Recent patents on anti-cancer drug discovery最新文献

{"title":"Updated Progress on Mass Spectrometry Imaging and its Application in Cancer Treatment and Drug Discovery.","authors":"Mingyue Li, Jingna Zhou, Tingting Zhang, Jingyang Lu, Yajie Wang, Junyu Liu, Xiaoyu Zhang, Haixia Chen","doi":"10.2174/0115748928269691231203164021","DOIUrl":"10.2174/0115748928269691231203164021","url":null,"abstract":"<p><strong>Background: </strong>Mass spectrometry imaging (MSI) is an imaging method based on mass spectrometry technology that can simultaneously visualize the spatial distribution of various biological molecules. The use of MSI in cancer detection and drug discovery has been extensively investigated in recent years.</p><p><strong>Objective: </strong>This review aims to summarize the latest advances of MSI and its specific applications in cancer detection and drug discovery, providing a basic understanding of the development and application of MSI in the past five years and offering references for the further application of MSI in cancer detection and drug discovery.</p><p><strong>Methods: </strong>In the database, \"mass spectrometry imaging\", \"cancer treatment\", and \"drug discovery\" were used as keywords for literature retrieval, and the time range was limited to \"2018- 2023\". After organizing and analyzing the literature and patents, a review was conducted.</p><p><strong>Results: </strong>Based on the literature, it was found that the updated progress of MSI in the past five years mostly focused on concrete methods, operation procedures, facilities, and composite applications. The patents of MSI were mainly correlated with the mass spectrometry imaging system and its application in cancer treatment. MSI is conducive to investigating the therapeutic schedule of cancer and searching for new drugs.</p><p><strong>Conclusion: </strong>MSI is a convenient, fast and powerful technology that has made great progress in sample preparation, instrumentation, quantitation, and multimodal imaging. MSI has emerged as a powerful technique in various biomedical applications, which has strong potential in cancer detection, treatment, formation mechanism research, discovery of biomarkers, and drug discovery process.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"319-334"},"PeriodicalIF":4.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139565416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Survival Benefits of <i>Ganoderma Lucidum</i> in Early-stage Triple-negative Breast Cancer: A Real World Study.","authors":"Baohong Jiang, Na Li, Wei Du, Lijun Zeng, Yuanbin Tang, Lunqi Luo, Hongbo Zhu, Feng Ye","doi":"10.2174/0115748928282946240111114448","DOIUrl":"10.2174/0115748928282946240111114448","url":null,"abstract":"<p><strong>Background: </strong>Ganoderma lucidum extracts are widely used as adjuvants in the treatment of triple-negative breast cancers (TNBC) in China. However, its clinical value in TNBC remains unclear. Therefore, we investigated the clinical effect of Ganoderma lucidum spore powder (GLSP) on prognosis in patients with early-stage TNBC in this study.</p><p><strong>Methods: </strong>A total of 388 patients who were diagnosed with TNBC at the Sun Yat-sen University Cancer Center from February 2012 to December 2017 were retrospectively reviewed. The propensity score matching (PSM) method was applied to balance baseline data. Kaplan-Meier method and Cox proportional hazards model were used to evaluate the relationship between GLSP and prognosis.</p><p><strong>Results: </strong>Of the 388 patients, 72 (18.6%) patients took GLSP. After PSM, 208 patients were selected for analysis, including 71 (34.1%) patients who took the powder. The median follow-up period was 51 months. The patients who took GLSP (the treatment group) and those who did not take GLSP (the control group) were similar in most clinico-pathological features before being matched. However, the proportion of patients who received breast-conserving surgery in the treatment group was higher (27.8% vs. 16.1%; p =0.021) than in the control group. No significant difference was found in the baseline data between the two groups for the matched cohort (all p >0.05). Univariate analysis and multivariate analysis showed that patients taking GLSP benefited from improved overall survival (OS) (HR=0.159, p = 0.002) and disease-free survival (DFS) (HR=0.232, p = 0.005) before being matched. The main result of the survival analysis after matching was similar to that described above. Patients in the treatment group achieved both greater OS and DFS benefits than patients in the control group (all p < 0.05). In stratified analysis according to TNM stages, after adjusting for the significant prognostic factors, multivariate analysis revealed that the treatment group had better OS than the control group for patients in stages II and III (HR=0.172, p =0.004).