Experimental cell research最新文献_第8页

Threonine and tyrosine kinase promotes multiple myeloma progression by regulating regucalcin expression

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-15 DOI: 10.1016/j.yexcr.2025.114454

Xiaofeng Zhu , Zuxi Feng , Xiaohuan Peng , Tianning Di , YanHong Li , Jun Bai , Tao Ma , Lijuan Li , Liansheng Zhang

{"title":"Threonine and tyrosine kinase promotes multiple myeloma progression by regulating regucalcin expression","authors":"Xiaofeng Zhu , Zuxi Feng , Xiaohuan Peng , Tianning Di , YanHong Li , Jun Bai , Tao Ma , Lijuan Li , Liansheng Zhang","doi":"10.1016/j.yexcr.2025.114454","DOIUrl":"10.1016/j.yexcr.2025.114454","url":null,"abstract":"<div><div>Multiple myeloma (MM) is a malignant proliferative disorder of plasma cells and remains an incurable disease. Threonine and tyrosine kinase (TTK) is a dual-specific protein kinase that targets serine/threonine and tyrosine residues for phosphorylation. Its elevated expression has been linked to unfavorable outcomes in several types of cancer. Although the role of TTK in MM are still incompletely understood. In this research, we assessed TTK mRNA and protein expression levels in 51 MM patients and 30 healthy donors using qRT-PCR and western blotting. The impact of TTK expression on MM cell apoptosis, proliferation, and the cell cycle were assessed through CCK-8 assay, flow cytometry, and western blotting. Our findings revealed a significant overexpression of TTK in multiple myeloma patients and cell lines. TTK knockdown promoted apoptosis and G0/G1 phase arrest while inhibiting proliferation in MM cells, whereas TTK overexpression reduced apoptosis and G0/G1 phase arrest, enhancing proliferation in MM cells. Next, we identified regucalcin (RGN) as a downstream target of TTK through proteomic analysis. In NDMM, the expression of RGN was decreased. Cell function experiments showed that RGN knockdown significantly promoted MM cell proliferation, inhibited apoptosis and reduced cell cycle arrest, and reversed the increased apoptosis, weakened proliferation, and enhanced cell cycle arrest caused by TTK knockdown. Finally, a xenograft mouse model showed that TTK significantly promotes MM development. In summary, we demonstrated that the TTK-RGN axis regulates cell apoptosis, G0/G1 phase arrest, and proliferation in MM, highlighting TTK as a potential target for therapeutic intervention in this cancer.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114454"},"PeriodicalIF":3.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ACSS3 promotes the tumorigenesis of non-small cell lung cancer via suppressing p53-mediated ferroptosis

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-15 DOI: 10.1016/j.yexcr.2025.114438

Jing Zhang , Xiuhong Wang , Jingyi Wang , Xiao Wen , Siyuan Chen , Tao Wang , Bei Wang , Wenquan Hu

{"title":"ACSS3 promotes the tumorigenesis of non-small cell lung cancer via suppressing p53-mediated ferroptosis","authors":"Jing Zhang , Xiuhong Wang , Jingyi Wang , Xiao Wen , Siyuan Chen , Tao Wang , Bei Wang , Wenquan Hu","doi":"10.1016/j.yexcr.2025.114438","DOIUrl":"10.1016/j.yexcr.2025.114438","url":null,"abstract":"<div><div>Non-small cell lung cancer (NSCLC) is a subtype of the most frequently diagnosed cancer, causing a considerable number of deaths globally. Mitochondrial dysfunction was found to promote malignant progression. However, the underlying mechanism remains unclear. Acyl-CoA synthetase short chain family member 3 (ACSS3) is mainly located in mitochondria, which abnormal regulation is usually accompanied by the occurrence and development of tumors. In this study, we found that the expression level of ACSS3 was correlated with poor prognosis in patients with NSCLC. Moreover, we demonstrated that ACSS3 knockdown led to mitochondrial contraction, increased reactive oxygen species levels, decreased mitochondrial membrane potential, and subsequently inhibited tumor growth of NSCLC cells <em>in vitro</em> and <em>in vivo</em>, whereas its overexpression promoted these processes. Mechanistically, ACSS3 knockdown promoted ferroptosis through transcriptional control of SLC7A11 and GPX4. Further investigations indicated that ACSS3 loss inhibited the SLC7A11/GPX4 axis by enhancing p53 stability. Taken together, our data confirmed that ACSS3 promotes NSCLC tumorigenesis through inhibiting the p53-mediated ferroptosis. Hence, ACSS3 emerges as a promising therapeutic target for NSCLC treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114438"},"PeriodicalIF":3.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

