Current cancer drug targets最新文献

{"title":"Screening miRNAs to Hinder the Tumorigenesis of Renal Clear Cell Carcinoma Associated with KDR Expression","authors":"Kaviyaprabha R, Miji TV, Suseela R, Muthusami S, Thangaleela S, Almoallim HS, Priyadarshini S, Bharathi M","doi":"10.2174/0115680096321287240826065718","DOIUrl":"https://doi.org/10.2174/0115680096321287240826065718","url":null,"abstract":"Introduction: This study delved into the role of Kinase Insert Domain Receptor (KDR) and its associated miRNAs in renal cell carcinoma through an extensive computational analysis. The potential of our findings to guide future research in this area is significant. Methods: Our methods, which included the use of UALCAN and GEPIA2 databases, as well as miRDB, MirDIP, miRNet v2.0, miRTargetLink, MiEAA v2.1, TarBase v8.0, INTERNET, and miRTarBass, were instrumental in identifying the regulation of miRNA associated with KDR expression. The predicted miRNA was validated with the TCGA-KIRC patients’ samples by implementing CancerMIRNome. The TargetScanHuman v8.0 was implemented to identify the associations between human miRNAs and KDR. A Patch Dock server analyzed the interactions between hsa-miR-200b-3p-KDR and hsa-miR-200b-3p with KDR. Results: The KDR expression rate was investigated in the Kidney Renal Cell Carcinoma (KIRC) samples, and adjacent normal tissues revealed that the expression rate was significantly higher than the normal samples, which was evident from the strong statistical significance (P = 1.63e-12). Likely, the KDR ex-pression rate was estimated as high at tumor grade 1 and gradually decreased till the metastasis grade, reducing the survival rate of the KIRC patients. To identify these signals early, we predicted a miRNA that could trigger the expression of KDR. Furthermore, we uncovered the potential associations between miR-200c-3p expressions by regulating KDR towards the progression of KIRC. Discussion: Upon examining the outcome, it became evident that miR-200c-3p was significantly down-regulated in KIRC compared to the normal samples. Moreover, the negative correlation was obtained for hsa-miR-200c-3p (R = - 0.276) along with the KDR expression describing that the increased rate of hsa-miR-200c-3p might reduce the KDR expression rate, which may suppress the KIRC initiation or progres-sion. Conclusion: The in-silico analysis indicated that the significant increase in KDR expression during the initiation of KIRC could serve as an early diagnostic marker. Moreover, KDR could be utilized to identify advancements in KIRC stages. Additionally, hsa-miR-200c-3p was identified as a potential regulator capable of downregulating and upregulating KDR expression among the 24 miRNAs screened. This find-ing holds promise for future research endeavors. Concurrent administration of the FDA-approved 5-fluor-ouracil with KIRC drugs, such as sorafenib, zidovudine, and everolimus, may have the potential to en-hance the therapeutic efficacy in downregulating hsa-miR-200c-3p. However, further in vitro studies are imperative to validate these findings and gain a comprehensive understanding of the intricate regulatory interplay involving hsa-miR-200c-3p, KDR, 5-fluorouracil, and other FDA-approved drugs for the treat-ment of KIRC. This will facilitate the identification of KIRC stage progression and its underlying pre-ventative mechanisms.","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142251399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dendrobine Suppresses Tumor Growth by Regulating the PD-1/PD-L1 Checkpoint Pathway in Lung Cancer.","authors":"Linmao Li, Jiejin Nong, Jingui Li, Lini Fang, Meini Pan, Haixian Qiu, Shiqing Huang, Yepeng Li, Meijuan Wei, Haiying Yin","doi":"10.2174/0115680096305416240820040314","DOIUrl":"https://doi.org/10.2174/0115680096305416240820040314","url":null,"abstract":"<p><strong>Background: </strong>Dendrobine is a bioactive alkaloid isolated from Dendrobium nobile. Studies have evaluated the anti-tumor effect of dendrobine in cancers, including lung cancer. However, the mechanism of dendrobine inhibiting tumors requires further study.