Current Issues in Molecular Biology最新文献

{"title":"Chronic Oral D-Galactose Induces Oxidative Stress but Not Overt Organ Dysfunction in Male Wistar Rats.","authors":"Jelena Martinovic, Ivana Gusevac Stojanovic, Sladjan Nesic, Ana Todorovic, Katarina Bobic, Sanja Stankovic, Dunja Drakulic","doi":"10.3390/cimb47030161","DOIUrl":"10.3390/cimb47030161","url":null,"abstract":"<p><p>D-galactose (d-gal) plays numerous roles in the organism as an energy-providing nutrient and also an important constituent of the complex glycoconjugates. However, excessive amounts of d-gal activate alternative metabolic pathways that can lead to the development of a pro-oxidative environment. This feature is used in numerous aging studies which implied intraperitoneal (i.p.) or subcutaneous (s.c.) administration of d-gal for a prolonged time. The present study aims to investigate the systemic effects of orally administered d-gal (200 mg/kg and 500 mg/kg, dissolved in tap water, for 6 weeks) by analyzing oxidative stress parameters in the liver, kidney, and heart. For comparison with natural aging, the effects were studied in rats aged 12, 18, 24, and 30 months. In addition, histopathologic analyzes and serum biochemical measurements were performed to investigate the potential structural and functional organ damage induced by d-gal administration. Our findings show that chronic oral administration of d-gal induces oxidative stress in rat organs and mimics some aspects of natural aging similar to those of 30-month-old rats. Consistent with its primary role in galactose metabolism, the liver exhibited the most pronounced oxidative damage. However, despite the increased oxidative stress, only minor histopathological changes were observed, while organ function remained largely unaffected. Oral intake of d-gal was found to have milder effects compared to i.p. or s.c. injections, suggesting that this model may induce some features of natural aging but without overt organ dysfunction.</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708433","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}

{"title":"The Proliferation of Chang Liver Cells After Simulated Microgravity Induction.","authors":"Huy Nghia Quang Hoang, Chi Nguyen Quynh Ho, Loan Thi Tung Dang, Nhan Lu Chinh Phan, Chung Chinh Doan, Han Thai Minh Nguyen, Cuong Phan Minh Le, Son Nghia Hoang, Long Thanh Le","doi":"10.3390/cimb47030164","DOIUrl":"10.3390/cimb47030164","url":null,"abstract":"<p><p>This study aimed to assess the recovery capability of Chang liver cells (CCL-13) following simulated microgravity (SMG) induction. CCL-13 cells were cultured under SMG conditions for 72 h, and control group cells were cultured under 1G conditions for an identical duration. Cells from the SMG and control groups were further cultured under 1G conditions and assessed after 24 h and 72 h intervals in the gravity recovery experiment. The WST1 results indicated that CCL-13 proliferation was more evident in the control group than in the SMG group after both the 24 h and 72 h intervals. The control group had a lower percentage of CCL-13 cells in the G0/G1 phase compared with the SMG group at both time points, and it exhibited a higher total percentage of cells in the S and G2/M phases. The control group exhibited elevated levels of cell-cycle-related proteins, including cyclin A, cyclin D, and cdk6, compared with the SMG group. The flow cytometry results revealed that the apoptotic rate in the control group was significantly lower than that in the SMG group at both the 24 h and 72 h time points. However, the apoptotic percentage in the SMG group at the 72-h mark was significantly lower than that at the 24-h mark. SMG reduces the viability and proliferation ability of CCL-13 cells. After a period of recovery and adaptation to normal gravity conditions (1G), the CCL-13 cells in the SMG group showed better signs of recovery after 72 h than after 24 h.</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708792","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}

{"title":"Editorial for Special Issue: \"Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment\".","authors":"Haibo Dong","doi":"10.3390/cimb47030160","DOIUrl":"10.3390/cimb47030160","url":null,"abstract":"<p><p>Metabolic-dysfunction-associated fatty liver disease (MAFLD) and alcohol-associated liver disease (ALD) represent two of the most prevalent chronic liver diseases globally, collectively affecting hundreds of millions of individuals [...].</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11940956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708806","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}