</p><p><strong>Conclusion: </strong>The results of this real-world propensity-score-matched study suggest that GLSP can improve OS and DFS in early-stage TNBC patients. A higher OS was observed for patients taking GLSP, particularly in stage II and stage III.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"476-488"},"PeriodicalIF":4.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139934890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP31 Activates the Wnt/β-catenin Signaling Pathway and Promotes Gastric Cancer Cell Proliferation, Invasion and Migration.","authors":"Lan Li, Limin Ye, Yinying Cui, Yueting Wu, Ling Shui, Zheng Zong, Zhao Nie","doi":"10.2174/0115748928297343240425055552","DOIUrl":"10.2174/0115748928297343240425055552","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) has a poor prognosis because it is highly aggressive, yet there are currently few effective therapies available. Although protein ubiquitination has been shown to play a complex role in the development of gastric cancer, to date, no efficient ubiquitinating enzymes have been identified as treatment targets for GC.</p><p><strong>Methods: </strong>The TCGA database was used for bioinformatic investigation of ubiquitin-specific protease 31 (USP31) expression in GC, and experimental techniques, including Western blotting, qRT-PCR, and immunohistochemistry, were used to confirm the findings. We also analyzed the relationship between USP31 expression and clinical prognosis in patients with GC. We further investigated the effects of USP31 on the proliferation, invasion, migration, and glycolysis of GC cells <i>in vitro</i> and <i>in vivo</i> by using colony formation, CCK-8 assays, Transwell chamber assays, cell scratch assays, and cell-derived xenograft. Furthermore, we examined the molecular processes by which USP31 influences the biological development of GC.</p><p><strong>Results: </strong>Patients with high USP31 expression have a poor prognosis because USP31 is abundantly expressed in GC. Therefore, USP31 reduces the level of ubiquitination of the Wnt/β-catenin pathway by binding to β-catenin, thereby activating glycolysis, which ultimately promotes GC proliferation and aggressive metastasis.</p><p><strong>Conclusion: </strong>USP31 inhibits ubiquitination of β-catenin by binding to it, stimulates the Wnt/β-- catenin pathway, activates glycolysis, and accelerates the biology of GCs, which are all demonstrated in this work.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"232-247"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140878254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Single-arm, Open-label, Phase Ib Clinical Study Evaluating the Efficacy and Safety of Durvalumab in Combination with Albumin-bound Paclitaxel and Carboplatin as Neoadjuvant Therapy for Resectable Stage III Non-small Cell Lung Cancer.","authors":"Yuejiao Zhong, Tao Li, Zhaoshi Bai, Ninglei Qiu, Siwen Liu, Wenjia Xia, Qiang Wei, Lingxiang Chen","doi":"10.2174/0115748928304000240429120252","DOIUrl":"10.2174/0115748928304000240429120252","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to explore the clinical efficacy and safety of durvalumab combined with albumin-bound paclitaxel and carboplatin as neoadjuvant therapy for resectable stage III Non-small Cell Lung Cancer (NSCLC).</p><p><strong>Methods: </strong>A single-arm open-label phase Ib study was conducted. A total of 40 patients with driver gene-negative resectable stage III NSCLC were enrolled. All patients received neoadjuvant treatment with durvalumab in combination with albumin-bound paclitaxel and carboplatin. The clinical efficacy, Major Pathological Response (MPR), Complete Pathological Response (pCR), and safety were assessed. Flow cytometry was used to detect the expression of programmed cell death receptor 1 (PD-1) on total T, helper T, and cytotoxic T lymphocytes in peripheral blood before and after neoadjuvant treatment. Adverse reactions during the treatment were recorded. Disease- free Survival (DFS) and Overall Survival (OS) curves were constructed.</p><p><strong>Results: </strong>After the neoadjuvant treatment, the overall Objective Response Rate (ORR) in the 40 patients with NSCLC was 65.00%. MPR was achieved in 27 patients (67.50%), and pCR was achieved in nine patients (22.50%). The expression levels of PD-1 on total T, helper T, and cytotoxic T lymphocytes in patients with NSCLC significantly decreased after treatment (all p < 0.05). The most common adverse events were hair loss (47.50%), nausea and vomiting (42.50%), and fatigue (40.00%). The majority of adverse events were grades 1 and 2, with a small number of events being grades 3 and 4. At the end of the follow-up period, the average DFS was 21.49 ± 0.99 months, and the average OS was 24.79 ± 0.53 months.</p><p><strong>Conclusion: </strong>Neoadjuvant treatment with durvalumab combined with albumin-bound paclitaxel and carboplatin as first-line therapy for driver gene-negative stage III NSCLC achieved a high pathological response rate and improved immune function. It is expected to extend patient survival with good tolerability.