Anti-cancer agents in medicinal chemistry最新文献

{"title":"Recurrent Missense Driver STAT5B N642H Mutation in Children Transiting into Adolescence, with Acute Lymphoid Leukemia and its In silico Inhibition.","authors":"Rehana Yasmin, Rashda Abbasi, Tajdar Jahangir Gohar, Hina, Nafees Ahmad, Sajid Malik","doi":"10.2174/0118715206350463241226032324","DOIUrl":"https://doi.org/10.2174/0118715206350463241226032324","url":null,"abstract":"<p><strong>Background: </strong>The occurrence of gain of function mutations in STAT5B has been associated to survival, and drug resistance in Leukemia. In silico screening of compounds having inhibitory potential towards mutated proteins, can be helpful in the development of specific inhibitors.</p><p><strong>Objective: </strong>This study was designed to screen selected JAK-STAT mutations in leukemia patients and virtual exploration of molecular interaction of potential inhibitors with their mutated products.</p><p><strong>Methods: </strong>In total 276 patients were randomly recruited for this study. Demographic and clinical data were summarized. The genetic status of JAK1V623A, JAK2 S473 and STAT5BN642H were screened through allele specific PCR. In-silico analysis was performed on wild type and mutant protein sequences retrieved from Protein databank. The ligands and protein were prepared through standard protocols, and docking was performed through Auto Dock Vina 1.2.0.</p><p><strong>Results: </strong>Acute lymphoblastic leukemia comprises 70% of the total patients. Male to female ratio was 3:1. All the patients were homozygous for JAK1V623A, JAK2 S473 major allele. However, 6 patients (5 male, 1 female) with ALL were STAT5BN642H+. The molecular docking of the ligands to wild type and STAT5BN642H+revealed that AC- 4-130, Pimozide, Indirubin and Stafib-2 have higher but differential docking affinities for SH2-domain of both normal and mutated STAT5B. However, AC-4-130 has a higher affinity for wild type and Stafib-2 has stable molecular interaction with STAT5BN642H+.</p><p><strong>Conclusion: </strong>The aggressive form of pediatric leukemia, carrying STAT5BN642H+ mutation is identified in the studied population. It is predicted that AC-14-30 and stafib-2 have potential for inhibition of constitutively active STAT5B if optimized for use in combination therapy.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490536","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":"A Systematic Quantitative Approach to Rational Drug Design and the Discovery of Novel Human Antigen R (HuR) Inhibitors.","authors":"Juhi Dey, Kumari Kaushiki, K M Abha Mishra, Paga Sudheer, Kalyan Kumar Sethi","doi":"10.2174/0118715206354755241220062707","DOIUrl":"https://doi.org/10.2174/0118715206354755241220062707","url":null,"abstract":"<p><strong>Background: </strong>1,4-Naphthoquinone and its derivatives are recognized for their potent anticancer effects, establishing this pharmacophore as a key focus in cancer research. Their potential to modulate cellular pathways suggests they could be effective in developing new HuR inhibitors, targeting a protein crucial for regulating cancer-related gene expression. Compounds C1-C20 were designed by using Discovery Studio (DS) software.</p><p><strong>Methods: </strong>In this study, a systematic approach involves scaffold hopping followed by additional research such as molecular docking, ADMET, drug-likeness, toxicity prediction, molecular dynamic (MD) simulation, and binding free energy analysis was used to discover novel Human Antigen R (HuR) inhibitors.</p><p><strong>Results: </strong>In molecular docking, 1,4-Naphthoquinone derivatives showed better interactions with the HuR protein compared to that of the conventional HuR inhibitor MS-444. Among twenty 1,4-Naphthoquinone derivatives, most of the compounds showed favorable pharmacokinetic characteristics. In the toxicity prediction model, most of the designed compounds were neither mutagenic nor carcinogenic. According to MD simulation, C5 is more stable than MS-444.</p><p><strong>Conclusion: </strong>The designed 1,4-Naphthoquinone derivatives have been found to be crucial structural motifs for the discovery of novel HuR inhibitors, which was well supported by the in-silico screening and molecular modeling methods.