Cell Biochemistry and Biophysics最新文献

{"title":"Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.","authors":"Megh Pravin Vithalkar, Shreya Pradhan, K S Sandra, H B Bharath, Yogendra Nayak","doi":"10.1007/s12013-025-01696-4","DOIUrl":"https://doi.org/10.1007/s12013-025-01696-4","url":null,"abstract":"<p><p>Idiopathic Pulmonary Fibrosis (IPF) is a severe, rapidly advancing disease that drastically diminishes life expectancy. Without treatment, it can progress to lung cancer. The precise etiology of IPF remains unknown, but inflammation and damage to the alveolar epithelium are widely thought to be pivotal in its development. Research has indicated that activating the NLRP3 inflammasome is a crucial mechanism in IPF pathogenesis, as it triggers the release of pro-inflammatory cytokines such as IL-1β, IL-18, and TGF-β. These cytokines contribute to the myofibroblast differentiation and extracellular matrix (ECM) accumulation. Currently, treatment options for IPF are limited. Only two FDA-approved medications, pirfenidone and nintedanib, are available. While these drugs can decelerate disease progression, they come with a range of side effects and do not cure the disease. Additional treatment strategies primarily involve supportive care and therapy. Emerging research has highlighted that numerous flavonoids derived from traditional medicines can inhibit the critical regulators responsible for activating the NLRP3 inflammasome. These flavonoids show promise as potential therapeutic agents for managing IPF, offering a new avenue for treatment that targets the core inflammatory processes of this debilitating condition.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143447376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suyin Detoxification Prescription Regulates the Klotho and ERK/NF-κB Signaling Pathways to Alleviate Renal Injury.","authors":"Lianghui Shu, Li Quan, Yanping Wang, Yanlin Chen, Chen Yong, Fang Tian, Kun Gao, Enchao Zhou","doi":"10.1007/s12013-025-01695-5","DOIUrl":"https://doi.org/10.1007/s12013-025-01695-5","url":null,"abstract":"<p><p>Chronic Kidney Disease (CKD) is an irreversible pathological condition resulting from the gradual accumulation of nephrotoxic substances. The application of the \"Kidney Toxicity\" theory in CKD treatment holds significant research potential and promising clinical prospects. We established a murine model of unilateral ureteral obstruction (UUO) and administered the traditional Chinese medicine prescription Suyin detoxification prescription (SDP). The efficacy of SDP was assessed by comparing the expression levels of Klotho, NF-κB, pNF-κB, VEGF, α-SMA, pERK1/2, and ERK1/2 proteins with those in the Sham operation group using immunohistochemistry, RT-qPCR, and Western Blot techniques. The study revealed a significant reduction in the expression of Klotho and VEGF proteins during the progression of renal fibrosis in mice, while there was a marked increase in the levels of pNF-κB, α-SMA, and pERK1/2 proteins, demonstrating statistical significance (p < 0.05). In UUO mice treated with a high dose of SDP, these proteins exhibited an opposite expression trend compared to that observed in pure operated model mice, with statistically significant differences (p < 0.05). Subsequently, we investigated the relationship between Klotho protein and the ERK/NF-κB signaling pathway-related proteins in human umbilical vein endothelial cells (HUVECs). Knockdown of Klotho protein in HUVECs confirmed its potential as a target for SDP's renal protective effects in vivo by regulating ERK/NF-κB signaling pathway-related proteins to some extent. The renoprotective effect of SDP is mediated through modulation of Klotho protein expression in renal tissues, thereby influencing the ERK/NF-κB signaling pathway and ameliorating the inflammatory processes associated with renal fibrosis. The present study has significantly contributed to the advancement and refinement of the pathogenesis of \"Kidney Toxicity\" as well as the therapeutic approach of \"Kidney Detoxification\".