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"648-654"},"PeriodicalIF":4.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Present State and Potential Applications of Artificial Intelligence in Cancer Diagnosis and Treatment.","authors":"Anuja Mishra, Srishti Sharma, Swaroop Kumar Pandey","doi":"10.2174/0115748928361472250123105507","DOIUrl":"10.2174/0115748928361472250123105507","url":null,"abstract":"<p><p>An aberrant increase in cancer incidences has demanded extreme attention globally despite advancements in diagnostic and management strategies. The high mortality rate is concerning, and tumour heterogeneity at the genetic, phenotypic, and pathological levels exacerbates the problem. In this context, lack of early diagnostic techniques and therapeutic resistance to drugs, sole awareness among the public, coupled with the unavailability of these modern technologies in developing and low-income countries, negatively impact cancer management. One of the prime necessities of the world today is the enhancement of early detection of cancers. Several independent studies have shown that screening individuals for cancer can improve patient survival but are bogged down by risk classification and major problems in patient selection. Artificial intelligence (AI) has significantly advanced the field of oncology, addressing various medical challenges, particularly in cancer management. Leveraging extensive medical datasets and innovative computational technologies, AI, especially through deep learning (DL), has found applications across multiple facets of oncology research. These applications range from early cancer detection, diagnosis, classification, and grading, molecular characterization of tumours, prediction of patient outcomes and treatment responses, personalized treatment, and novel anti-cancer drug discovery. Over the past decade, AI/ML has emerged as a valuable tool in cancer prognosis, risk assessment, and treatment selection for cancer patients. Several patents have been and are being filed and granted. Some of those inventions were explored and are being explored in clinical settings as well. In this review, we will discuss the current status, recent advancements, clinical trials, challenges, and opportunities associated with AI/ML applications in cancer detection and management. We are optimistic about the potential of AI/ML in improving outcomes for cancer and the need for further research and development in this field.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"287-305"},"PeriodicalIF":4.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143124249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Matrix Metalloproteinase-2 (MMP-2): As an Essential Factor in Cancer Progression.","authors":"Ramakkamma Aishwarya Reddy, Magham Sai Varshini, Raman Suresh Kumar","doi":"10.2174/0115748928251754230922095544","DOIUrl":"10.2174/0115748928251754230922095544","url":null,"abstract":"<p><p>The development of cancer has been a multistep process involving mutation, proliferation, survival, invasion, and metastasis. Of all the characteristics of cancer, metastasis is believed to be the hallmark as it is responsible for the highest number of cancer-related deaths. In connection with this, Matrix metalloproteinases (MMPs), that has a role in metastasis, are one of the novel therapeutic targets. MMPs belong to the family of zinc-dependent endopeptidases and are capable of degrading the components of the extracellular matrix (ECM). The role of MMPs in ECM remodeling includes tissue morphogenesis, uterine cycling, growth, tissue repair, and angiogenesis. During pathological conditions, MMPs play a critical role in the excessive degradation of ECM which includes arthritis, tumour invasion, tumour metastasis, and several other autoimmune disorders. Moreover, they are believed to be involved in many physiological aspects of the cell, such as proliferation, migration, differentiation, angiogenesis, and apoptosis. It is reported that dysregulation of MMP in a variety of cancer subtypes have a dual role in tumour growth and metastasis processes. Further, multiple studies suggest the therapeutic potential of targeting MMP in invading cancer. The expression of MMP-2 correlates with the clinical characteristics of cancer patients, and its expression profile is a new diagnostic and prognostic biomarker for a variety of human diseases. Hence, manipulating the expression or function of MMP-2 may be a potential treatment strategy for different diseases, including cancers. Hence, the present review discusses the therapeutic potential of targeting MMP in various types of cancers and their recent patents.