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143363583","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":"The Function of Poly (U) Binding Splicing Factor 60 (PUF60) in Disease Regulation.","authors":"Huijuan Chen, Tian Guan, Jingfeng Song, Yihua Chen","doi":"10.2174/0118715206346843241119105519","DOIUrl":"https://doi.org/10.2174/0118715206346843241119105519","url":null,"abstract":"<p><p>The alternative splicing (AS) of pre-mRNA is an important process in controlling the expression of human genes, which can enrich the diversity of the proteome and regulate gene function. On the contrary, aberrant splicing contributes significantly to numerous human diseases progression, including tumors, neurological diseases, metabolic diseases, infections, and immune diseases. The PUF60, a protein related to RNA splicing, plays critical functions in RNA splicing and gene transcription regulation. In addition, it can achieve synergistic binding with U2AF65 on RNA through interactions in the pyrimidine region, promoting the splicing of introns with weak 3'- splice sites and pyrimidine bundles. Nevertheless, an increasing amount of evidence supports that it shows a significant overexpression pattern in the vast majority of cancer cells and is crucial for embryonic development, indicating that PUF60 may hold the post of a potential therapeutic target for such diseases. These studies have significantly increased our interest in PUF60. Thus, we briefly reviewed the structural domain characteristics of the PUF60, splicing mutants of PUF60, and the roles and functions in human diseases, including various cancers, infections of bacterium and viruses, myositis, and Verheij syndrome. Furthermore, the targeted PUF60 inhibitors and boundedness of the current research were elaborated on in the article. The article effectively communicates critical perception and insight, making it a precious resource for those interested in PUF60 research and treatment.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942994","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":"Novel Celecoxib Derivative, RF26, Blocks Colon Cancer Cell Growth by Inhibiting PDE5, Activating cGMP/PKG Signaling, and Suppressing β-catenin-dependent Transcription.","authors":"Sara Sigler, Mohammad Abdel-Halim, Reem K Fathalla, Luciana Madeira Da Silva, Adam B Keeton, Yulia Y Maxuitenko, Kristy L Berry, Gang Zhou, Matthias Engel, Ashraf H Abadi, Gary A Piazza","doi":"10.2174/0118715206318802240821114353","DOIUrl":"10.2174/0118715206318802240821114353","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have reported that the cGMP-specific PDE5 isozyme is overexpressed in colon adenomas and adenocarcinomas and essential for colon cancer cell proliferation, while PDE5 selective inhibitors (e.g., sildenafil) have been reported to have cancer chemopreventive activity.</p><p><strong>Aim: </strong>This study aimed to determine the anticancer activity of a novel PDE5 inhibitor, RF26, using colorectal cancer (CRC) cells and the role of PDE5 in CRC tumor growth <i>in vivo</i>.</p><p><strong>Objective: </strong>The objective of this study was to characterize the anticancer activity of a novel celecoxib derivative, RF26, in CRC cells previously reported to lack COX-2 inhibition but have potent PDE5 inhibitory activity.</p><p><strong>Methods: </strong>Anticancer activity of RF26 was studied using human CRC cell lines. Effects on cell growth, cGMPdependent protein kinase (PKG) activity, β-catenin levels, TCF/LEF transcriptional activity, cell cycle distribution, and apoptosis were measured. CRISPR/cas9 PDE5 knockout techniques were used to determine if PDE5 mediates the anticancer activity of RF26 and validate PDE5 as a cancer target.</p><p><strong>Results: </strong>RF26 was appreciably more potent than celecoxib and sildenafil to suppress CRC cell growth and was effective at concentrations that activated PKG signaling. RF26 suppressed β-catenin levels and TCF/LEF transcriptional activity and induced G1 cell cycle arrest and apoptosis within the same concentration range. CRISPR/cas9 PDE5 knockout CRC cells displayed reduced sensitivity to RF26, proliferated slower than parental cells, and failed to establish tumors in mice.</p><p><strong>Conclusion: </strong>Further evaluation of RF26 for the prevention or treatment of cancer and studying the role of PDE5 in tumorigenesis are warranted.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":"52-62"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118831","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":"Therapeutic Effects of Crocin Nanoparticles Alone or in Combination with Doxorubicin against Hepatocellular Carcinoma <i>In vitro</i>.","authors":"Noha S Basuony, Tarek M Mohamed, Doha M Beltagy, Ahmed A Massoud, Mona M Elwan","doi":"10.2174/0118715206327654240823074318","DOIUrl":"10.2174/0118715206327654240823074318","url":null,"abstract":"<p><strong>Objective: </strong>Crocin (CRO), the primary antioxidant in saffron, is known for its anticancer properties. However, its effectiveness in topical therapy is limited due to low bioavailability, poor absorption, and low physicochemical stability. This study aimed to prepare crocin nanoparticles (CRO-NPs) to enhance their pharmaceutical efficacy and evaluate the synergistic effects of Cro-NPs with doxorubicin (DOX) chemotherapy on two cell lines: human hepatocellular carcinoma cells (HepG2) and non-cancerous cells (WI38).