</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143447457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"STYX Interacts with FBXW7 to Promote AML Proliferation via Inhibiting the Ubiquitination of CCNE1.","authors":"Rui Yang, Jing Ning, Hainan Wang, Hui Ma, Lijuan Cui","doi":"10.1007/s12013-025-01692-8","DOIUrl":"https://doi.org/10.1007/s12013-025-01692-8","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is a challenging hematologic malignancy with a poor prognosis. STYX, a catalytically inactive phosphatase, is overexpressed in various cancers and has been shown to promote cellular proliferation. However, its clinical relevance and impact on AML cell behavior remain poorly understood. This study investigates the role of STYX in AML and elucidates its underlying molecular mechanisms. Peripheral blood samples were collected from 50 patients with AML and 25 healthy controls, and the expression of STYX and FBXW7 was analyzed using RT-qPCR and Western blot. THP-1 cells (AML cell line) were transfected with lentivirus vectors to overexpress STYX, FBXW7, or CCNE1. The effects of these proteins on THP-1 cell proliferation and apoptosis were assessed by RT-qPCR, Western blot, CCK-8, EdU, and TUNEL assays. Interactions between STYX and FBXW7, as well as FBXW7 and CCNE1, were confirmed via STRING analysis and endogenous co-immunoprecipitation (CO-IP). Furthermore, the ubiquitination level of CCNE1 was examined through immunoprecipitation (IP) and Western blot. Upregulated STYX mRNA and protein levels, along with downregulated FBXW7 mRNA and protein levels, were observed in peripheral blood samples from MLL-AF9 fusion gene-positive AML cases, with a negative correlation between STYX and FBXW7. Overexpression of STYX in AML cells increased cell viability, promoted proliferation, and inhibited apoptosis, thus accelerating AML progression. STYX overexpression also facilitated the interaction with FBXW7, downregulated FBXW7 expression, and impaired the ubiquitin-mediated degradation of CCNE1. FBXW7 overexpression reversed STYX-induced proliferation and apoptosis effects in AML cells, while CCNE1 overexpression counteracted the suppressive effects of FBXW7 on AML progression. STYX promotes AML proliferation by disrupting the ubiquitin degradation pathway of CCNE1 through its interaction with FBXW7, thereby accelerating disease progression. These findings indicate that targeting STYX may offer a promising therapeutic approach for AML.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MICAL1 Mediates TGF-β1-Induced Epithelial-to-Mesenchymal Transition and Metastasis of Hepatocellular Carcinoma by Activating Smad2/3.","authors":"Xun Zhuang, Chunrong Wang, Zhenghui Ge, Mengjie Wu, Mengjiao Chen, Zhen Chen, Jianghong Hu","doi":"10.1007/s12013-025-01668-8","DOIUrl":"https://doi.org/10.1007/s12013-025-01668-8","url":null,"abstract":"<p><p>Epithelial-mesenchymal transition (EMT) induced by transforming growth factor-β (TGF-β) is involved in hepatocellular carcinoma (HCC) growth and metastasis. Our study aimed to investigate the role of molecules interacting with CasL 1 (MICAL1) in regulating TGF-β-triggered EMT in HCC and the related mechanisms. After detecting MICAL1 expression and prognostic value in HCC, in vitro assays including CCK-8 assay, EdU staining, flow cytometry assay, Transwell assay, western blotting, and RT-qPCR and in vivo metastasis assay was conducted to evaluate the influence of MICAL1 knockdown on the proliferation and apoptosis as well as TGF-β-induced EMT and metastasis of Huh7 and MHCC97H cells. MICAL1 was highly expressed in HCC, and its high expression was related to histological grade, TNM stage, and shorter overall survival of HCC patients. MICAL1 silencing suppressed proliferation, promoted apoptosis, and curbed TGF-β1-triggered cytoskeletal remodeling, EMT, and metastasis of HCC cells. MICAL1 knockdown impeded TGF-β1-induced upregulation in phosphorylated-Smad2/3 protein levels and reduced Smad2/3 mRNA levels in HCC cells. MICAL1 downregulation enhanced the polyubiquitination and proteasomal degradation of TβRI. Additionally, MICAL1 silencing suppressed tumor growth and lung metastasis in Huh7-derived xenograft mouse models. Collectively, MICAL1 knockdown impairs TGF-β1-stimulated EMT and metastasis of HCC cells by restraining Smad2/3 phosphorylation and activation.