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"26-44"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49686893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Construction and Identification of a Human Colorectal Adenoma Epithelial Cell Line by SV40 Large T-antigen Transfection.","authors":"Xiangxue Meng, Xinyue Han, Xiangying Lin, Guanhong Li, Jingnan Wang, Ao Sun, Xiaochen Fu, Bowen Xu, Donghua Yang, Yanping Wu, Min Zhang, Xiaoling Fu","doi":"10.2174/0115748928297500240522080820","DOIUrl":"10.2174/0115748928297500240522080820","url":null,"abstract":"<p><strong>Background: </strong>Colorectal adenoma represents the critical step in the development of colorectal cancer. The establishment of an immortalized epithelial cell line of colorectal adenoma of human origin would provide a tool for studying the mechanism of precancerous lesions, screening the efficacy of novel drugs, and constructing in vivo disease models. Currently, there is no commercially available stable supply of epithelial cells from precancerous lesions.</p><p><strong>Aims: </strong>This study aimed to establish a natural LHPP low-expressing precancerous epithelial cell line by SV40-LT antigen gene transfection.</p><p><strong>Methods: </strong>Simian vacuolating virus 40(SV40), SV40-LT overexpressed lentivirus vector, was transfected into primary human colorectal adenomatous polyp epithelial cells. The transfected cells were screened, and the screened cells were amplified to obtain the epithelial cell line: IHCRA- CELL. The cells were identified by morphological observation, cell proliferation, Quantitative real-time PCR (qPCR), and Short Tandem Repeats (STR) experiments. Morphologically, the cells showed epithelial-like characteristics, such as polygon shape, desmosomes mitochondria, and strong positive keratin staining. There was no significant difference between the transfected cells and the primary cells. Through the STR identification experiment, no matching cell lines were found in the cell lines retrieval.</p><p><strong>Conclusion: </strong>We successfully established a natural LHPP low-expressing precancerous epithelial cell line by SV40-LT antigen gene transfection, which has been patented and is now preserved in the Chinese Typical Culture Preservation Center. It was verified that the transformed cells maintained the phenotype and biological characteristics of epithelial cells. This cell line can be used to study the mechanism of precancerous lesions, screen the efficacy of novel drugs, and construct in vivo disease models.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"621-633"},"PeriodicalIF":4.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patents on PARP-1 Inhibitors for the Management of Cancer from 2017-2023.","authors":"Harshwardhan Singh, Ankit Kumar Singh, Adarsh Kumar, Pradeep Kumar","doi":"10.2174/0115748928315021240603073902","DOIUrl":"10.2174/0115748928315021240603073902","url":null,"abstract":"<p><strong>Background: </strong>There are eighteen members of the Poly (ADP-ribose) polymerases (PARPs) family, which oversees various cellular processes such as maintaining the integrity of the genome, regulating transcription, cell cycle progression, initiating the DNA damage response, and apoptosis. PARP1 is an essential member of the PARP family and plays a crucial role in repairing single-strand breaks in eukaryotic cells through a process called BER (base excision repair). It is the most extensively studied and commonly found member of this family.</p><p><strong>Area covered: </strong>This article discusses the advancements in developing PARP inhibitors for human cancers. It covers the discovery of new PARP1 inhibitors with chemical classifications that selectively target multiple areas using cancer models in vitro and in vivo and evaluate them critically. The focus is on patents that have been published from 2017 to 2023, except tankyrase inhibitors.</p><p><strong>Expert opinion: </strong>PARP1 inhibitors were developed by various companies and academic groups from the 1990s to enhance the effectiveness of chemo and radiotherapy. However, their progress was hindered due to their severe toxicity when combined with these treatments. Therefore, on finding PARP1 inhibitors that can amplify the ability of chemotherapy agents to kill tumors while causing minimal toxicity, these substances can either be used alone as part of the synthetic lethality approach or in conjunction with radiotherapy or chemotherapy, resulting in a mutually beneficial outcome.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"532-547"},"PeriodicalIF":4.