Cancer Cell International最新文献

{"title":"STAT3: Key targets of growth-promoting receptor positive breast cancer.","authors":"Rui-Yuan Jiang, Jia-Yu Zhu, Huan-Ping Zhang, Yuan Yu, Zhi-Xin Dong, Huan-Huan Zhou, Xiaojia Wang","doi":"10.1186/s12935-024-03541-9","DOIUrl":"10.1186/s12935-024-03541-9","url":null,"abstract":"<p><p>Breast cancer has become the malignant tumor with the first incidence and the second mortality among female cancers. Most female breast cancers belong to luminal-type breast cancer and HER2-positive breast cancer. These breast cancer cells all have different driving genes, which constantly promote the proliferation and metastasis of breast cancer cells. Signal transducer and activator of transcription 3 (STAT3) is an important breast cancer-related gene, which can promote the progress of breast cancer. It has been proved in clinical and basic research that over-expressed and constitutively activated STAT3 is involved in the progress, proliferation, metastasis and chemotherapy resistance of breast cancer. STAT3 is an important key target in luminal-type breast cancer and HER2-positive cancer, which has an important impact on the curative effect of related treatments. In breast cancer, the activation of STAT3 will change the spatial position of STAT3 protein and cause different phenotypic changes of breast cancer cells. In the current basic research and clinical research, small molecule inhibitors activated by targeting STAT3 can effectively treat breast cancer, and enhance the efficacy level of related treatment methods for luminal-type and HER2-positive breast cancers.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"356"},"PeriodicalIF":5.3,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Th17 cell function in cancers: immunosuppressive agents or anti-tumor allies?","authors":"Milad Taghizadeh Anvar, Kimiya Rashidan, Nima Arsam, Ashkan Rasouli-Saravani, Hamidreza Yadegari, Ali Ahmadi, Zeynab Asgari, Ahmad Ghorbani Vanan, Farid Ghorbaninezhad, Safa Tahmasebi","doi":"10.1186/s12935-024-03525-9","DOIUrl":"10.1186/s12935-024-03525-9","url":null,"abstract":"<p><p>T helper (Th) 17 cells, a distinct subset of Th lymphocytes, are known for their prominent interleukin (IL)-17 production and other pro-inflammatory cytokines. These cells exhibit remarkable plasticity, allowing them to exhibit different phenotypes in the cancer microenvironment. This adaptability enables Th17 cells to promote tumor progression by immunosuppressive activities and angiogenesis, but also mediate anti-tumor immune responses through employing immune cells in tumor setting or even by directly converting toward Th1 phenotype and producing interferon-gamma (IFN-γ). This dual role of Th17 cells in cancer makes it a double-edged sword in encountering cancer. In this review, we aim to elucidate the complexities of Th17 cell function in cancer by summarizing recent studies and, ultimately, to design novel therapeutic strategies, especially targeting Th17 cells in the tumor milieu, which could pave the way for more effective cancer treatments.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"355"},"PeriodicalIF":5.3,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acid affairs in anti-tumour immunity.","authors":"Federica Cappellesso, Massimiliano Mazzone, Federico Virga","doi":"10.1186/s12935-024-03520-0","DOIUrl":"10.1186/s12935-024-03520-0","url":null,"abstract":"<p><p>Metabolic rewiring of cancer cells is one of the hallmarks of cancer. As a consequence, the metabolic landscape of the tumour microenvironment (TME) differs compared to correspondent healthy tissues. Indeed, due to the accumulation of acid metabolites, such as lactate, the pH of the TME is generally acidic with a pH drop that can be as low as 5.6. Disruptions in the acid-base balance and elevated lactate levels can drive malignant progression not only through cell-intrinsic mechanisms but also by impacting the immune response. Generally, acidity and lactate dampen the anti-tumour response of both innate and adaptive immune cells favouring tumour progression and reducing the response to immunotherapy. In this review, we summarize the current knowledge on the functional, metabolic and epigenetic effects of acidity and lactate on the cells of the immune system. In particular, we focus on the role of monocarboxylate transporters (MCTs) and other solute carrier transporters (SLCs) that, by mediating the exchange of lactate (among other metabolites) and bicarbonate, participate in pH regulation and lactate transport in the cancer context. Finally, we discuss advanced approaches to target pH or lactate in the TME to enhance the anti-tumour immune response.