</p><p><strong>Methods: </strong>Bioinformatics was performed to screen the potential targets of dendrobine. The in-tersection of dendrobine and lung cancer targets was performed for KEGG analysis. CCK-8 was used to detect cell viability after dendrobine treatment. A xenograft mouse model was es-tablished to explore the effect of dendrobine on lung cancer. The percentages of PD-L1+, CD4+, CD8+, CD11b+, CD25+FOXP3+ cells, the expression of Ki-67 and caspase-3, the ex-pression of pathway-related proteins, the levels of IL-2, IFN-γ, and TGF-β, and the changes of indicators of liver and renal function were measured.</p><p><strong>Results: </strong>Dendrobine regulated the PD1/PD-L1 checkpoint signaling pathway and affected the occurrence and development of lung cancer. Dendrobine decreased the cell viability of lung cancer. Dendrobine and anti-PD-L1 decreased tumor growth, increased caspase-3 expression, and reduced Ki-67 expression in tumor tissues. Dendrobine and anti-PD-L1 suppressed pro-tein expression of PD-L1, p-JAK1/JAK1, and p-JAK2/JAK2 in tumor tissues. Greatly, den-drobine and anti-PD-L1 decreased the percentages of PD-L1+, CD11b+, and CD25+FOXP3+ cells, increased the percentages of CD4+ and CD8+cells, and enhanced the levels of IL-2, IFN-γ, and TGF-β in tumor tissues. Dendrobine demonstrated no hepatorenal toxicity to the tumor mice. The combination of dendrobine and anti-PD-L1 greatly strengthened the effects of dendrobine on tumors.</p><p><strong>Conclusion: </strong>Dendrobine inhibited tumor immune escape by suppressing the PD-1/PD-L1 checkpoint pathway, thus restricting tumor growth of lung cancer.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnesium as a Co-Factor: A Vital Cation with Pro- and Anti-Tumor Effects.","authors":"Muthu Krishnan Dhivya Dharshini, Dhamodharan Prabhu, Subash C B Gopinath","doi":"10.2174/0115680096346615240907210849","DOIUrl":"https://doi.org/10.2174/0115680096346615240907210849","url":null,"abstract":"","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progressive Dynamics of Cancer Stem Cells in Oral Squamous Cell Carcinoma.","authors":"Gopalakrishnan Shankari, Rajmichael Raji, Dhamodharan Prabhu, Jeyaraman Jeyakanthan, Subash C B Gopinath","doi":"10.2174/0115680096340994240906111400","DOIUrl":"https://doi.org/10.2174/0115680096340994240906111400","url":null,"abstract":"","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SELENBP1 Inhibits the Warburg Effect and Tumor Growth by Reducing the HIF1α Expression in Colorectal Cancer.","authors":"Tao Song, Xiaotian Zhang, Jun Ren, Zhiqing Hu, Xin Wang, Gengming Niu","doi":"10.2174/0115680096320837240806172245","DOIUrl":"https://doi.org/10.2174/0115680096320837240806172245","url":null,"abstract":"<p><strong>Introduction: </strong>Colorectal cancer (CRC) is experiencing a significant increase in both incidence and mortality rates globally. The expression of Selenium-binding protein 1 (SELENBP1) has been reported to be notably downregulated in various malignancies, yet its biological functions and cellular mechanisms in CRC remain incompletely understood.</p><p><strong>Method: </strong>In our investigation, we observed the downregulation of SELENBP1 in CRC tissues through quantitative real-time PCR and western blotting and identified a positive correlation between higher SELENBP1 expression and improved survival prognosis using Kaplan-Meier survival analysis. Through loss-of-function and gain-of-function studies, we demonstrated the tumor-suppressive roles of SELENBP1 in CRC, supported by results from both in vitro and in vivo experiments. Furthermore, we uncovered the pivotal functions of SELENBP1 in suppressing aerobic glycolysis in CRC cells by regulating glucose uptake, lactate generation, and extracellular acidification rate.</p><p><strong>Result: </strong>At a mechanistic level, we found that SELENBP1 inhibits the expression of the key glycolytic modulator hypoxia-inducible factor 1 subunit alpha (HIF1α), and the inhibition of glycolysis by SELENBP1 can be reversed by ectopic expression of HIF1α. Therefore, our study highlights the potential of SELENBP1 as a promising target for CRC therapy, given its significant impact on tumor suppression and reprogrammed glucose metabolism.