</p><p><strong>Methods: </strong>CRO-NPs were prepared using the emulsion diffusion technique and characterized by transmission electron microscopy (TEM), scanning electron microscopy (SEM), Zeta potential, and Fourier transform infrared spectroscopy (FT-IR). Cell proliferation inhibition was assessed using the MTT assay for DOX, CRO, CRO-NPs, and DOX+CRO-NPs. Apoptosis and cell cycle were evaluated by flow cytometry, and changes in the expression of apoptotic gene (P53) and autophagic genes (ATG5 & LC3) were analyzed using real-time polymerase chain reaction.</p><p><strong>Results: </strong>TEM and SEM revealed that CRO-NPs exhibited a relatively spherical shape with an average size of 9.3 nm, and zeta potential analysis indicated better stability of CRO-NPs compared to native CRO. Significantly higher antitumor effects of CRO-NPs were observed against HepG2 cells (IC₅₀ = 1.1 mg/ml and 0.57 mg/ml) compared to native CRO (IC₅₀ = 6.1 mg/ml and 3.2 mg/ml) after 24 and 48 hours, respectively. Annexin-V assay on HepG2 cells indicated increased apoptotic rates across all treatments, with the highest percentage observed in CRO-NPs, accompanied by cell cycle arrest at the G2/M phase. Furthermore, gene expression analysis showed upregulation of P53, ATG5, and LC3 genes in DOX/CRO-NPs co-treatment compared to individual treatments. In contrast, WI38 cells exhibited greater sensitivity to DOX toxicity but showed no adverse response to CRONPs.</p><p><strong>Conclusion: </strong>Although more in vivo studies in animal models are required to corroborate these results, our findings suggest that CRO-NPs can be a potential new anticancer agent for hepatocellular carcinoma. Moreover, they have a synergistic effect with DOX against HepG2 cells and mitigate the toxicity of DOX on normal WI38 cells.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":"194-206"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456294","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":"The Dual Role of ADAMTS9-AS1 in Various Human Cancers: Molecular Pathogenesis and Clinical Implications.","authors":"Haodong He, Jingjie Yang, Yan Zhou, Xinyan Zheng, Lihan Chen, Zhujun Mao, Chuyuan Liao, Tongtong Li, Haoran Liu, Gang Zhou, Houdong Li, Chengfu Yuan","doi":"10.2174/0118715206359325241119075640","DOIUrl":"10.2174/0118715206359325241119075640","url":null,"abstract":"<p><p>Long non-coding RNA (lncRNA) is a type of non-coding RNA distinguished by a length exceeding 200 nucleotides. Recent studies indicated that lncRNAs participate in various biological processes, such as chromatin remodeling, transcriptional and post-transcriptional regulation, and the modulation of cell proliferation, death, and differentiation, hence influencing gene expression and cellular function. ADAMTS9-AS1, an antisense long non-coding RNA situated on human chromosome 3p14.1, has garnered significant interest due to its pivotal involvement in the advancement and spread of diverse malignant tumors. ADAMTS9-AS1 functions as a competitive endogenous RNA (ceRNA) that interacts with multiple microRNAs (miRNAs) and plays a crucial role in regulating gene expression and cellular functions by modulating essential signaling pathways, including PI3K/AKT/mTOR, Wnt/β-catenin, and Ras/MAPK pathways. Dysregulation of this factor has been linked to tumor development, migration, invasion, and resistance to apoptotic mechanisms, including as iron-induced apoptosis, underscoring its intricate function in cancer pathology. While current research has clarified certain pathways involved in cancer formation, additional clinical and <i>in vivo</i> investigations are necessary to enhance comprehension of its specific involvement across various cancer types. This review encapsulates the recent discoveries on the correlation of ADAMTS9-AS1 with numerous malignancies, clarifying its molecular mechanisms and its prospective role as a therapeutic target in oncology. Furthermore, it identifies ADAMTS9-AS1 as a potential early diagnostic biomarker and therapeutic target, offering novel opportunities for targeted intervention in oncology.