Biologics : Targets & Therapy最新文献

{"title":"Molecular Biology Mechanisms and Emerging Therapeutics of Triple-Negative Breast Cancer.","authors":"Zhiying Zhang,&nbsp;Rui Zhang,&nbsp;Donghai Li","doi":"10.2147/BTT.S426392","DOIUrl":"https://doi.org/10.2147/BTT.S426392","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer that is conventionally characterized by the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2), accounting for approximately 15-20% of all breast cancers. Compared to other molecular phenotypes, TNBC is typically associated with high malignancy and poor prognosis. Cytotoxic agents have been the mainstay of treatment for the past few decades due to the lack of definitive targets and limited therapeutic interventions. However, recent developments have demonstrated that TNBC has peculiar molecular classifications and biomarkers, which provide the possibility of evolving treatment from basic cytotoxic chemotherapy to an expanding domain of targeted therapies. This review presents a framework for understanding the current clinical experience surrounding molecular biology mechanisms in TNBC (Figure 1). Including immunotherapy, polymerase (PARP) and PI3K/AKT pathway inhibitors, antibody-drug conjugates, and androgen receptor (AR) blockade. Additionally, the role of miRNA therapeutics targeting TNBC and potential strategies targeting cancer stem cells (CSCs) are discussed and highlighted. As more and more treatments arise on the horizon, we believe that patients with TNBC will have a new sense of hope.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"113-128"},"PeriodicalIF":4.0,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/85/41/btt-17-113.PMC10520847.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41096964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Demonstration of Safety in Wild Type Mice of npFOXF1, a Novel Nanoparticle-Based Gene Therapy for Alveolar Capillary Dysplasia with Misaligned Pulmonary Veins.","authors":"Fatemeh Kohram, Zicheng Deng, Yufang Zhang, Abid A Al Reza, Enhong Li, Olena A Kolesnichenko, Samriddhi Shukla, Vladimir Ustiyan, Jose Gomez-Arroyo, Anusha Acharya, Donglu Shi, Vladimir V Kalinichenko, Alan P Kenny","doi":"10.2147/BTT.S400006","DOIUrl":"10.2147/BTT.S400006","url":null,"abstract":"<p><strong>Introduction: </strong>Alveolar Capillary Dysplasia with Misaligned Pulmonary Veins (ACDMPV) is a fatal congenital disease resulting from a pulmonary vascular endothelial deficiency of FOXF1, producing abnormal morphogenesis of alveolar capillaries, malpositioned pulmonary veins and disordered development of lung lobes. Affected neonates suffer from cyanosis, severe breathing insufficiency, pulmonary hypertension, and death typically within days to weeks after birth. Currently, no treatment exists for ACDMPV, although recent murine research in the Kalinichenko lab demonstrates nanoparticle delivery improves survival and reconstitutes normal alveolar-capillary architecture. The aim of the present study is to investigate the safety of intravenous administration of FOXF1-expressing PEI-PEG nanoparticles (npFOXF1), our pioneering treatment for ACDMPV.</p><p><strong>Methods: </strong>npFOXF1 was constructed, validated, and subsequently administered in a single dose to postnatal day 14 (P14) mice via retro-orbital injection. Biochemical, serologic, and histologic safety were monitored at postnatal day 16 (P16) and postnatal day 21 (P21).</p><p><strong>Results: </strong>With treatment we observed no lethality, and the general condition of mice revealed no obvious abnormalities. Serum chemistry, whole blood, and histologic toxicity was assayed on P16 and P21 and revealed no abnormality.</p><p><strong>Discussion: </strong>In conclusion, npFOXF1 has a very good safety profile and combined with preceding studies showing therapeutic efficacy, npFOXF1 can be considered as a good candidate therapy for ACDMPV in human neonates.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"43-55"},"PeriodicalIF":4.0,"publicationDate":"2023-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bb/46/btt-17-43.PMC10031269.