tumor cell self-renewal capacity. TET3 was highly expressed in tumor-promoting cells. Its knockdown significantly reduced cell proliferation, migration, and tumor growth in vivo. Tumors with TET3 knockdown had lower volumes, weights, and Ki67-positive cells. Mechanistically, TET3 regulated key tumor-related genes and pathways and reduced DNA 5hmC levels. Notably, TET3 knockdown downregulated multiple stemness-related transcription factors such as SOX2 and NANOG, and impaired sphere-forming efficiency, suggesting its essential role in maintaining cancer cell stemness. This study reveals that TET3 promotes tumor growth and progression in bladder cancer partly through modulation of the stemness pathway, highlighting its potential as a therapeutic target and prognostic marker.
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ALLERGOLOGY INTERNATIONAL
·
2025
·
IF 6.7
Maoxin Huang,Liping Dong,Yue He,Xinying Cai,Yun Lu,Jinlei Xu,Fengli Xiao
Background YTHDF1, a critical regulator of cellular processes, has attracted attention for its involvement in some inflammatory diseases. However, its specific association with atopic dermatitis (AD) remains unclear. The objective is to investigate the functional roles and underlying mechanisms of YTHDF1 in AD. Methods The expression of YTHDF1 was investigated by bioinformatics analysis and skin lesions of AD patients. The functional role and upstream and downstream regulatory mechanisms of YTHDF1 were examined through a series of in vitro and in vivo experiments. Adeno-associated virus (AAV)-mediated delivery of YTHDF1 in the AD mouse model was evaluated for its therapeutic potential. Results Bioinformatics analysis revealed that the YTHDF1 mRNA level in the skin lesions of AD was significantly higher than that in healthy people. YTHDF1 expression was significantly elevated in AD skin lesions, the DNCB-induced AD mouse model, and primary human keratinocytes and HaCaT cells stimulated with interleukin (IL)-4/IL-13, compared to controls. Both in vitro and in vivo experiments revealed that upregulation of YTHDF1 in AD exacerbated cell proliferation and inhibited keratinization by activating the PI3K/AKT pathway, which was modulated via the IL-4/IL-13/STAT3 axis. Moreover, topical application of AAV-YTHDF1 significantly improved AD-like lesions in the mouse model. Conclusions This study identifies YTHDF1 as a contributor to AD pathogenesis by influencing keratinocyte proliferation and differentiation. It also suggests that YTHDF1 could be a potential therapeutic target for AD treatment.
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Journal of Translational Medicine
·
2026
·Vol. 24
·期 1
·492
·
IF 9.7
Li Ze,Ling Yimin,Xiao Wei,Li JiaZheng,Rong JiaHui,Zhang Zewen,Wei Yan,Huo Zhongchao,Li Dong
Background Scutellarin (SCU) is a natural flavonoid compound exhibiting anti-tumor activity. This study aimed to elucidate the molecular mechanism underlying SCU’s therapeutic effects in liver cancer. Methods An integrated approach combining network pharmacology and transcriptomic analysis was employed to identify SCU-related targets, followed by the identification of core targets through protein–protein interaction (PPI) network construction and topological analysis using MCC and MCODE algorithms. A circular RNA (circRNA)-mediated competing endogenous RNA (ceRNA) regulatory network was constructed by integrating data from databases including miRWALK and circBANK with whole-transcriptome sequencing. Molecular interactions were experimentally validated using Western blotting, dual-luciferase reporter assays, and RNA immunoprecipitation (RIP). In Huh7 and HepG2 cells, overexpression and knockdown models of key RNAs were established to evaluate their functional roles, with cell proliferation, cell cycle distribution, and apoptosis assessed via CCK-8, colony formation, and flow cytometry assays. To investigate in vivo anti-tumor efficacy and associated mechanisms, a subcutaneous xenograft tumor model was established in nude mice. Results Integrated network pharmacology and transcriptomic analysis identified 11 core genes significantly enriched in the estrogen signaling pathway, among which ESR1 was validated as a key target. SCU downregulated ESR1 expression in a dose-dependent manner. Mechanistically, SCU upregulated miR-2682-5p while downregulating circSRBD1. Dual-luciferase reporter assays confirmed that miR-2682-5p directly binds to the 3′UTRs of both circSRBD1 and ESR1, supporting the existence of a circSRBD1/miR-2682-5p/ESR1 ceRNA regulatory axis. Functional studies demonstrated that overexpression of circSRBD1 attenuated SCU-induced cell cycle arrest, apoptosis, and suppression of proliferation, whereas silencing circSRBD1 enhanced these effects. Furthermore, SCU and fulvestrant exhibited synergistic anti-tumor activity both in vitro and in vivo. Conclusion This study identifies a novel circSRBD1/miR-2682-5p/ESR1 ceRNA regulatory axis that plays a critical role in mediating SCU’s inhibitory effects on liver cancer progression, highlighting the potential therapeutic value of combining SCU with fulvestrant. Clinical trial number Not applicable.
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