{"title":"Drug Pipeline for MASLD: What Can Be Learned from the Successful Story of Resmetirom.","authors":"Elizabeta Knezović, Marija Hefer, Suzana Blažanović, Ana Petrović, Vice Tomičić, Nika Srb, Damir Kirner, Robert Smolić, Martina Smolić","doi":"10.3390/cimb47030154","DOIUrl":"10.3390/cimb47030154","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), represent a growing global health problem linked to obesity, insulin resistance, and dyslipidemia. MASLD often leads to fibrosis, cirrhosis, and hepatocellular carcinoma. Currently, therapeutic options are limited, emphasizing the need for novel, targeted pharmacological interventions. Resmetirom, a selective thyroid hormone receptor beta (THR-β) agonist, offers a promising approach by specifically enhancing hepatic metabolism while minimizing systemic effects. Clinical trials have demonstrated its capacity to reduce hepatic triglyceride accumulation and improve lipid profiles. Early- and advanced-phase studies, including the MAESTRO program, highlight significant reductions in hepatic fat content and favorable impacts on noninvasive biomarkers of fibrosis with minimal side effects. This review highlights evidence from pivotal studies, explores resmetirom's mechanism of action, and compares its efficacy and safety with other emerging therapeutic agents. While resmetirom marks a breakthrough in non-cirrhotic MASH management, further long-term studies are essential to fully evaluate its clinical benefits and potential regulatory approval for broader use in MASLD and MASH.</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941580/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708802","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}

{"title":"A Comprehensive Review Exploring the Role of Bone Morphogenetic Proteins [BMP]: Biological Mechanisms.","authors":"Akanksha A Kalal, Satyajit Mohapatra","doi":"10.3390/cimb47030156","DOIUrl":"10.3390/cimb47030156","url":null,"abstract":"<p><p>Bone morphogenetic proteins (BMPs) belong to the TGF-β family. They perform diverse roles in development, osteogenesis, and vasculogenesis. BMPs have crucial functions in embryonic development and regulate the specialization of various cell types. The dysregulation of BMP activity at various stages in signal transduction is associated with a diverse range of human diseases. It is not surprising that BMPs also have a role in tumor formation and control the progression of cancer through different phases. Nevertheless, their specific roles remain ambiguous and the findings regarding this have been inconsistent. The objective of this review is to highlight the important functions of BMP ligands, receptors, and signaling mediators and the subsequent effects on final cellular responses resulting from these signaling modalities. This review elucidates the dysregulation of BMPs identified in various cancer types, which serves as a predictive sign for favorable results in cancer therapy. Alterations in the BMP pathway can represent a crucial milestone in the genetic and molecular mechanisms that facilitate cancer formation. This review has shown that alterations in certain components of the BMP pathway are evident in various tumor forms, including breast, gastric, colorectal, and myeloma cancer. This review reinforces the conclusion that BMPs exert both beneficial and detrimental effects on cancer biology. Collectively, these findings indicate that BMPs serve multiple functions in cancer; therefore, directing therapeutic efforts to focus on BMP may be a highly effective method for treating several cancers.</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708967","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}

{"title":"Linoleic Fatty Acid from Rwandan Propolis: A Potential Antimicrobial Agent Against <i>Cutibacterium acnes</i>.","authors":"Florent Rouvier, Lydia Abou, Emmanuel Wafo, Jean Michel Brunel","doi":"10.3390/cimb47030162","DOIUrl":"10.3390/cimb47030162","url":null,"abstract":"<p><p>Acne is a very common skin condition that causes pimples in 80% of adolescents despite the many effective treatments developed. Various compounds have been employed in the treatment of acne, including erythromycin ointments and antiseptics, yielding mixed results. The rise in erythromycin-resistant <i>C. acnes</i> strains has driven the pursuit of new antimicrobial agents, especially those obtained from natural sources. Propolis that was collected in Rwanda was extracted, fractioned, and analyzed for its activity against <i>C. acnes</i> growth in accordance with NCLSI guidelines. Our work revealed that linoleic acid has a significant effect on <i>C. acnes</i> growth at a low concentration (16 µg/mL). A comparison of the antimicrobial activities of a broad panel of well-known fatty acids revealed a specific mode of action for linoleic acid, characterized by a significant membranotropic effect on <i>Bacillus cereus</i> established by measuring extracellular ATP levels as an indicator of membrane permeability. Our data suggest that linoleic acid is effective against <i>C. acnes</i> and could be a promising candidate for developing a propolis-based ointment for acne treatment.</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708975","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}