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9587136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Significance of Interleukin 23 in Systemic Lupus Patients: Relation to Disease Activity and Damage Indices.","authors":"Maysa M Haroon,&nbsp;Gehan A Hegazy,&nbsp;Mohammed A Hassanien,&nbsp;Olfat Shaker,&nbsp;Wafaa H Hussein","doi":"10.2147/BTT.S389021","DOIUrl":"https://doi.org/10.2147/BTT.S389021","url":null,"abstract":"<p><strong>Background: </strong>Dysregulation of both cellular and humoral immune responses is central in systemic lupus erythematosus (SLE) pathogenetic mechanisms. Proinflammatory cytokines, such as interleukin 23 (IL23), and their roles in promoting such dysregulation have recently been highly considered. This research compared IL23 serum levels in 85 Egyptian SLE patients and 85 healthy controls. Then, IL23 level was correlated to various SLE disease parameters, disease activity, and damage indices.</p><p><strong>Results: </strong>IL23 serum levels were significantly elevated in SLE patients versus healthy individuals. Furthermore, IL23 levels were positively correlated with SLE disease activity index (SLEDAI) and were positively correlated with arthritis, seizures, consumption of complements (C3, C4), and with parameters of nephritis (hematuria, pyuria, casts, and proteinuria). A positive correlation was also found between IL23 levels and oral prednisolone dose.</p><p><strong>Conclusion: </strong>IL23 has higher levels in the serum of SLE patients, and is correlated to activity of the disease, especially lupus nephritis. Further researchis needed to explore its exact role in SLE pathogenesis and whether it can be considered a potential biomarker or therapeutic target in SLE.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"1-9"},"PeriodicalIF":4.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7a/46/btt-17-1.PMC9868139.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10622308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness of RCTs Pooling Evidence on Mesenchymal Stem Cell (MSC) Therapeutic Applications During COVID-19 Epidemic: A Systematic Review.","authors":"Usha Rani Kandula,&nbsp;Addisu Dabi Wake","doi":"10.2147/BTT.S404421","DOIUrl":"https://doi.org/10.2147/BTT.S404421","url":null,"abstract":"<p><strong>Background: </strong>Global pandemic identified as coronavirus disease 2019 (COVID-19) has resulted in a variety of clinical symptoms, from asymptomatic carriers to those with severe acute respiratory distress syndrome (SARS) and moderate upper respiratory tract symptoms (URTS). This systematic review aimed to determine effectiveness of stem cell (SC) applications among COVID-19 patients.</p><p><strong>Methods: </strong>Multiple databases of PubMed, EMBASE, Science Direct, Google Scholar, Scopus, Web of Science, and Cochrane Library were used. Studies were screened, chosen, and included in this systematic review using Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 flowchart diagram and PRISMA checklist. Included studies' quality was assessed employing Critical Appraisal Skills Programme (CASP) quality evaluation criteria for 14 randomized controlled trials (RCTs).</p><p><strong>Results: </strong>Fourteen RCTs were performed between the years of 2020 to 2022, respectively, with a sample size n = 574 (treatment group (n = 318); control group (n = 256)) in multiple countries of Indonesia, Iran, Brazil, Turkey, China, Florida, UK, and France. The greatest sample size reported from China among 100 COVID-19 patients, while the lowest sample of 9 COVID-19 patients from Jakarta, Indonesia, and the patient's age ranges from 18 to 69 years. Studies applied to the type of SC were \"Umbilical cord MSCs, MSCs secretome, MSCs, Placenta-derived MSCs, Human immature dental pulp SC, DW-MSC infusion, Wharton Jelly-derived MSCs\". The injected therapeutic dose was 1 × 10⁶ cells/kg, 1 × 10⁷ cells/kg, 1 × 10⁵ cells/kg, and 1 million cells/kg as per the evidence from the different studies. Studies focused on demographic variables, clinical symptoms, laboratory tests, Comorbidities, respiratory measures, concomitant therapies, Sequential Organ Failure Assessment score, mechanical ventilation, body mass index, adverse events, inflammatory markers, and PaO₂/FiO₂ ratio were all recorded as study characteristics.