Cancer Biology & Therapy最新文献_第3页

Correction. 更正。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-08-19 DOI: 10.1080/15384047.2024.2392996

引用次数: 0

Tumor microenvironment in primary central nervous system lymphoma (PCNSL). 原发性中枢神经系统淋巴瘤（PCNSL）的肿瘤微环境。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-11-18 DOI: 10.1080/15384047.2024.2425131

Qiqi Jin, Haoyun Jiang, Ye Han, Litian Zhang, Cuicui Li, Yurong Zhang, Ye Chai, Pengyun Zeng, Lingling Yue, Chongyang Wu

{"title":"Tumor microenvironment in primary central nervous system lymphoma (PCNSL).","authors":"Qiqi Jin, Haoyun Jiang, Ye Han, Litian Zhang, Cuicui Li, Yurong Zhang, Ye Chai, Pengyun Zeng, Lingling Yue, Chongyang Wu","doi":"10.1080/15384047.2024.2425131","DOIUrl":"10.1080/15384047.2024.2425131","url":null,"abstract":"Primary central nervous system lymphoma (PCNSL) is one of the rare lymphomas limited to the central nervous system. With the availability of immunotherapy, the tumor microenvironment (TME) attracts much attention nowadays. However, the systematic studies on the TME of PCNSL are lacking. By reviewing the existing research, we found that the TME of PCNSL is infiltrated with abundant TAMs and TILs, among which cytotoxic T cells (CTLs) and M2-polarized macrophages are principal. However, the counts of immune cells infiltrated in the TME of PCNSL are significantly lower than systemic diffuse large B-cell lymphoma (DLBCL). In addition, PCNSL can attract the infiltration of immunosuppressive cells and the loss of HLA I/II expression, overexpress inhibitory immune checkpoints, and release immunosuppressive cytokines to form an immunosuppressive TME. The immunosuppressive effect of TME in PCNSL is significantly stronger than that in systemic DLBCL. These characteristics of TME highlight the immunosuppression of PCNSL.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2425131"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11581175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeting autophagy promotes the antitumor effect of radiotherapy on cervical cancer cells. 靶向自噬促进放疗对宫颈癌细胞的抗肿瘤作用。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-12-05 DOI: 10.1080/15384047.2024.2431136

Fanjie Meng, Ying Yan, Li Zhou, Song Zhao, Lingyan Sun, Huiying Yu

引用次数: 0

The polymeric fluoropyrimidine CF10 overcomes limitations of 5-FU in pancreatic ductal adenocarcinoma cells through increased replication stress. 聚合氟嘧啶 CF10 通过增加复制应激克服了 5-FU 在胰腺导管腺癌细胞中的局限性。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-11-08 DOI: 10.1080/15384047.2024.2421584

Jennifer M Finan, Roberto Di Niro, Soon Young Park, Kang Jin Jeong, Madeline D Hedberg, Alexander Smith, Grace A McCarthy, Alex O Haber, John Muschler, Rosalie C Sears, Gordon B Mills, William H Gmeiner, Jonathan R Brody

{"title":"The polymeric fluoropyrimidine CF10 overcomes limitations of 5-FU in pancreatic ductal adenocarcinoma cells through increased replication stress.","authors":"Jennifer M Finan, Roberto Di Niro, Soon Young Park, Kang Jin Jeong, Madeline D Hedberg, Alexander Smith, Grace A McCarthy, Alex O Haber, John Muschler, Rosalie C Sears, Gordon B Mills, William H Gmeiner, Jonathan R Brody","doi":"10.1080/15384047.2024.2421584","DOIUrl":"10.1080/15384047.2024.2421584","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease soon to become the second leading cause of cancer deaths in the US. Beside surgery, current therapies have narrow clinical benefits with systemic toxicities. FOLFIRINOX is the current standard of care, one component of which is 5- Fluorouracil (5-FU), which causes serious gastrointestinal and hematopoietic toxicities and is vulnerable to resistance mechanisms. Recently, we have developed polymeric fluoropyrimidines (F10, CF10) which unlike 5-FU, are, in principle, completely converted to the thymidylate synthase inhibitory metabolite FdUMP, without generating appreciable levels of ribonucleotides that cause systemic toxicities while displaying much stronger anti-cancer activity. Here, we confirm the potency of CF10 and investigate enhancement of its efficacy through combination with inhibitors in vitro targeting replication stress, a hallmark of PDAC cells. CF10 is 308-times more potent as a single agent than 5-FU and was effective in the nM range in primary patient derived models. Further, we find that activity of CF10, but not 5-FU, is enhanced through combination with inhibitors of ATR and Wee1 that regulate the S and G2 DNA damage checkpoints and can be reversed by addition of dNTPs indicative of CF10 acting, at least in part, through inducing replication stress. Our results indicate CF10 has the potential to supersede the established benefit of 5-FU in PDAC treatment and indicate novel combination approaches that should be validated in vivo and may be beneficial in established regimens that include 5-FU.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2421584"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11552260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction. 更正。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-05-15 DOI: 10.1080/15384047.2024.2352926