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phellodendrine Exerts Protective Effects on Intra-abdominal Sepsis by Inactivating AKT/NF-kB Signaling.","authors":"Ang Li, Peng Liu, Jiaohong Gan, Weijun Fang, Anjie Liu","doi":"10.1007/s12013-024-01658-2","DOIUrl":"https://doi.org/10.1007/s12013-024-01658-2","url":null,"abstract":"<p><p>Acute kidney injury (AKI) and acute lung injury (ALI) are major complications of intra-abdominal sepsis, leading to increased mortality. Phellodendrine (PHE) is a characteristic and important active ingredient of Phellodendri Cortex, possessing multiple pharmacological properties. This study intends to explore the effect of PHE on intra-abdominal sepsis-induced AKI and ALI. An intra-abdominal infection-induced rat model of sepsis was established by fecal intraperitoneal injection, followed by the administration of PHE. ELISA was used to determine plasma levels of inflammatory cytokines. Hematoxylin-eosin, Periodic acid Schiff, and Masson trichrome staining were employed for histopathological analysis of rat kidney and lung tissues. Western blotting was used to estimate the AKT/NF-κB signaling-related protein levels. The results showed that PHE improved the survival rate of septic rats and reduced plasma levels of proinflammatory cytokines. PHE administration attenuated pathological lesions in the kidneys and lungs of septic rats. Mechanistically, PHE treatment blocked AKT/NF-κB signaling in septic rats' kidneys and lungs. In conclusion, PHE ameliorates intra-abdominal sepsis-induced kidney and lung injury possibly by inactivating AKT/NF-kB signaling.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-634 Mediated Aquaporin 5 Expression Regulates the Inflammatory Response and Apoptosis in Lipopolysaccharide-Induced Human Nasal Epithelial Cells.","authors":"Kai Wang, Nan Zhang","doi":"10.1007/s12013-025-01689-3","DOIUrl":"https://doi.org/10.1007/s12013-025-01689-3","url":null,"abstract":"<p><p>To investigate the effects and potential mechanism of miR-634 that regulates aquaporin 5 (AQP5) to regulate the inflammatory response and apoptosis in LPS-induced human nasal epithelial cells (HNEpCs). The mRNA expressions of miR-634 and AQP5 in the tissues of patients with chronic rhinosinusitis (CRS) and LPS-induced HNEpCs were detected by qRT-PCR. Western blotting was performed to detect the protein expression of AQP5 in HNEpCs. The apoptosis was assessed by flow cytometry. The cell viability was detected by CCK-8 kit. Combined with bioinformatics analysis, dual-luciferase reporter and western blotting, the interaction between AQP5 and miR-634 were predicted and verified. It proved that the mRNA expression of miR-634 in CRS group was significantly up-regulated, while AQP5 was down-regulated. And the expression of AQP5 in CRS group was down-regulated compared with control group. In vitro experiments indicated that the expression of miR-634 increased gradually, while AQP5 decreased gradually with the increase of LPS concentration. The cell viability was inhibited and apoptosis was promoted in LPS-induced group. In addition, it was found that miR-634 could inhibit cell viability and promote apoptosis. QRT-PCR results implied that miR-634 up-regulated the expression of inflammatory factor-related mRNA in LPS-induced HNEpCs. Combined with bioinformatics analysis and qRT-PCR, it was confirmed that AQP5 was the direct target of miR-634. MiR-634 directly targeted AQP5 to regulate CRS progression, including inhibiting cell viability, promoting apoptosis and aggravating inflammatory response, which may provide theoretical basis for its use as a biomarker for CRS treatment.