BRAF V600E in cancer: Exploring structural complexities, mutation profiles, and pathway dysregulation

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-15 DOI: 10.1016/j.yexcr.2025.114440

Jayhind Bharti , Priyadharshini Gogu , Sarvesh Kumar Pandey , Amita Verma , Jagat Pal Yadav , Ankit Kumar Singh , Pradeep Kumar , Ashish Ranjan Dwivedi , Prateek Pathak

{"title":"BRAF V600E in cancer: Exploring structural complexities, mutation profiles, and pathway dysregulation","authors":"Jayhind Bharti , Priyadharshini Gogu , Sarvesh Kumar Pandey , Amita Verma , Jagat Pal Yadav , Ankit Kumar Singh , Pradeep Kumar , Ashish Ranjan Dwivedi , Prateek Pathak","doi":"10.1016/j.yexcr.2025.114440","DOIUrl":"10.1016/j.yexcr.2025.114440","url":null,"abstract":"<div><div>BRAF, a fundamental component of cellular signaling pathways regulating growth and survival, is frequently mutated in cancer development. Among entire BRAF mutations, the V600E substitution stands out as a dominant alteration in various malignancies, including melanoma, colorectal cancer, and thyroid cancer. Understanding the structural differences between wild-type BRAF and BRAFV600E is crucial for elucidating the molecular mechanisms underpinnings tumorigenesis and identifying dysregulation associated with the same. V600E mutation results in a constitutively active kinase domain, leading to dysregulated downstream signaling independent of extracellular stimuli. This sustained activation promotes cell proliferation, survival, angiogenesis, and hallmark features of the cancer cells. The study describes three distinct classes of BRAF mutations where Class 1 mutations predominantly involve point mutations within the BRAF gene, while Class 2 encompasses in-frame insertions and deletions, and Class 3 comprises gene fusions with large-scale chromosomal rearrangements. Further, we have discussed dysregulated pathways associated with mutation of BRAFV600E, which includes MAPK/ERK, PI3K/AKT/mTOR, TP53, DNA damage response, and WNT/β-Catenin from schematic representation. In the current review, we have shown how these dysregulated pathways play pivotal roles in tumorigenesis, tumor progression in BRAF-mutant cancers and highlighted the critical role of BRAF dysregulation in cancer development followed by its therapeutic implications of targeting dysregulated pathways in BRAF-driven malignancies.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114440"},"PeriodicalIF":3.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to “MOTS-c relieves hepatocellular carcinoma resistance to TRAIL-induced apoptosis under hypoxic conditions by activating MEF2A” [Exp. Cell Res., Volume 444, Issue 1, 1 January 2025, 114354] “MOTS-c在低氧条件下通过激活MEF2A来缓解肝癌细胞对trail1诱导的凋亡的抵抗”[j].细胞研究，vol . 444, Issue 1, 2025, 114354。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-15 DOI: 10.1016/j.yexcr.2024.114376

Haiying Shen , Junjie Nie , Xiaojun Wang , Guangqing Li , Liwei Zhao , Yuji Jin , Lianhai Jin

引用次数: 0

Modeling amyotrophic lateral sclerosis with amniotic membrane-derived mesenchymal stem cells: A novel approach for disease modeling

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-15 DOI: 10.1016/j.yexcr.2025.114449

B.S. Soumya , Naisarg Gamit , Manasi Patil , V.P. Shreenidhi , Arun Dharmarajan , Sudha Warrier