</p><p><strong>Conclusion: </strong>Clinical evidence on MSC's therapeutic applications during COVID-19 pandemic has proven to be a promising therapy for COVID-19 patient recovery with no consequences and applied as a routine treatment for challenging ailments.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"85-112"},"PeriodicalIF":4.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/cc/94/btt-17-85.PMC10202141.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9516657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Critical Response: \"Does the Mutation of Cancer Driver Genes <i>IDH1</i>/<i>2</i> and CD204 Influence Cancer Metabolism and Tumor Associated Macrophage Recruitment in Tumor Microenvironment\" [Letter].","authors":"Novaria Sari Dewi Panjaitan,&nbsp;Sarwo Handayani,&nbsp;Rita Marleta Dewi","doi":"10.2147/BTT.S410506","DOIUrl":"https://doi.org/10.2147/BTT.S410506","url":null,"abstract":"","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"41-42"},"PeriodicalIF":4.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8e/b2/btt-17-41.PMC10038000.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9545575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Cancer Driver Genes IDH1 and IDH2 and CD204 in WHO-Grade 4 Astrocytoma: Crosstalk Between Cancer Metabolism and Tumour Associated Macrophage Recruitment in Tumour Microenvironment.","authors":"Maher Kurdi,&nbsp;Nasser Mulla,&nbsp;Yousef Katib,&nbsp;Taghreed Alsinani,&nbsp;Sahar Hakamy,&nbsp;Bassam Mj Addas,&nbsp;Husam Malibary,&nbsp;Taher F Halawa,&nbsp;Marwa S Farhan,&nbsp;Eyad Faizo,&nbsp;Saleh Baeesa","doi":"10.2147/BTT.S394556","DOIUrl":"https://doi.org/10.2147/BTT.S394556","url":null,"abstract":"<p><strong>Purpose: </strong>IDH1 and IDH2 are hotspot mutations commonly identified in WHO-grade 4 astrocytomas. Their association with TAMs has never been investigated. We aim to explore the crosstalk between the IDH1/2 mutation metabolic effect and TAMs in tumour microenvironment and how this relationship affects the tumour recurrence.</p><p><strong>Patients and methods: </strong>The study included 20 samples of patients with WHO-grade 4 astrocytoma. The alteration hotspot in codon IDH1^R132 and IDH2^R172 was examined using direct sequencing. The protein expression of CD204 on TAM was detected through immunohistochemistry.</p><p><strong>Results: </strong>IDH1^R132 and IDH2^R172 were symmetrically identified as wildtype in 18/20 tumours (90%) and the remaining 2 tumours (10%) showed synonymous mutations on both codons. Tumours with IDH1/2-wildtype showed high expression of CD204⁺TAMs in 10 cases and low expression in 8 cases. Typical expression was seen equally in IDH1/2 mutant tumours. There was no significant association between IDH1/2 and CD204⁺TAM expression (p= 0.999). The association between the two groups was significantly observed among IDH-wildtype tumours (p=0.027). Highly expressed CD204 in IDH-wildtype tumours showed a median recurrence at 10 months compared to low CD204 expression, showed a median recurrence interval at 24 months.</p><p><strong>Conclusion: </strong>IDH1^R132 or IDH^R172 has the same impact on the classification and prognosis of WHO-grade 4 astrocytoma. There was no crosstalk between IDH1/2 metabolic effect and CD204⁺TAM. However, IDH-wildtype glioblastomas with dense CD204⁺TAM are associated with early recurrence. Because the sample size is small, a larger study is recommended to determine the impact of IDH1/2 on TAMs.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"15-22"},"PeriodicalIF":4.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b7/d8/btt-17-15.PMC9912343.