</p><p><strong>Conclusion: </strong>These findings contribute to a deeper understanding of the molecular mechanisms underlying CRC progression and may pave the way for the development of targeted therapies for this challenging disease.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antibody-drug conjugates (ADCs): a novel therapy for triple-negative breast cancer (TNBC).","authors":"Gaurav Gupta, Md Sadique Hussain, Kumud Pant, Haider Ali, Riya Thapa, Asif Ahmad Bhatt","doi":"10.2174/0115680096343056240828190900","DOIUrl":"https://doi.org/10.2174/0115680096343056240828190900","url":null,"abstract":"<p><p>NA.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantum Dots Functionalized Polymeric Nanoparticles as Cancer Theranostics: An Advanced Nanomedicine Strategy.","authors":"Honey Panchal, Drishti Panjwani, Shruti Patel, Priyanka Ahlawat, L D Patel, Abhay Dharamsi, Asha Patel","doi":"10.2174/0115680096299455240621070820","DOIUrl":"https://doi.org/10.2174/0115680096299455240621070820","url":null,"abstract":"<p><strong>Background: </strong>Cancer is a life-threatening disease prevalent worldwide, but its proper treatment has not yet been developed. Conventional therapies, like chemotherapy, sur-gery, and radiation, have shown relapse and drug resistance. Nanomedicine comprising cancer theranostics based on imaging probes functionalized with polymeric nanoconjugates is acquir-ing importance due to its targeting capability, biodegradability, biocompatibility, capacity for drug loading, and long blood circulation time. The application of synthetic polymers contain-ing anti-cancer agents and functionalizing their surface amenities with diagnostic probes offer a nano-combinatorial model in cancer theranostics.</p><p><strong>Objective: </strong>This study aimed to highlight the recent advancements in quantum dots-functionalized nanoconjugates and substantial progress in advanced polymeric nanomaterials in cancer theragnostics.</p><p><strong>Methods: </strong>This review details the synthetic methods for fabricating Quantum Dots (QDs) and QDs-functionalized polymeric nanoparticles, such as the hydrothermal method, solvothermal technique, atomic layer desorption, electrochemical method, microwave, and ultrasonic method.</p><p><strong>Results: </strong>Conjugating nanoparticles with photo-emitting quantum dots has shown efficacy for real-time monitoring and treating multi-drug-resistant cancer.</p><p><strong>Conclusion: </strong>Quantum dots are used in phototherapy, bioimaging, and medication delivery for cancer therapy. Real-time monitoring of therapy is possible and multiple models of hybridized quantum dots may be created to treat cancer. This review has discovered that numerous at-tempts have been made to conjugate carbon and graphene-based quantum dots with various biomolecules.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CNDP1 Suppresses the Malignant Behavior of Hepatoma Cell via Restricting PI3K-AKT-mTOR Activation.","authors":"Youwen Du, Linxin Pan, Wenchen Zhang, Shuangbiao Wei, Xu Fan, Na Zhang, Pengjun Wei, Xiaoqian Chen, Zhi Qiao, Li Xie","doi":"10.2174/0115680096332450240827070033","DOIUrl":"https://doi.org/10.2174/0115680096332450240827070033","url":null,"abstract":"<p><strong>Introduction: </strong>Hepatocellular carcinoma (HCC) is a global health problem with increasing morbidity and mortality, and exploring the diagnosis and treatment of HCC at the gene level has been a research hotspot in recent years.</p><p><strong>Methods: </strong>In this paper, a series of differentially expressed genes were found from the biochip related to HCC by bioinformatic analysis, then CNDP1 was finally selected for in-depth study according to the function and research progress of each gene. As the rate-limiting enzyme of carnosine hydrolysis, CNDP1 participates in the progress of many diseases, but its function has not been revealed in HCC. In the follow-up study, the low expression of CNDP1 in liver cancer tissues and cells was verified, then the pcDNA3.1-CNDP1 was used to improve the expression level of CNDP1 in HCC cell lines. Furthermore, this paper found that CNDP1 overexpression could significantly suppress cell prolifer-ation, migration, and invasion of HCC cell lines.