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"354"},"PeriodicalIF":5.3,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The recent advancements of ferroptosis of gynecological cancer.","authors":"Shenglan Tang, Li Chen","doi":"10.1186/s12935-024-03537-5","DOIUrl":"10.1186/s12935-024-03537-5","url":null,"abstract":"<p><p>Ovarian, endometrial, and cervical cancer are the most common types of gynecologic tumor in women. Surgery, combined with radiotherapy and chemotherapy, is commonly used to treat these tumors. Unfortunately, difficulties in early diagnosis and acquired drug resistance have resulted in poor outcomes for most patients. Ferroptosis is a form of regulated cell death that depends on iron and is characterized by iron accumulation, reactive oxygen species production, and lipid peroxidation. The strong association between ferroptosis and many diseases, especially tumor diseases, has been confirmed by numerous studies. Many studies have demonstrated that ferroptosis is involved in initiating, progressing and metastasizing gynecologic tumors. This review summarizes the pathogenesis of ferroptosis and its association with the development, treatment, and prognosis of gynecologic tumors, and further explore the potential utility of ferroptosis in treating gynecologic tumors.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"351"},"PeriodicalIF":5.3,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The development of the occurrence and metastasis of breast cancer by single-cell sequencing.","authors":"Man Chen, Mengya Feng, Hai Lei, Dan Mo, Shengnan Ren, Dechun Yang","doi":"10.1186/s12935-024-03531-x","DOIUrl":"10.1186/s12935-024-03531-x","url":null,"abstract":"<p><p>Breast cancer is currently the most frequent malignant tumor and the leading cause of cancer death among women globally. Although the five-year survival rate for early breast cancer has risen to more than 90%, medication resistance persists in advanced breast cancer and some intractable breast cancer, resulting in a poor prognosis, a high recurrence rate, and a low survival rate. Single-cell sequencing (SCS) is the study of a single cell's gene structure and expression level differences in order to discover unusual molecular subgroups, disease development, and a variety of mechanisms. This review briefly discusses single-cell sequencing and its application, and lists the research on single-cell sequencing in the development and metastasis of breast cancer, in order to bring fresh ideas for the comprehensive treatment of breast cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"349"},"PeriodicalIF":5.3,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11515250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Celastrol attenuates the invasion and migration and augments the anticancer effects of olaparib in prostate cancer.","authors":"Mengqiu Huang, Lin Chen, Xiaoyan Ma, Houqiang Xu","doi":"10.1186/s12935-024-03542-8","DOIUrl":"10.1186/s12935-024-03542-8","url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer (PCa) is a leading malignancy among men globally, with rising incidence rates emphasizing the critical need for better detection and therapeutic approaches. The roles of HSP90AB1 and PARP1 in prostate cancer cells suggest potential targets for enhancing treatment efficacy.</p><p><strong>Methods: </strong>This study investigated the overexpression of HSP90AB1 and PARP1 in prostate cancer cells and the impact of HSP90AB1 knockdown on the sensitivity of these cells to the PARP inhibitor olaparib. We also explored the combined effect of olaparib and celastrol, an HSP90 inhibitor, on the clonogenic survival, migration, proliferation, and overall viability of prostate cancer cells, alongside the modulation of the PI3K/AKT pathway. An in vivo PC3 xenograft mouse model was used to assess the antitumor effects of the combined treatment.</p><p><strong>Results: </strong>Our findings revealed significant overexpression of HSP90AB1 and PARP1 in prostate cancer cells. Knockdown of HSP90AB1 increased cell sensitivity to olaparib. The combination of olaparib and celastrol significantly reduced prostate cancer cell survival, migration, proliferation, and enhanced cumulative DNA damage. Celastrol also downregulated the PI3K/AKT pathway, increasing cell susceptibility to olaparib. In vivo experiments demonstrated that celastrol and olaparib together exerted strong antitumor effects.