引用次数: 0

The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer. Cdk抑制剂dinaciclib作为一种有前途的抗胆道肿瘤药物。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-12-12 DOI: 10.1080/15384047.2024.2439057

Celina Ablinger, Daniel Neureiter, Theresa Mähr, Christian Mayr, Tobias Kiesslich, Nicole Maeding, Irina Valenta, Maximilian Ardelt, Fabian Wilhelm, Elen Neureiter, Markus Ritter, Johanna Pachmayr, Petra Huber-Cantonati

{"title":"The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer.","authors":"Celina Ablinger, Daniel Neureiter, Theresa Mähr, Christian Mayr, Tobias Kiesslich, Nicole Maeding, Irina Valenta, Maximilian Ardelt, Fabian Wilhelm, Elen Neureiter, Markus Ritter, Johanna Pachmayr, Petra Huber-Cantonati","doi":"10.1080/15384047.2024.2439057","DOIUrl":"10.1080/15384047.2024.2439057","url":null,"abstract":"Biliary tract cancer (BTC) is a rare malignancy with rising incidence. The therapeutic options are limited and the overall survival remains poor. Cyclin-dependent kinases, drivers of cell cycle and transcription have numerous biological functions and are known to be dysregulated in numerous tumor entities. Dinaciclib is a selective Cdk1/2/5/9 inhibitor with anti-tumor activity. In the present study, the efficacy of dinaciclib was tested on a comprehensive BTC cell-line model. The results indicate a heterogeneous expression pattern of Cdk1/2/5/9, as well as various differentiation tumor markers in BTC cells. We demonstrated that dinaciclib reduces cell viability, ATP levels, and proliferation rates. Moreover, dinaciclib induces apoptosis via increased caspase 3/7 activity and reduced expression levels of the anti-apoptotic protein Mcl-1 in a concentration- and cell line -dependent manner. 3D cell culture confirms the cytotoxic impact of dinaciclib under more physiologic tumor conditions. Additionally, dinaciclib affects different cell growth regulators like EGFR and STAT3 on gene and protein level, thus decreasing tumor growth. In summary, our study indicates that dinaciclib acts as a promising anti-tumorigenic agent in 2D and 3D in vitro BTC models and thus encourages further investigation.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2439057"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11789727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-10b-5p promotes tumor growth by regulating cell metabolism in liver cancer via targeting SLC38A2. miR-10b-5p 通过靶向 SLC38A2 调节肝癌细胞代谢促进肿瘤生长

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-23 DOI: 10.1080/15384047.2024.2315651