</p><p><strong>Results: </strong>Mechanismly, the GeneMANIA database predicted that CNDP1 could interact with various proteins that regulate the PI3K-AKT-mTOR signaling pathway, which is overactivated in HCC. And this study showed that CNDP1 overexpression could effectively inhibit the activation of PI3K-AKT-mTOR signaling pathways, more significantly, inhibition of PI3K-AKT-mTOR signaling pathway could disrupt the anti-cancer effect of CNDP1 on HCC.</p><p><strong>Conclusion: </strong>In conclusion, we confirmed that CNDP1 was lowly expressed in HCC tissues and cells, and had potential anti-cancer activity. This discovery will lay a cytological foundation for expanding the biological function of CNDP1 and the diagnosis and treatment of HCC in the future.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation and Crosstalk of Cells and Factors in the Pancreatic Cancer Microenvironment.","authors":"Jia Xu, Songmei Lou, Hui Huang, Jian Xu, Feng Luo","doi":"10.2174/0115680096317840240723071018","DOIUrl":"https://doi.org/10.2174/0115680096317840240723071018","url":null,"abstract":"<p><p>Pancreatic cancer is a highly malignant form of cancer that distinguishes itself from other gastrointestinal tumors through significant fibrosis and unique perineural invasion. These characteristics underscore the complexity of neural regulation within the pancreatic cancer Tumor Microenvironment (TME). This review aimed to explore the regulatory mechanisms and crosstalk among stromal cells and their factors within the pancreatic cancer microenvironment. We begin by reviewing the major components of the pancreatic cancer microenvironment, analyzing interactions among crucial cell types, such as Cancer-associated Fibroblasts (CAFs) and immune cells, and revealing the dynamic changes between tumor cells and surrounding nerves, immune, and stromal cells. We discuss the role of neural factors, including the Nerve Growth Factor (NGF) and Brain-derived Neurotrophic Factor (BDNF), in the progression of pancreatic cancer and the mechanisms by which the sympathetic and parasympathetic nervous systems regulate tumor cell growth, migration, and invasion. Interactions among stromal cells, cytokines, and neural factors in the pancreatic cancer microenvironment promote fibrosis and perineural invasion. A deeper understanding of the regulation and crosstalk among components in the pancreatic cancer microenvironment offers new perspectives for inhibiting fibrosis and perineural invasion in pancreatic cancer.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neomorphic IDH Heterodimer Mutants: An Underestimated Point in Cancer Pathogenesis.","authors":"Olga V Dorovatovskaia, Mikhail Yu Oliferenko, Anatoly A Sorokin, Daniil I Sobolev, Galina S Stupnikova, Danil S Sobakin, Eugene N Nikolaev, Igor A Popov, Stanislav I Pekov","doi":"10.2174/0115680096317314240723054739","DOIUrl":"https://doi.org/10.2174/0115680096317314240723054739","url":null,"abstract":"<p><p>Mutations in an essential metabolic enzyme, isocitrate dehydrogenase (IDH), were found in many cancers. The impact of IDH1 and IDH2 proteoforms mutations can vary and de-pend on the cancer type and other genetic alterations. The wild-type IDH1/2 consists of two identical subunits, but the mutant enzyme is a heterodimer of mutant and wild-type subunits, while the mutant homodimer loses its catalytic activity. Thus, the balance of expression of wild-type and mutant proteoforms directly affects enzyme neomorphic activity, cell metabolic por-trait, and, therefore, cell survival and proliferation rates. Here, we generalize the influence of the presence of IDH mutations and the expression of mutant and wild-type proteoforms for various nosologies to demonstrate the deficiency in knowledge about the mutual distribution of the pro-teoforms in cancer cells. The review is supplemented with a brief description of IDH mutations' role in cell metabolic reprogramming and a summary of methods for IDH mutation detection. Eventually, we highlight the necessity of assessing the expression of wild-type and mutated IDH quantitatively, which can help create and deliver personalized approaches for tumor therapy.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142105192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}