{"title":"Lycobetaine Has Therapeutic Efficacy in Lung Squamous Cell Carcinoma by Targeting USP32 to Trigger Ferroptosis.","authors":"Shangping Xing, Hua Chai, Zhenlong Chen, Shuye Deng, Feifei Nong","doi":"10.3390/cimb47030163","DOIUrl":"10.3390/cimb47030163","url":null,"abstract":"<p><p>Ubiquitin-specific protease 32 (USP32), a deubiquitylating enzyme that controls the ubiquitin process, is overexpressed in multiple cancers and serves as a promising therapeutic target for cancer therapy. Drugs targeting ferroptosis have exhibited promising anticancer activity. Lycobetaine (LBT), a natural alkaloid, holds promise against various cancers, yet its specific targets and anticancer mechanisms remain unclear. In this study, we show that LBT induced ferroptosis in lung squamous cell carcinoma (LUSC) cells, accompanied by glutathione depletion and the accumulation of lipid peroxidation, malondialdehyde, and ferrous iron. Mechanistically, drug affinity responsive target stability-based mass spectrometry analysis, molecular dynamics simulations, and a cellular thermal shift assay confirmed that USP32 is a potential target of LBT in LUSC cells. Moreover, a strong interaction between USP32 and nuclear factor erythroid 2-related factor 2 (NRF2) was found via immunoprecipitation-mass spectrometry and co-immunoprecipitation. In addition, the ubiquitination assay results demonstrated that LBT treatment significantly increased NRF2 ubiquitination and degradation by targeting USP32. Importantly, USP32 overexpression effectively attenuated the effects of LBT on proliferation and ferroptosis in LUSC cells. In orthotopic LUSC xenografts, the administration of LBT significantly inhibited tumor growth and metastasis and induced ferroptosis by targeting the USP32-NRF2 signaling axis. Taken together, these data suggest that LBT exerts its anticancer effects by inhibiting USP32-mediated NRF2 deubiquitination to induce ferroptosis and that LBT may serve as a prospective USP32-targeting agent for LUSC treatment.</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709034","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}

{"title":"The Function of Myostatin in Ameliorating Bone Metabolism Abnormalities in Individuals with Type 2 Diabetes Mellitus by Exercise.","authors":"Chenghao Zhong, Xinyu Zeng, Xiaoyan Yi, Yuxin Yang, Jianbo Hu, Rongbin Yin, Xianghe Chen","doi":"10.3390/cimb47030158","DOIUrl":"10.3390/cimb47030158","url":null,"abstract":"<p><strong>Purpose: </strong>The molecular mechanisms involved in bone metabolism abnormalities in individuals with type 2 diabetes mellitus (T2DM) are a prominent area of investigation within the life sciences field. Myostatin (MSTN), a member of the TGF-β superfamily, serves as a critical negative regulator of skeletal muscle growth and bone metabolism. Current research on the exercise-mediated regulation of MSTN expression predominantly focuses on its role in skeletal muscle. However, due to the intricate and multifaceted mechanical and biochemical interactions between muscle and bone, the precise mechanisms by which exercise modulates MSTN to enhance bone metabolic disorders in T2DM necessitate additional exploration. The objective of this review is to systematically synthesize and evaluate the role of MSTN in the development of bone metabolism disorders associated with T2DM and elucidate the underlying mechanisms influenced by exercise interventions, aiming to offer novel insights and theoretical recommendations for enhancing bone health through physical activity.</p><p><strong>Methods: </strong>Relevant articles in Chinese and English up to July 2024 were selected using specific search terms and databases (PubMed, CNKI, Web of Science); 147 studies were finally included after evaluation, and the reference lists were checked for other relevant research.</p><p><strong>Results: </strong>Myostatin's heightened expression in the bone and skeletal muscle of individuals with T2DM can impede various pathways, such as PI3K/AKT/mTOR and Wnt/β-catenin, hindering osteoblast differentiation and bone mineralization. Additionally, it can stimulate osteoclast differentiation and bone resorption capacity by facilitating Smad2-dependent NFATc1 nuclear translocation and PI3K/AKT/AP-1-mediated pro-inflammatory factor expression pathways, thereby contributing to bone metabolism disorders. Physical exercise plays a crucial role in ameliorating bone metabolism abnormalities in individuals with T2DM. Exercise can activate pathways like Wnt/GSK-3β/β-catenin, thereby suppressing myostatin and downstream Smads, CCL20/CCR6, and Nox4 target gene expression, fostering bone formation, inhibiting bone resorption, and enhancing bone metabolism in T2DM.</p><p><strong>Conclusion: </strong>In the context of T2DM, MSTN has been shown to exacerbate bone metabolic disorders by inhibiting the differentiation of osteoblasts and the process of bone mineralization while simultaneously promoting the differentiation and activity of osteoclasts. Exercise interventions have demonstrated efficacy in downregulating MSTN expression, disrupting its downstream signaling pathways, and enhancing bone metabolism.</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708498","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}