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":"533-543"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942992","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":"Emerging Claudin18.2-targeting Therapy for Systemic Treatment of Gastric Cancer: Seeking Nobility Amidst Danger.","authors":"Xueshuai Ye, Yongqiang Wu, Haiqiang Zhang","doi":"10.2174/0118715206329892240927081033","DOIUrl":"10.2174/0118715206329892240927081033","url":null,"abstract":"<p><p>Gastric cancer in advanced stages lacked effective treatment options. claudin18.2 (CLDN18.2) is a membrane protein that is crucial for close junctions in the differentiated epithelial cells of the gastric mucosa, playing a vital role in barrier function, and can be hardly recognized by immune cells due to its polarity pattern. As the polarity of gastric tumor cells changes, claudin18.2 is exposed on the cell surface, resulting in immune system recognition, and making it an ideal target. In this review, we summarized the expression regulation mechanism of claudin18.2 both in normal cells and malignant tumor cells. Besides, we analyzed the available clinical results and potential areas for future research on claudin18.2-positive gastric cancer and claudin18.2-targeting therapy. In conclusion, claudin18.2 is an ideal target for gastric cancer treatment, and the claudin18.2-targeting therapy has changed the treatment pattern of gastric cancer.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":"223-231"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370794","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":"Schisanhenol Inhibits the Proliferation of Hepatocellular Carcinoma Cells by Targeting Programmed Cell Death-ligand 1 <i>via</i> the STAT3 Pathways.","authors":"Zhihong Zhang, Yiwen Zhong, Xu Han, Xueyang Hu, Yuhan Wang, Lei Huang, Siying Li, Ziqing Li, Chunmei Wang, He Li, Jinghui Sun, Wenyue Zhuang, Mengyang Wang, Jianguang Chen, Wei Liu, Chang Liu, Xin Guo, Siyu Yuan, Jiping Wu","doi":"10.2174/0118715206349131241121091834","DOIUrl":"10.2174/0118715206349131241121091834","url":null,"abstract":"<p><strong>Background: </strong>Programmed cell death-ligand 1 (PD-L1) is overexpressed in tumor cells, which promotes tumor cell survival and cell proliferation and causes tumor cells to escape T-cell killing. Schisanhenol, a biphenyl cyclooctene lignin-like compound, was extracted and isolated from the plant named <i>Schisandra rubriflora</i> (Franch.).</p><p><strong>Purpose: </strong>In this work, we studied the anticancer potential of schisanhenol and explored whether schisanhenol mediated its effect by inhibiting the expression of PD-L1 <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Materials and methods: </strong><i>In vitro</i>, we performed western blot, immunofluorescence, immunoprecipitation, and colony formation assays to study the proteins, genes, and pathways related to the anti-tumour activity of schisanhenol. <i>In vivo</i>, we explored the antitumor activity of schisanhenol through orthotopic liver transplantation and subcutaneous transplantation tumor models of hepatocellular carcinoma (HCC) cells.</p><p><strong>Results: </strong>We found that schisanhenol decreased the viability of HCC cells. It inhibited the expression of programmed cell death ligand-1 (PD-L1), which plays a pivotal role in tumorigenesis. Subsequently, schisanhenol suppressed the expression of PD-L1 by decreasing the activation of STAT3. Furthermore, we found that schisanhenol inhibited the activation of STAT3 <i> via</i> JAK/STAT3 (T705), Src/STAT3 (T705), and PI3K/AKT/mTOR/STAT3 (S727) pathways. Colony formation tests showed that schisanhenol suppressed cell proliferation by inhibiting PD-L1. Schisanhenol also enhanced cytotoxic T lymphocytes (CTL) activity and regained their ability to kill tumour cells in co-culture. Finally, <i>in vivo</i> observation confirmed the antitumor activity of schisanhenol.</p><p><strong>Conclusion: </strong>Schisanhenol inhibits the proliferation of HCC cells by targeting PD-L1 <i> via</i> the STAT3 pathways. These findings prove that schisanhenol is a valuable candidate for HCC therapeutics and reveal previously unknown characteristics of schisanhenol.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":"697-710"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982533","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":"Recent Prospectives of Cellular Signaling Role for Mammary Gland Carcinogenesis.","authors":"Monu Kumar Kashyap, Sikma Roy, Shiwani Jaiswal, Shweta Verma, Siddharth Srivastava, Amit Kumar Nigam, Awadhesh Kumar, Bandana Singh, Ved Prakash Tiwari, Mahima Mahima, Akash Ved, Karuna S Shukla, Namrata Singh","doi":"10.2174/0118715206319933241104100736","DOIUrl":"10.2174/0118715206319933241104100736","url":null,"abstract":"<p><p>In women globally, breast cancer ranks as the second most frequent cause of cancer-related deaths, making up about 25% of female cancer cases, which is pretty standard in affluent countries. Breast cancer is divided into subtypes based on aggressive, genetic and stage. The precise