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9275805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypereosinophilic Dermatitis: Successful Treatment with Dupilumab.","authors":"Chenyu Wu,&nbsp;Jianzhong Zhang,&nbsp;Yan Zhao","doi":"10.2147/BTT.S400073","DOIUrl":"https://doi.org/10.2147/BTT.S400073","url":null,"abstract":"<p><p>Hypereosinophilic dermatitis (HED) is a subtype of hypereosinophilic syndrome. HED is characterized by eosinophilic granulocytes increased in peripheral blood and bone marrow and infiltrated in skin. The clinical manifestations of HED are diffussed by erythema, papule and maculopapule with severe itching. The etiology of HED is unknown. At present, in addition to HED with FIP1L1-PDGFRA fusion gene positive, whose treatment is tyrosine kinase inhibitor, other types of HED first-line treatment are oral glucocorticoids, supplemented by antihistamines and immunosuppressants. Dupilumab is a human monoclonal antibody, which inhibits the IL-4 and IL-13 signaling by binding to the IL-4R-α and IL-13R-α-1 subunits of the receptor. We report a 76-year-old male patient with HED whose peripheral blood eosinophils decreased from 20.7% to 4.1% after 8 weeks of dupilumab, and his pruritus was completely relieved. Dupilumab was discontinued after 6 months of treatment. It is exciting that the patient has not experienced relapse for 17 months after the discontinuation. No adverse event was reported.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"57-60"},"PeriodicalIF":4.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/36/fe/btt-17-57.PMC10124617.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9356810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preliminary Assessment of Safety and Tolerability of Avacopan During the Early Access Program for ANCA-Associated Vasculitis.","authors":"Jolijn R van Leeuwen,&nbsp;Tamara Popov,&nbsp;Achim Obergfell,&nbsp;Ton J Rabelink,&nbsp;Y K Onno Teng","doi":"10.2147/BTT.S394843","DOIUrl":"https://doi.org/10.2147/BTT.S394843","url":null,"abstract":"Introduction Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a heterogeneous group of rare, life-threatening, systemic autoimmune disorders characterized by necrotizing vasculitis that predominantly affects the small bloodto medium-sized vessels. Patients with ANCA vasculitis experience side effects from immunosuppression used to achieve disease remission, notably from long-term use of glucocorticoids. Both a Phase 2 trial (CLEAR) and a Phase 3 pivotal trial (ADVOCATE) have demonstrated the potential for avacopan to reduce steroid use in patients with newly diagnosed or relapsing severe ANCA-associated vasculitis while maintaining efficacy and safety. Avacopan is an orally administered small-molecule C5a receptor (C5aR) antagonist that selectively blocks the effects of C5a through the C5aR, including blocking neutrophil chemoattraction and activation. Most recently, avacopan has been approved by the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA) for the treatment of ANCAassociated vasculitis. In between the completion of the ADVOCATE study (2019) and the approval of regulatory agencies, 30 patients with a high unmet medical need have been treated with avacopan through the Early Access Program (EAP). Eligible for the EAP were patients with new or relapsing lifeor organ-threatening ANCA-associated vasculitis, requiring an induction treatment, who also had a high risk of steroid-related complications.","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"11-14"},"PeriodicalIF":4.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/18/03/btt-17-11.PMC9884459.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10602784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New Uracil Analog with Exocyclic Methylidene Group Can Reverse Resistance to Taxol in MCF-7 Cancer Cells.","authors":"Angelika Długosz-Pokorska,&nbsp;Renata Perlikowska,&nbsp;Tomasz Janecki,&nbsp;Anna Janecka","doi":"10.2147/BTT.S405080","DOIUrl":"https://doi.org/10.2147/BTT.S405080","url":null,"abstract":"<p><strong>Introduction: </strong>Taxol (Tx), a microtubule-stabilizing drug, has been widely used as a chemotherapeutic in several types of cancer. However, the development of resistance limited its application. One of the strategies used to prevent the emergence of drug resistance is combination treatment, involving at least two drugs. The aim of the current study was to assess if a new uracil analog, 3-<i>p</i>-bromophenyl-1-ethyl-5-methylidenedihydrouracil (U-359) can prevent the development of Tx resistance in breast cancer cells.