{"title":"Modeling amyotrophic lateral sclerosis with amniotic membrane-derived mesenchymal stem cells: A novel approach for disease modeling","authors":"B.S. Soumya , Naisarg Gamit , Manasi Patil , V.P. Shreenidhi , Arun Dharmarajan , Sudha Warrier","doi":"10.1016/j.yexcr.2025.114449","DOIUrl":"10.1016/j.yexcr.2025.114449","url":null,"abstract":"<div><div>Advancement of therapeutics for neurodegenerative diseases like amyotrophic lateral sclerosis (ALS) has been predominantly hampered by the dearth of relevant disease models. Despite numerous animal models, significant challenges remain in correlating these with human disease complexities. In this study, the ALS model was created using amniotic membrane-derived mesenchymal stem cells (AM-MSCs) which were differentiated into motor neurons (MN) with specific MN induction media and transiently transfected with mutated human SOD1 G93A plasmid to induce ALS-like condition. Characterization included gene expression analysis, immunocytochemistry, flow cytometry, and Western blot. Functional assays assessed the extent of degeneration and model efficiency. AM-MSCs demonstrated multipotency and were positive for MSC markers. Upon differentiation, the expression of MN markers like MNX1, Olig2, and ChAT were found to be elevated. SOD1 G93A overexpression, downregulated MN markers, upregulated NURR1 gene, reduced acetylcholine (ACh), reduced glutathione, and elevated oxidative stress markers. This robust <em>in-vitro</em> ALS model derived from AM-MSCs offers an alternative to animal models to provide an efficient and cost-effective platform to conduct rapid drug screening.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114449"},"PeriodicalIF":3.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Knockdown of PLOD2 inhibits pulmonary artery smooth muscle cell glycolysis under chronic intermittent hypoxia via PI3K/AKT signal

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-15 DOI: 10.1016/j.yexcr.2025.114453

Shenwen Yi , Tiange Qu , Heling Wu, Chenyu Xu, Jun Xu, Fei Yu, Liang Ye

{"title":"Knockdown of PLOD2 inhibits pulmonary artery smooth muscle cell glycolysis under chronic intermittent hypoxia via PI3K/AKT signal","authors":"Shenwen Yi , Tiange Qu , Heling Wu, Chenyu Xu, Jun Xu, Fei Yu, Liang Ye","doi":"10.1016/j.yexcr.2025.114453","DOIUrl":"10.1016/j.yexcr.2025.114453","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to investigate the role and potential mechanism of procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2) in chronic intermittent hypoxia (CIH)-induced mice and pulmonary arterial smooth muscle cells (PASMCs).</div></div><div><h3>Methods</h3><div>CIH mouse model was pre-injected with AAV-shPLOD2 by tail vein, and the pathological changes of lung was evaluated using hematoxylin-eosin (H&E) and α-SMA immunostaining. Enriched KEGG pathway analyses of PLOD2 targeted genes were performed using GSE11341 and GSE131425 datasets. Next, primary PASMCs were exposed to CIH environment, and then measured its proliferation, migration and glycolysis by CCK8, EdU assay, wound healing assay, Transwell and western blotting.</div></div><div><h3>Results</h3><div>PLOD2 expression was increased in the lungs of CIH-induced mice and in PASMCs under CIH conditions. Moreover, glycolysis and PI3K/AKT pathway were regulated by PLOD2. Silencing of PLOD2 significantly inhibited the increase of RV/(LV + S) and RVSP, alleviated pathological changes of lung in CIH-induced mice and restrained the proliferation, migration, glycolysis and activation of PI3K/AKT in CIH-induced PASMCs. The inhibitory effects of PLOD2 silencing on PASMC proliferation and migration were accelerated by 2-DG (an inhibitor of glycolysis) and were reversed by lactate (the end product of glycolysis). In addition, the inhibitory effects of PLOD2 silencing on PASMC proliferation, migration and glycolysis were accelerated by PI3K/AKT inhibitor LY294002 and were reversed by the agonist 740Y-P.</div></div><div><h3>Conclusions</h3><div>Silencing of PLOD2 inhibits PI3K/AKT signaling to limit PASMC glycolysis which allows PASMC proliferation and migration in CIH-induced pulmonary arterial hypertension (PAH).</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114453"},"PeriodicalIF":3.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143437791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MYG1 interacts with HSP90 to promote breast cancer progression through Wnt/β-catenin and Notch signaling pathways