Mingzhi Xia, Jie Chen, Yingyun Hu, Bin Qu, Qianqian Bu, Haoming Shen

{"title":"miR-10b-5p promotes tumor growth by regulating cell metabolism in liver cancer via targeting SLC38A2.","authors":"Mingzhi Xia, Jie Chen, Yingyun Hu, Bin Qu, Qianqian Bu, Haoming Shen","doi":"10.1080/15384047.2024.2315651","DOIUrl":"10.1080/15384047.2024.2315651","url":null,"abstract":"Metabolic reprogramming plays a critical role in hepatocarcinogenesis. However, the mechanisms regulating metabolic reprogramming in primary liver cancer (PLC) are unknown. Differentially expressed miRNAs between PLC and normal tissues were identified using bioinformatic analysis. RT-qPCR was used to determine miR-10b-5p and SCL38A2 expression levels. IHC, WB, and TUNEL assays were used to assess the proliferation and apoptosis of the tissues. The proliferation, migration, invasion, and apoptosis of PLC cells were determined using the CCK-8 assay, Transwell assay, and flow cytometry. The interaction between miR-10b-5p and SLC38A2 was determined using dual-luciferase reporter assay. A PLC xenograft model in BALB/c nude mice was established, and tumorigenicity and SLC38A2 expression were estimated. Finally, liquid chromatography - mass spectrometry (LC-MS) untargeted metabolomics was used to analyze the metabolic profiles of xenograft PLC tissues in nude mice. miR-10b-5p was a key molecule in the regulation of PLC. Compared with para-carcinoma tissues, miR-10b-5p expression was increased in tumor tissues. miR-10b-5p facilitated proliferation, migration, and invasion of PLC cells. Mechanistically, miR-10b-5p targeted SLC38A2 to promote PLC tumor growth. Additionally, miR-10b-5p altered the metabolic features of PLC in vivo. Overexpression of miR-10b-5p resulted in remarkably higher amounts of lumichrome, folic acid, octanoylcarnitine, and Beta-Nicotinamide adenine dinucleotide, but lower levels of 2-methylpropanal, glycyl-leucine, and 2-hydroxycaproic acid. miR-10b-5p facilitates the metabolic reprogramming of PLC by targeting SLC38A2, which ultimately boosts the proliferation, migration, and invasion of PLC cells. Therefore, miR-10b-5p and SLC38A2 are potential targets for PLC diagnosis and treatment.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2315651"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10896153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MiR-378a-5p exerts a radiosensitizing effect on CRC through LRP8/β-catenin axis. MiR-378a-5p通过LRP8/β-catenin轴对CRC产生放射增敏作用。

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-22 DOI: 10.1080/15384047.2024.2308165

Guolin Hu, Pengbiao Che, Ling Deng, Lei Liu, Jia Liao, Qi Liu

{"title":"MiR-378a-5p exerts a radiosensitizing effect on CRC through LRP8/β-catenin axis.","authors":"Guolin Hu, Pengbiao Che, Ling Deng, Lei Liu, Jia Liao, Qi Liu","doi":"10.1080/15384047.2024.2308165","DOIUrl":"10.1080/15384047.2024.2308165","url":null,"abstract":"Background: MiRNAs are closely related to tumor radiosensitivity. MiR-378a-5p level is down-regulated in colorectal cancer (CRC). Therefore, this study intends to explore the role of miR-378a-5p in CRC, especially radiosensitivity.Methods: The expression of miR-378a-5p was analyzed in CRC samples. CRC cell lines were treated with different doses of X-rays. Bioinformatics analysis, dual-luciferase reporter assay and RT-qPCR were used to detect the expressions and binding relationship of miR-378a-5p and low-density lipoprotein receptor-related protein 8 (LRP8). MiR-378a-5p inhibitor or/and siLRP8 were transfected into CRC cells with or without irradiation. Subsequently, clonogenic assay, flow cytometry and in vivo experiments including tumorigenesis assay, immunohistochemistry, RT-qPCR and Western blot were performed to clarify the role of miR-378a-5p/LRP8 axis in the radiosensitivity of CRC.Results: The down-regulated expression of miR-378a-5p in CRC is related to histological differentiation and tumor-node-metastasis (TNM) stage. After irradiation, the survival fraction of CRC cells was decreased, while the apoptotic rate and the level of miR-378a-5p were increased. Restrained miR-378a-5p repressed apoptosis and apoptosis-related protein expressions, yet promoted the proliferation and the radioresistance of cells by regulating β-catenin in CRC cells. LRP8 was highly expressed in CRC, and targeted by miR-378a-5p. SiLRP8 improved radiosensitivity and reversed the effect of miR-378a-5p down-regulation on CRC cells. Overexpressed miR-378a-5p and irradiation enhanced the level of miR-378a-5p, yet suppressed the expressions of Ki67 and LRP8 as well as tumorigenesis.Conclusion: MiR-378a-5p may exert a radiosensitizing effect on CRC through the LRP8/β-catenin axis, which may be a new therapeutic target for CRC radioresistance.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2308165"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10896128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A positive feedback loop of SRSF9/USP22/ZEB1 promotes the progression of ovarian cancer. SRSF9/USP22/ZEB1的正反馈回路促进了卵巢癌的进展。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-11-12 DOI: 10.1080/15384047.2024.2427415