</p><p><strong>Conclusions: </strong>The study indicates that targeting both HSP90AB1 and PARP1 presents a promising therapeutic strategy for prostate cancer. The synergistic combination of celastrol and olaparib enhances the efficacy of treatment against prostate cancer, offering a potent approach to combat this disease.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"352"},"PeriodicalIF":5.3,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of a prognostic model based on three TLS-Related genes in oral squamous cell carcinoma.","authors":"Bincan Sun, Chengwen Gan, Yan Tang, Qian Xu, Kai Wang, Feiya Zhu","doi":"10.1186/s12935-024-03543-7","DOIUrl":"10.1186/s12935-024-03543-7","url":null,"abstract":"<p><strong>Background: </strong>The tertiary lymphoid structures (TLSs) have an immunomodulatory function and have a positive impact on the survival outcomes of patients with oral squamous cell carcinoma (OSCC). However, there is a lack of standard approaches for quantifying TLSs and prognostic models using TLS-related genes (TLSRGs). These limitations limit the widespread use of TLSs in clinical practice.</p><p><strong>Methods: </strong>A convolutional neural network was used to automatically detect and quantify TLSs in HE-stained whole slide images. By employing bioinformatics and diverse statistical methods, this research created a prognostic model using TCGA cohorts and explored the connection between this model and immune infiltration. The expression levels of three TLSRGs in clinical specimens were detected by immunohistochemistry. To facilitate the assessment of individual prognostic outcomes, we further constructed a nomogram based on the risk score and other clinical factors.</p><p><strong>Results: </strong>TLSs were found to be an independent predictor of both overall survival (OS) and disease-free survival in OSCC patients. A larger proportion of the TLS area represented a better prognosis. After analysis, we identified 69 differentially expressed TLSRGs and selected three pivotal TLSRGs to construct the risk score model. This model emerged as a standalone predictor for OS and exhibited close associations with CD4 + T cells, CD8 + T cells, and macrophages. Immunohistochemistry revealed high expression levels of CCR7 and CXCR5 in TLS + OSCC samples, while CD86 was highly expressed in TLS- OSCC samples. The nomogram demonstrates excellent predictive ability for overall survival in OSCC patients.</p><p><strong>Conclusions: </strong>This is the first prognostic nomogram based on TLSRGs, that can effectively predict survival outcomes and contribute to individual treatment strategies for OSCC patients.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"350"},"PeriodicalIF":5.3,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11515094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting sphingosine 1-phosphate and sphingosine kinases in pancreatic cancer: mechanisms and therapeutic potential.","authors":"Khem Raj Limbu, Rashmi Bhandari Chhetri, Subin Kim, Jitendra Shrestha, Yoon Sin Oh, Dong Jae Baek, Eun-Young Park","doi":"10.1186/s12935-024-03535-7","DOIUrl":"10.1186/s12935-024-03535-7","url":null,"abstract":"<p><p>Pancreatic cancer is known to be the most lethal cancer. Fewer new treatments are being developed for pancreatic cancer as compared to other cancers. The bioactive lipid S1P, which is mainly regulated by sphingosine kinase 1 (SK1) and sphingosine kinase 2 (SK2) enzymes, plays significant roles in pancreatic cancer initiation and exacerbation. S1P controls many signaling pathways to modulate the progression of pancreatic cancer through the G-coupled receptor S1PR1-5. Several papers reporting amelioration of pancreatic cancer via modulation of S1P levels or downstream signaling pathways have previously been published. In this paper, for the first time, we have reviewed the results of previous studies to understand how S1P and its receptors contribute to the development of pancreatic cancer, and whether S1P can be a therapeutic target. In addition, we have also reviewed papers dealing with the effects of SK1 and SK2, which are kinases that regulate the level of S1P, on the pathogenesis of pancreatic cancer. We have also listed available drugs that particularly focus on S1P, S1PRs, SK1, and SK2 for the treatment of pancreatic cancer. Through this review, we would like to suggest that the SK/S1P/S1PR signaling system can be an important target for treating pancreatic cancer, where a new treatment target is desperately warranted.