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Juglone Encapsulation in PLGA Nanoparticles Improves Solubility and Enhances Apoptosis in HeLa Cells.","authors":"Duygu Elif Yilmaz, Busra Gumus, Hasan Demirci","doi":"10.1007/s12013-025-01691-9","DOIUrl":"https://doi.org/10.1007/s12013-025-01691-9","url":null,"abstract":"<p><p>The anticancer potential of juglone, a naphthoquinone derived from walnut trees, has been extensively studied; however, its hydrophobicity and toxicity obstruct its therapeutic applications. This study aimed to overcome these challenges by encapsulating juglone into poly (lactic-co-glycolic acid) (PLGA) nanoparticles and evaluating their antiproliferative and apoptotic effects on HeLa cells. Juglone nanoparticles (JNP) were obtained by single emulsion solvent evaporation method. Its key physicochemical properties, such as particle size, zeta potential, drug loading, release yield, and encapsulation efficiency values were calculated as 207.45 ± 1.67 nm, -24.12 ± 2.21 mV, 47.80, 66.90 and 90.12%, respectively. JNP's antiproliferative effects were compared to those of free juglone on HeLa cells. The calculated IC₅₀ values for free juglone and JNPs were 17.07 µM and 20.64 µM, respectively. Both formulations exhibited comparable dose-dependent antiproliferative effects across the tested concentrations. However, the nanoparticle-based delivery system demonstrated enhanced apoptotic activity, as evidenced by increased caspase-3 activation and greater suppression of BCL-2 levels relative to free juglone. These findings were further corroborated by TUNEL and immunocytochemical analyses, which confirmed the superior apoptotic induction by the nanosystem. Collectively, the results highlight the potential advantages of PLGA-based nanoparticle systems for the delivery of juglone, thereby improving its water solubility-a key limiting factor for its use-while minimizing its toxicity. These findings offer a promising approach for its application as an effective anticancer agent via nanoparticle-based delivery.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioinformatics-based Prognosis Effect of Ferroptosis-related Genes on Gastric Cancer.","authors":"Tao Wang, Aoran Zeng, Lili Zhu, Fengzhi Liu, Bowen Pang, Yan Liu, Zijian Liu, Jing Wang","doi":"10.1007/s12013-024-01634-w","DOIUrl":"https://doi.org/10.1007/s12013-024-01634-w","url":null,"abstract":"<p><p>This study investigated the relationship between ferroptosis related genes and the prognosis of gastric cancer patients. Gene expression and corresponding clinical data were obtained from the TCGA database. Differentially expressed genes in gastric cancer were identified using R software, and prognostic-related genes were screened using univariate Cox regression analysis. Prognostic genes related to ferroptosis were determined using a Venn diagram. A prognostic model was constructed using LASSO-Cox regression analysis. Additionally, the expression of DUSP1 in gastric cancer was validated through immunohistochemistry, Western blot, and qRT-PCR. The impact of DUSP1 on ferroptosis was analyzed by measuring iron and lipid content in gastric cancer cell lines. A total of 407 gastric cancer patients were included as the training cohort. Fifteen prognostic genes related to ferroptosis were identified, and an 11-gene prognostic model was constructed. Risk scores were calculated for each patient, revealing that the overall survival rate was higher in the low-risk group compared to the high-risk group. ROC curves, PCA plots, and Kaplan-Meier survival curves demonstrated the model's efficacy in predicting 5-year survival rates (AUC = 0.716). Increased DUSP1 expression, correlated with higher Fe2+ and lipid ROS levels, was observed in gastric cancer cells with increasing Erastin concentration. The prognostic model effectively predicts gastric cancer patient outcomes. DUSP1 is lowly expressed in gastric cancer tissues and is associated with malignancy and metastasis, playing a role in ferroptosis in gastric cancer cells.