Jing Wang, Ming Hu, Jie Min, Xin Li

{"title":"A positive feedback loop of SRSF9/USP22/ZEB1 promotes the progression of ovarian cancer.","authors":"Jing Wang, Ming Hu, Jie Min, Xin Li","doi":"10.1080/15384047.2024.2427415","DOIUrl":"10.1080/15384047.2024.2427415","url":null,"abstract":"Ovarian cancer (OC) is recognized as the most lethal type of gynecological malignancy, making treatment options challenging. Discovering novel therapeutic targets will benefit OC patients. This study aimed to reveal the mechanism by which SRSF9 regulates OC progression. Cell proliferation was determined via CCK-8 assays, whereas cell migration and invasion were monitored via Transwell assays. Western blotting and qPCR assays were used to detect protein and mRNA alterations. RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were performed to investigate the relationships between SRSF9 and USP22. Co-IP was used to validate the interaction between USP22 and ZEB1. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays were used to verify the regulatory effect of ZEB1 on the transcription of SRSF9. Subcutaneous xenograft models were established to evaluate the impact of SRSF9 on tumor development. Knockdown of SRSF9 significantly suppressed the proliferation, invasion, migration, tumorigenicity, and epithelial‒mesenchymal transition (EMT) of OC cells. SRSF9 can bind to USP22 mRNA, increasing its stability. Moreover, the overexpression of USP22 reversed the impact of SRSF9 silencing on malignant phenotypes. USP22 can mediate the deubiquitination of ZEB1, thereby enhancing the progression of OC. Furthermore, ZEB1 upregulated SRSF9 expression through transcriptional activation, thus establishing a positive feedback loop. SRSF9 enhanced the malignant characteristics of OC through a positive feedback loop of SRSF9/USP22/ZEB1. This functional circuit may help in the development of novel therapeutic approaches for treating OC.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2427415"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11559372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dynamic evolution of bone marrow adipocyte in B cell acute lymphoblastic leukemia: insights from diagnosis to post-chemotherapy. 骨髓脂肪细胞在 B 细胞急性淋巴细胞白血病中的动态演变：从诊断到化疗后的启示。

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-03-11 DOI: 10.1080/15384047.2024.2323765

Xi Jia, Naying Liao, Yunqian Yao, Xutao Guo, Kai Chen, Pengcheng Shi

{"title":"Dynamic evolution of bone marrow adipocyte in B cell acute lymphoblastic leukemia: insights from diagnosis to post-chemotherapy.","authors":"Xi Jia, Naying Liao, Yunqian Yao, Xutao Guo, Kai Chen, Pengcheng Shi","doi":"10.1080/15384047.2024.2323765","DOIUrl":"10.1080/15384047.2024.2323765","url":null,"abstract":"Adipocyte is a unique and versatile component of bone marrow microenvironment (BMM). However, the dynamic evolution of Bone Marrow (BM) adipocytes from the diagnosis of B cell Acute Lymphoblastic Leukemia (B-ALL) to the post-treatment state, and how they affect the progression of leukemia, remains inadequately explicated. Primary patient-derived xenograft models (PDXs) and stromal cell co-culture system are employed in this study. We show that the dynamic evolution of BM adipocytes from initial diagnosis of B-ALL to the post-chemotherapy phase, transitioning from cellular depletion in the initial leukemia niche to a fully restored state upon remission. Increased BM adipocytes retards engraftment of B-ALL cells in PDX models and inhibits cells growth of B-ALL in vitro. Mechanistically, the proliferation arrest of B-ALL cells in the context of adipocytes-enrichment niche, might attribute to the presence of adiponectin secreted by adipocytes themselves and the absence of cytokines secreted by mesenchymal stem cell (MSCs). In summary, our findings offer a novel perspective for further in-depth understanding of the dynamic balance between BMM and B-ALL.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2323765"},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140093445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0