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"353"},"PeriodicalIF":5.3,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review of current developments in RNA modifications in lung cancer.","authors":"Shujun Zhang, Yafeng Liu, Kaijie Liu, Xinjun Hu, Xinyu Gu","doi":"10.1186/s12935-024-03528-6","DOIUrl":"10.1186/s12935-024-03528-6","url":null,"abstract":"<p><p>Lung cancer has the highest incidence and mortality rates worldwide and is the primary cause of cancer-related death. Despite the rapid development of diagnostic methods and targeted drugs in recent years, many lung cancer patients do not benefit from effective therapies. The emergence of drug resistance has led to a reduction in the therapeutic effectiveness of targeted drugs, highlighting a crucial need to explore novel therapeutic targets. Many studies have found that epigenetic plays an important role in the occurrence of lung cancer. This review describes the biological function of epigenetic RNA modifications, such as m6A, m5C, m7G, and m1A, and recent advancements in their role in the development, progression, and prognosis of lung cancer. This review aims to provide new guidance for the treatment of lung cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"347"},"PeriodicalIF":5.3,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11515118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erianin inhibits the progression of pancreatic cancer by directly targeting AKT and ASK1.","authors":"Ruxue Liu, Minghan Qiu, Xinxin Deng, Meng Zhang, Zhanhua Gao, Yayun Wang, Hanwei Mei, Mengting Zhai, Qiaonan Zhang, Jie Hao, Zhen Yang, Huaqing Wang","doi":"10.1186/s12935-024-03533-9","DOIUrl":"10.1186/s12935-024-03533-9","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic cancer is a malignant tumor of the digestive tract with a high mortality rate. Erianin has antitumor activity, but the regulatory targets and mechanism of action in pancreatic cancer are unclear. The objective of this study was to evaluate the anti-pancreatic cancer activity of Erianin and explore its underlying mechanisms.</p><p><strong>Methods: </strong>A network pharmacology approach was used to investigate the mechanism of action of Erianin in pancreatic cancer cells. Cell proliferation was analyzed using CCK8, colony-formation, and EdU proliferation assays. Cell migration was evaluated through wound healing and transwell assays, as well as determination of the protein expression levels of EMT markers and β-catenin. Apoptosis and the cell cycle were measured using flow cytometry and JC-1 staining, respectively. The protein expression levels of p-Rb, CyclinB1, P21, Cleaved-PARP, and Cleaved-Caspase3 were assessed using western blotting. RNA sequencing (RNA-seq) and bioinformatics analyses were performed to elucidate the mechanism underlying the action of Erianin in pancreatic cancer. Western blotting was used to examine the expression levels of key proteins in the AKT, JNK, and p38 MAPK signaling pathways. Molecular docking and CETSA were used to test hypotheses. The tumor-suppressive ability of Erianin in vivo was assessed using a tumor-bearing assay in nude mice.</p><p><strong>Results: </strong>Network pharmacology revealed that Erianin inhibited pancreatic cancer through multiple pathways. Erianin significantly inhibited pancreatic cancer cell proliferation and migration while promoting intracellular ROS and inducing apoptosis. Mechanistically, Erianin inhibited pancreatic cancer cell proliferation by regulating the AKT/FOXO1 and ASK1/JNK/p38 MAPK signaling pathways. In vivo experiments showed that Erianin inhibited subcutaneous tumor growth and promoted tumor tissue apoptosis in nude mice.</p><p><strong>Conclusions: </strong>The component-target-pathway network revealed that Erianin exerted anti-cancer effects through multiple components, targets, and pathways. Erianin inhibited the proliferation and migration of pancreatic cancer cells and induced apoptosis through the AKT/FOXO1 and ASK1/JNK/p38 MAPK signaling pathways. These results indicate that Erianin is a promising agent for pancreatic cancer treatment.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"348"},"PeriodicalIF":5.3,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11515188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}