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141319411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ruthenium Complex Suppresses Proliferation of Residual Hepatocellular Carcinoma after Incomplete Radiofrequency Ablation Therapy.","authors":"Zhi-Jie Yu, Shun-Wen Guo, Bi-Shu Wang, Shi Ouyang, Xian-Huan Zhang, Zi-Zhuo Zhao, Jin-Quan Wang","doi":"10.2174/0115748928320508240802055846","DOIUrl":"10.2174/0115748928320508240802055846","url":null,"abstract":"<p><strong>Background: </strong>Radiofrequency ablation (RFA) is an effective therapy for hepatocellular carcinoma (HCC). However, incomplete radiofrequency ablation (IRFA) can promote the progression of residual cancer cells, which is a serious problem in the clinical application of RFA. Therefore, it is of great significance to explore the mechanism and countermeasures of the progression of residual tumors after IRFA. Our previous study confirmed that IRFA can activate the hypoxia/ autophagy pathway of residual tumors in mice and then induce the proliferation of residual tumor cells. Additionally, we found a metal ruthenium complex [Ru(bpy)2(ipad)](ClO₄)₂ (Ru, where bpy = 2,2'-bipyridine and ipad = 2-(anthracene-9,10-dione-2-yl)imidazo[4,5-f][1,10]phenanthroline) can effectively inhibit hypoxia-inducible factor (HIF-1α) and has good anti-tumor effect in a hypoxic environment; however, whether Ru could suppress the proliferation of residual tumor cells after IRFA is unknown.</p><p><strong>Objectives: </strong>This study intends to evaluate the effect of Ru in suppressing the proliferation of residual hepatocellular carcinoma after IRFA in a mice model.</p><p><strong>Methods: </strong>The Hepa1-6 xenograft mouse model was established in C57BL/6 mice to simulate clinical IRFA. H&E staining was used to evaluate the biosafety of major organs in the treated mice. TUNEL assay was employed to assess the antitumor effect. Immunohistochemically and immunofluorescence staining was performed to detect the expression of HIF-1α and autophagy-related proteins. The ELISA assay was used to examine the cytokines of interferon-gamma (IFN-γ) and interleukin 10 (IL-10).</p><p><strong>Results: </strong>Our findings revealed that the residual tumor relapsed via the HIF-1α/LC3B/P62 autophagy- related pathway after IRFA, while Ru could suppress this process. In addition, it was demonstrated that Ru could effectively activate the immune system of the mice and reverse the tumor immune suppression microenvironment after IRFA.</p><p><strong>Conclusion: </strong>The ruthenium complex Ru could suppress the proliferation of residual hepatocellular carcinoma cells after IRFA in the mice model. This study introduces a novel approach that combines the use of ruthenium complexes with IRFA, offering a potential solution to address the reoccurrence of residual liver cancer following IRFA in clinical settings.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"765-775"},"PeriodicalIF":4.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141972451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphofructokinase-1 in Cancer: A Promising Target for Diagnosis and Therapy.","authors":"Ali Raza Ishaq, Tahira Younis, Shankun Lin, Muhammad Usman, Tingfang Wang, Zhe-Sheng Chen","doi":"10.2174/0115748928321372240813080131","DOIUrl":"10.2174/0115748928321372240813080131","url":null,"abstract":"<p><p>Tumor cells have distorted enzymatic houses, which change the metabolic state from oxidative phosphorylation to glycolysis with high lactate levels in a hypoxic environment. Redrafting the metabolic profile is an emerging hallmark of cancer. Glycolytic enzyme amplification occurs in about 70% of all malignancies. Current studies have found that PFK-1 overexpression is linked to cell migration, proliferation, and Overall Survival (OS) rate in various human cancer cell lines. This review intended to uncover the bona fide therapeutic target for cancer therapy and elucidate the role of PFK-1 in cancer. Furthermore, this review has outlined the listed pharmacological and genetic inhibitors of PFK-1. Following this review, future studies on PFK-1 should emphasize the molecular pathways implicated in PFK-1 overexpression in cancer development. The terms \"PFK-1\", \"PFKP-1\", \"PFKL-1\", \"PFKM-1\", \"PFKM-1 and cancer\", \"PFKP-1 and cancer\", \"PFKL-1 and cancer\", and \"inhibitors of PFK-1\" were used to retrieve the information from a variety of databases, including PubMed, Scopus, Google Scholar, and ScienceDirect. In a variety of malignancies, inhibiting the expression of PFK-1 isoforms has been reported to be the most effective therapeutic method. Overexpression of PFK-1 isoforms induces the Warburg effect, cell proliferation, and carcinogenesis by downregulating apoptotic proteins, such as active caspase-3, caspase-9, and caspase-8. YY1, synoviolin, Sh-RNA-507, SNAI, miR-520a/b/e, miR-128, and β-miR-6517 are some of the putative genetic inhibitors against PFK-1 that have been used to manage the development of malignancies. Pharmacological inhibitors, such as penfluridol, synoviolin/HRD1, quercetin, ginsenoside 20(S)-Rg3, triptolide, worenine, acetylsalicylic acid, and salicylic acid, can regulate the advancement of malignancies by inhibiting PFK-1. Thus, PFK-1 is a promising molecular biomarker for cancer treatment. A prospective investigation can validate the unbiased approaches for discovering brandnew PFK-1 inhibitors for cancer treatment.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":"667-680"},"PeriodicalIF":4.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142019986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}