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-14 DOI: 10.1016/j.yexcr.2025.114448

Xuming Liu , Yurong Zhu , Wenqing Huang , Jianxiong Chen , Jiawen Lan , Xiaoli Long , Jun Zhou

{"title":"MYG1 interacts with HSP90 to promote breast cancer progression through Wnt/β-catenin and Notch signaling pathways","authors":"Xuming Liu , Yurong Zhu , Wenqing Huang , Jianxiong Chen , Jiawen Lan , Xiaoli Long , Jun Zhou","doi":"10.1016/j.yexcr.2025.114448","DOIUrl":"10.1016/j.yexcr.2025.114448","url":null,"abstract":"<div><h3>Background</h3><div>As an evolutionarily conserved gene involved in embryonic development, cell differentiation, and immune metabolism, <em>MYG1</em> exhibits a dynamic expression pattern related to development in human and mouse embryonic tissues, especially upregulates in undifferentiated or pluripotent stem cells. However, <em>MYG1</em> has been poorly studied in breast cancer and its functional mechanism still remains unclear.</div></div><div><h3>Method</h3><div>Immunohistochemistry and immunofluorescence were used to study <em>MYG1</em> expression and localization in breast cancer. Lentivirus transfection combined with CCK8, colony formation, matrix gel experiment and breast fat pad tumor formation in nude mice were used for in vivo and in vitro functional assessment. GSEA enrichment analysis, immunofluorescence and Western blot were conducted to explore functional mechanism.</div></div><div><h3>Result</h3><div><em>MYG1</em> expression was upregulated in breast cancer and its higher expression correlated with a variety of clinicopathological characteristics indicating poor prognosis. In vitro and in vivo experiments showed that overexpression of <em>MYG1</em> promoted breast cancer cells proliferation, migration, invasion and tumorigenesis, while downregulation of <em>MYG1</em> had an opposite effect. Mechanistically, MYG1 interacted with HSP90 to significantly activate Wnt/β-catenin and Notch signaling pathways in breast cancer cells, thus promoting EMT, cell cycle process and breast cancer progression.</div></div><div><h3>Conclusion</h3><div><em>MYG1</em> is highly expressed in breast cancer and functions as an oncogene. Mechanistically, MYG1 interacts with HSP90 to accelerate EMT and cell cycle process by activating both Wnt/β-catenin and Notch signaling pathways.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114448"},"PeriodicalIF":3.3,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cell death-associated lncRNAs in cancer immunopathogenesis: An exploration of molecular mechanisms and signaling pathways

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-11 DOI: 10.1016/j.yexcr.2025.114439

Safia Obaidur Rab , Ahmed Hussein Zwamel , Enwa Felix Oghenemaro , Muktesh Chandra , Irwanjot Kaur , Bindu Rani , Vikrant Abbot , M. Ravi Kumar , Muhammad Ikram Ullah , Abhinav Kumar

{"title":"Cell death-associated lncRNAs in cancer immunopathogenesis: An exploration of molecular mechanisms and signaling pathways","authors":"Safia Obaidur Rab , Ahmed Hussein Zwamel , Enwa Felix Oghenemaro , Muktesh Chandra , Irwanjot Kaur , Bindu Rani , Vikrant Abbot , M. Ravi Kumar , Muhammad Ikram Ullah , Abhinav Kumar","doi":"10.1016/j.yexcr.2025.114439","DOIUrl":"10.1016/j.yexcr.2025.114439","url":null,"abstract":"<div><div>Cancer remains one of the foremost causes of mortality worldwide, highlighting the urgent need for novel therapeutic targets due to the insufficient efficacy and adverse side effects associated with existing cancer treatments. Long non-coding RNAs (lncRNAs), defined as RNA transcripts longer than 200 nucleotides, have emerged as pivotal regulators in the initiation and progression of various malignancies. In oncology, programmed cell death (PCD) serves as the primary mechanism for tumor cell elimination, comprising processes such as apoptosis, pyroptosis, autophagy, and ferroptosis. Recent studies have elucidated a substantial relationship between lncRNAs and these PCD pathways, indicating that lncRNAs can modulate the apoptotic and non-apoptotic death mechanisms. This regulation may influence not only the dynamics of cancer progression but also the therapeutic response to clinical interventions. This review delves into the intricate role of lncRNAs within the context of PCD in cancer, unveiling the underlying pathogenic mechanisms while proposing innovative strategies for cancer therapy. Additionally, it discusses the potential therapeutic implications of targeting lncRNAs in PCD and related signaling pathways, aiming to enhance treatment outcomes for patients facing cancer.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114439"},"PeriodicalIF":3.3,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bee venom: Yesterday's enemy becomes modern medicine for skin cancer