cause of the problem is still unknown. However, the following significant risk factors have been found: sex, age, heredity, not having children, breastfeeding, elevated hormone levels, and personal lifestyle. The presence or lack of three nuclear receptors ER, PR, and HER2/ERBB2 (triple negative) and the amplification of the HER2/ErbB2 gene are the clinical criteria used to classify breast cancer. Chemotherapy is still the cornerstone of treatment for triple-negative breast cancer (TNBC), even. If, for the first two groups of patients,receptor-specific therapy is used. The most often prescribed chemotherapy agents for the treatment of breast cancer include doxorubicin (DOX), curcumin paclitaxel (PTX), docetaxel (DCX), thioridazine (THZ), disulfiram (DSF), and camptothecin (CPT). Monoclonal antibodies (mAbs) were used in antibody-drug conjugates (ADCs) to bind tumor-associated target antigens selectively and deliver very effective cytotoxic agents. According to recent research, synthetic derivatives effectively combat both MCF- 7 and breast cancer cell lines that are resistant to many drugs. This review provides a wealth of information on the mechanism of action of synthetic derivatives on multidrug-resistant cell lines. This review includes information about how synthetic derivatives affect cancer cells that have developed multidrug resistance during chemotherapy. These mechanisms have been linked to factors such as increased drug efflux, genetic factors, growth factors, increased DNA repair capacity, and elevated xenobiotic metabolism. Because of this, more research is necessary to learn more about the effectiveness of synthetic derivatives against breast cancer and cell lines that are resistant to several drugs. This review aims to find recent prospects of various types of cellular signaling pathways (JAK/STAT, Akt, MAPK, etc.) involved in the progression of breast cancer disorder, and we also study different synthetic and natural drugs that are applied for treating breast cancer.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":"818-840"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926269","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":"Cytotoxic Effects of <i>Lecaniodiscus Cupanioides</i> (Planch.) Extract and Triterpenoids-derived Gold Nanoparticles On MCF-7 Breast Cancer Cell Lines.","authors":"Roshudufhadzwa Magadani, Derek Tantoh Ndinteh, Saartjie Roux, Louisiane Patrick Nangah, Item Justin Atangwho, Daniel Ejim Uti, Esther Ugo Alum, Simeon Ikechukwu Egba","doi":"10.2174/0118715206325529241004064307","DOIUrl":"10.2174/0118715206325529241004064307","url":null,"abstract":"<p><strong>Background: </strong>The prevalent disease known as breast cancer has a significant impact on both men's and women's health and quality of life.</p><p><strong>Aim: </strong>The aim of this study was to explore the potential roles of <i>Lecaniodiscus cupanioides</i> (planch.) extract and triterpenoid- derived gold nanoparticles (AuNPs) in cancer therapy, specifically targeting MCF-7 breast cancer cell lines.</p><p><strong>Methods: </strong>Gold nanoparticles were synthesized utilizing triterpenoid (ZJ-AuNPs) and leaf extract from <i>Lecaniodiscus cupanioides</i> (LC-AuNPs). Fourier transform infrared spectroscopy (FTIR), Dynamic light scattering (DLS), High-resolution transmission electron microscopy (HRTEM), and UV-vis spectroscopy were employed to characterize the nanoparticles. Additionally, the MTT assay was used to assess the impact of AuNPs on cancer cell viability using MCF-7 breast cancer cell lines.</p><p><strong>Results: </strong>Analysis of ZJ-AuNPs and LC-AuNPs revealed DLS zeta potentials of -31.8 and -35.8 mV, respectively, and a corresponding UV-vis absorption maxima at 540 and 550 nm. Also, the ZJ-AuNPs and LC-AuNPs had respective zeta-sizes that ranged from 25.84 to 35.98 nm and polydispersive index values between 0.2360 and 0.773. Furthermore, the presence of the chemical groups -OH and -NH was shown to be necessary for the green method of capping and reducing the gold nanoparticles. Nevertheless, a significant decrease in cell viability percentages was noted in the MTT experiment, accompanied by an increase in the quantity or concentration of the nanoparticles for both ZJ-AuNPs and LC-AuNPs.</p><p><strong>Conclusion: </strong>Given the data obtained in this study, the biosynthesized ZJ-AuNPs and LC-AuNPs were shown to possess potent cytotoxic effects on breast cancer cells. Hence, they may be valuable tools in the development of new cancer chemotherapy drugs.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":"841-850"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051395","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}