</p><p><strong>Methods: </strong>The cytotoxicity of the new drug was tested in MCF-7 (hormone receptor (ER, PR) positive cell-line) and MCF-10A cell lines using MTT method. For the detection of apoptosis and necrosis, the Wright and Giemsa staining was used. Gene expression was measured by real-time PCR, and changes in the protein levels were evaluated by ELISA and bioluminescent method.</p><p><strong>Results: </strong>We investigated the effect of Tx and U-359 on cancer MCF-7 and normal MCF-10A cells alone and in combination. Tx co-administered with U-359 inhibited proliferation of MCF-7 cells to 7% while the level of ATPase drastically decreased to 14%, compared with effects produced by Tx alone. The apoptosis process was induced through the mitochondrial pathway. These effects were not seen in MCF-10A cells, showing the wide safety margin. The obtained results have shown that U-359 produced a synergistic effect with Tx probably by reducing Tx resistance in MCF-7 cells. To elucidate the possible mechanism of resistance, expression of tubulin III (TUBIII), responsible for microtubule stabilization and tau and Nlp proteins, responsible for microtubule dynamics, was assessed.</p><p><strong>Conclusion: </strong>Combination of Tx with U-359 reduced overexpression of TUBIII and Nlp. Thus, U-359 may stand for a potential reversal agent for the treatment of MDR in cancer cells.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"69-83"},"PeriodicalIF":4.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7b/6c/btt-17-69.PMC10198386.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9495864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated Serum Vinculin in Patients with HBV/HCV-Associated Liver Cirrhosis and Hepatocellular Carcinoma: A Pilot Study.","authors":"Abdallah Essa,&nbsp;Enas Said Essa,&nbsp;Sara Mahmoud El-Deeb,&nbsp;Hossam Eldin Mostafa Seleem,&nbsp;Muthana Al Sahlawi,&nbsp;Omar Ahmed Al-Omair,&nbsp;Somaia Shehab-Eldeen","doi":"10.2147/BTT.S405500","DOIUrl":"https://doi.org/10.2147/BTT.S405500","url":null,"abstract":"<p><strong>Background: </strong>The stiffness of the extracellular matrix (ECM) controls many cellular processes, such as migration and differentiation. Cells detect stiffness through adhesion structures termed focal adhesions (FAs). Vinculin, an actin-binding FA protein, plays a pivotal role in FA-mediated mechanotransduction.</p><p><strong>Aim: </strong>This study aimed to explore the role of vinculin in the development of HBV/HCV-induced hepatocellular carcinoma (HCC).</p><p><strong>Methods: </strong>Vinculin levels in a total number of 100 serum samples from patients with HBV/HCV-induced liver cirrhosis and HCC, as well as healthy controls, were analyzed using an enzyme-linked immunosorbent assay (ELISA).</p><p><strong>Results: </strong>In patients with HCC and liver cirrhosis, the serum vinculin levels were significantly greater than in controls (503.8±242.2 and 728.4±1044.8 vs 77.7±36.1 respectively, p<0.001). However, results showed no link between serum vinculin and the clinicopathological features of HCC.</p><p><strong>Conclusion: </strong>Patients with HBVor HCV-induced liver cirrhosis and HCC have significantly higher serum levels of vinculin than do controls. This might point to a potential role for vinculin in the development of HCC. More research into how this protein affects the development of HCC at the molecular level could lead to better clinical treatments and the development of new molecular therapies.</p>","PeriodicalId":9025,"journal":{"name":"Biologics : Targets & Therapy","volume":"17 ","pages":"23-32"},"PeriodicalIF":4.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/cb/7a/btt-17-23.PMC10035354.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9560616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}