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-07 DOI: 10.1016/j.yexcr.2025.114435

Amr Ahmed El-Arabey , Hamed A. Ghramh

{"title":"Bee venom: Yesterday's enemy becomes modern medicine for skin cancer","authors":"Amr Ahmed El-Arabey , Hamed A. Ghramh","doi":"10.1016/j.yexcr.2025.114435","DOIUrl":"10.1016/j.yexcr.2025.114435","url":null,"abstract":"<div><div>Malignant melanoma is one of the most lethal human malignancies, particularly when it spreads from its initial site in the skin to distant locations with few therapeutic options. While a range of treatment approaches exist, such as chemotherapy, radiation, immunotherapy, and targeted therapy, they typically fail to treat skin cancer, particularly in its late stages. The complex cellular and molecular mechanisms that drive melanoma growth and metastatic dissemination are both varied and complicated, posing significant challenges to the development of effective treatment approaches. As the incidence and burden of this malignancy increase, there is an urgent need for innovative therapeutic techniques. Therefore, it is vital to research alternate therapy options. Several research undertaken in recent years have found that bee venom influences a variety of cancers. The more research into using bee venom to cure skin cancer, the less attention it receives. In this context, the purpose of this proposal is to review a comprehensive assessment of the clinical impact of bee venom against skin cancer, as well as to highlight challenges and excitement down the road.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 2","pages":"Article 114435"},"PeriodicalIF":3.3,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143372444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanisms behind the LncRNAs-mediated regulation of paclitaxel (PTX) resistance in human malignancies

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-05 DOI: 10.1016/j.yexcr.2025.114434

Ali G. Alkhathami , Harikumar Pallathadka , Sejal Shah , Subbulakshmi Ganesan , Abhishek Sharma , Seema Devi , Yasser Fakri Mustafa , Mohammed Qasim Alasheqi , Abed J. Kadhim , Ahmed Hussein Zwamel

{"title":"Mechanisms behind the LncRNAs-mediated regulation of paclitaxel (PTX) resistance in human malignancies","authors":"Ali G. Alkhathami , Harikumar Pallathadka , Sejal Shah , Subbulakshmi Ganesan , Abhishek Sharma , Seema Devi , Yasser Fakri Mustafa , Mohammed Qasim Alasheqi , Abed J. Kadhim , Ahmed Hussein Zwamel","doi":"10.1016/j.yexcr.2025.114434","DOIUrl":"10.1016/j.yexcr.2025.114434","url":null,"abstract":"<div><div>Paclitaxel (PTX) is extensively used to treat various cancers, including those of the breast, ovary, lung, esophagus, stomach, pancreas, and neck. However, despite its effectiveness in clinical settings, patients often experience cancer recurrence due to the emergence of resistance to PTX. The mechanisms underlying this resistance in cancer cells exposed to PTX involve modifications in β-tubulin, the primary target molecule associated with mitosis, the activation of pathways that facilitate drug efflux, and the dysregulation of apoptosis-related proteins. Long non-coding RNAs (lncRNAs), which are RNA molecules exceeding 200 nucleotides in length and lacking protein-coding capabilities, play various regulatory roles in cellular functions. A growing body of evidence underscores the role of lncRNAs in cancer progression and their involvement in PTX resistance across different cancer types. As a result, lncRNAs have been identified as promising therapeutic targets for overcoming drug resistance in cancer therapies. This review aims to provide an overview of the current knowledge regarding lncRNAs and their contributions to resistance mechanisms to promote further research in this field. A summary of key lncRNAs and their related pathways associated with PTX resistance will be presented.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 2","pages":"Article 114434"},"PeriodicalIF":3.3,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0