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TUFT1 Modulates Cell Proliferation, Migration, Invasion, Stemness and EGFR Signaling in Cervical Cancer through Interacting with and Targeting ATF1.","authors":"Chunhua Han, Huifen Gao, Fengqiong Li, Lin Lin, Muying Qian, Lin Feng","doi":"10.1007/s12013-025-01673-x","DOIUrl":"https://doi.org/10.1007/s12013-025-01673-x","url":null,"abstract":"<p><p>Cervical cancer remains a frequently-occurring gynecologic health problem posing a great threat to women. Tuftelin1 (TUFT1), an acidic protein possessing secretory capacity, has been reported to drive cisplatin resistance in cervical cancer cells. Accordingly, the current study is intended to figure out the specific impacts of TUFT1 on the aggressive behaviors of cervical cancer cells and make an in-depth study into the related regulatory mechanism. Firstly, analysis of TUFT1 expression in cervical cancer cells was performed by RT-qPCR and Western blotting. Cervical cancer cell proliferation was estimated via CCK-8 and colony formation assays. Wound healing, transwell as well as sphere formation assays were used to appraise cell migration, invasion, and stemness, respectively. Western blotting examined the expressions of metastasis- and stemness-associated factors and RT-qPCR also tested the expressions of stemness-associated factors. Co-IP assay was used to verify the binding between TUFT1 and activating transcription factor 1 (ATF1). Subsequent ATF1 expression was examined by RT-qPCR and Western blotting after TUFT1 was silenced. After co-transfected with TUFT1 interference and ATF1 overexpression plasmids, aforementioned functional experiments were conducted again. Western blotting also analyzed the expressions of epidermal growth factor receptor (EGFR) signaling-associated proteins. The experimental data determined that TUFT1 expression was fortified in cervical cancer cells and TUFT1 absence diminished cervical cancer cell proliferation, migration, invasion, and stemness. Besides, TUFT1 bond to ATF1 and positively modulated ATF1 expression. Moreover, ATF1 elevation countervailed the impacts of TUFT1 insufficiency on the proliferation, migration, invasion, stemness as well as EGFR signaling in cervical cancer cells. Anyway, TUFT1 might interact with ATF1 to elicit pro-proliferation, pro-metastasis, and pro-stemness properties and inactivate EGFR signaling in cervical cancer, supporting that TUFT1 might be valued as a potential hallmark for cervical cancer.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Gut Microbiome and Colorectal Cancer: An Integrative Review of the Underlying Mechanisms.","authors":"Farah Karam, Yara El Deghel, Rabah Iratni, Ali H Dakroub, Ali H Eid","doi":"10.1007/s12013-025-01683-9","DOIUrl":"https://doi.org/10.1007/s12013-025-01683-9","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is the second leading cause of cancer-related mortality worldwide. While the incidence and mortality of CRC have decreased overall due to better screening, rates in adults under 50 have risen. CRC can manifest as inherited syndromes (10%), familial clustering (20%), or sporadic forms (70%). The gut microbiota, comprising mainly firmicutes and bacteroidetes, play a key role in CRC development and prevention. Indeed, CRC progression is influenced by the dynamic interaction between the gut microbiota, the intestinal barrier, the immune system, and the production of short-chain fatty acids. Not surprisingly, imbalance in the gut microbiota, termed dysbiosis, has been linked to CRC due to ensuing chronic inflammation, DNA damage, and oxidative stress. This may explain the notion that probiotics and fecal microbiota transplantation offer potential strategies for CRC prevention and treatment by restoring microbial balance and enhancing anti-cancer immune responses. This review appraises the roles of gut microbiota in promoting or preventing CRC. It also discusses the mechanistic interplay between microbiota composition, the intestinal barrier, and the immune system, with the hope of developing potential therapeutic strategies.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}