{"title":"Development of an Anti-Zearalenone Nanobody Phage Display Library and Preparation of Specific Nanobodies.","authors":"Ying Zeng, Yiying Hu, Ganying Chen, Qingqing Feng, Ruiting Wang, Zhilin Zhang, Jinxian Chen, Junbin Liao, Danrong Lin, Wei Zhu","doi":"10.3390/cimb47030157","DOIUrl":"10.3390/cimb47030157","url":null,"abstract":"<p><p>Zearalenone (ZEN), a toxic estrogenic mycotoxin in cereals, threatens human and animal health through reproductive, immune, and cytotoxic effects, necessitating sensitive detection methods. While nanobodies offer advantages over conventional antibodies for on-site ZEN detection, their application remains unexplored. This study aimed to develop an anti-ZEN nanobody derived from an anti-ZEN phage display nanobody library. An alpaca was immunized with a ZEN-bovine serum albumin (ZEN-BSA) antigen, achieving peak serum antibody titers (1:25,600) following four immunizations. A high-capacity phage display nanobody library (1.0 × 10¹¹ plaque-forming units/mL) was constructed. Following four rounds of biopanning, an enrichment factor of 479 was achieved. Phage ELISA screening identified six phage display nanobodies with specific ZEN-binding activity, and multiple sequence alignment revealed four unique nanobody sequences. The selected phage display nanobody, designated phage-V44, was expressed and purified, and its presence was validated by SDS-PAGE and western blotting, which detected a single approximately 17 kDa band consistent with the expected nanobody size. We established a working curve for an indirect competitive enzyme-linked immunoassay (ELISA) for ZEN, which showed an IC50 value of 7.55 ng/mL. The specificity and affinity of the V44 were also verified. Collectively, the study successfully constructed an anti-ZEN phage display nanobody library, screened four specific ZEN-binding phage display nanobodies, and prepared the anti-ZEN nanobody V44. Thereby establishing a foundation for the nanobody's future integration into rapid on-site detection methods for ZEN in both animal feed and human food products.</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11940844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708799","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}

{"title":"SJB2-043, a USP1 Inhibitor, Suppresses A549 Cell Proliferation, Migration, and EMT via Modulation of PI3K/AKT/mTOR, MAPK, and Wnt Signaling Pathways.","authors":"Lipeng Wu, Meng Yu, Huosheng Liang, Long Lin, Huajian Li, Guangyang Chen, Halimulati Muhetaer, Jingjing Li, Bo Wu, Xuejing Jia, Yuanye Dang, Guodong Zheng, Chuwen Li","doi":"10.3390/cimb47030155","DOIUrl":"10.3390/cimb47030155","url":null,"abstract":"<p><strong>Objective: </strong>Non-small cell lung cancer (NSCLC) remains one of the most significant contributors to cancer-related mortality. This investigation explores the influence and underlying mechanisms of the USP1 inhibitor SJB2-043 on A549 cells, with the aim of advancing the development of anti-NSCLC therapeutics.</p><p><strong>Methods: </strong>Publicly available databases were utilized to assess USP1 expression and its association with the progression of NSCLC. Gene expression variations were ascertained through RNA sequencing, followed by the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology pathway enrichment evaluations. Various doses of SJB2-043 were administered to A549 cells to evaluate its impact on cell multiplication, motility, apoptosis, and the cell cycle using CCK-8 assays, colony formation, wound healing, flow cytometry, and Western blotting (WB).</p><p><strong>Results: </strong>USP1 was found to be overexpressed in NSCLC specimens and linked to adverse prognosis. Treatment with SJB2-043 markedly inhibited A549 cell proliferation and migration, diminished clonogenic potential, and triggered apoptosis in a dose-dependent manner. Modifications in the cell cycle were observed, showing an elevated percentage of cells in the G2 phase while exhibiting a parallel decline in the G₁ phase. WB examination demonstrated diminished protein levels of N-cadherin, CyclinB₁, CDK1, C-myc, Bcl-2, p-ERK/ERK, p-p38/p38, p-JNK/JNK, p-AKT/AKT, and p-mTOR/mTOR, alongside an upregulation of E-cadherin, ZO-1, occludin, p53, Bax, p-β-catenin/β-catenin, and GSK3β.</p><p><strong>Conclusions: </strong>SJB2-043 exerts a suppressive effect on A549 cell proliferation, migration, and epithelial-mesenchymal transition while enhancing apoptosis. These cellular effects appear to be mediated through the inhibition of the MAPK, Wnt/β-catenin, and PI3K/AKT/mTOR signaling cascades, in addition to modulation of the cell cycle.</p>","PeriodicalId":10839,"journal":{"name":"Current Issues in Molecular Biology","volume":"47 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709047","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}