Cancer Biology & Therapy最新文献_第5页

The prognostic marker KRT81 is involved in suppressing CD8 + T cells and predicts immunotherapy response for triple-negative breast cancer. 预后标志物 KRT81 参与抑制 CD8 + T 细胞，并预测三阴性乳腺癌的免疫疗法反应。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-05-22 DOI: 10.1080/15384047.2024.2355705

Zhideng Yan, Zhihui Zhong, Chuanke Shi, Muyin Feng, Xiaoqiang Feng, Tong Liu

{"title":"The prognostic marker KRT81 is involved in suppressing CD8 + T cells and predicts immunotherapy response for triple-negative breast cancer.","authors":"Zhideng Yan, Zhihui Zhong, Chuanke Shi, Muyin Feng, Xiaoqiang Feng, Tong Liu","doi":"10.1080/15384047.2024.2355705","DOIUrl":"10.1080/15384047.2024.2355705","url":null,"abstract":"Triple-negative breast Cancer (TNBC) is an aggressive subtype lacking estrogen, progesterone, and HER2 receptors. Known for limited targeted therapies, it poses challenges and requires personalized treatment strategies. Differential analysis revealed a significant decrease in keratin 81 (KRT81) expression in non-TNBC samples and an increase in TNBC samples, lower KRT81 expression correlated with better TNBC patient outcomes. It emerged as an independent predictive factor for TNBC, with associations found between its expression and clinically relevant features. We further developed a nomogram for survival probability assessment based on Cox regression results, demonstrating its accuracy through calibration curves. Gene annotation analysis indicated that KRT81 is involved in immune-related pathways and tumor cell adhesion. KRT81 is associated with immune cell infiltration of Follicular helper T cells (Tfh) and CD8 + T cells, suggesting its potential impact on the immunological microenvironment. The study delved into KRT81's predictive value for immunotherapy responses, high expression of KRT81 was associated with greater potential for immune evasion. Single-cell RNA sequencing analysis pinpointed KRT81 expression within a specific malignant subtype which was a risk factor for TNBC. Furthermore, KRT81 promoted TNBC cell proliferation, migration, invasion, and adhesion was confirmed by gene knockout or overexpression assay. Co-culture experiments further indicated KRT81's potential role in inhibiting CD8 + T cells, and correlation analysis implied KRT81 was highly correlated with immune checkpoint CD276, providing insights into its involvement in the immune microenvironment via CD276. In conclusion, this comprehensive study positions KRT81 as a promising prognostic marker for predicting tumor progression and immunotherapy responses in TNBC.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11123506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141080856","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 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-05-05 DOI: 10.1080/15384047.2024.2350871

引用次数: 0

Natural killer cell memory: challenges and opportunities for cancer immunotherapy. 自然杀伤细胞记忆：癌症免疫疗法的挑战与机遇。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-07-10 DOI: 10.1080/15384047.2024.2376410

Yuhua Qu, Anhui Zeng, Yulu Cheng, Shengchun Li

引用次数: 0

Amino-truncated NOV expression and its correlation with clinicopathologic features, prognosis, metastasis, and chemoresistance in bladder cancer. 氨基截短 NOV 的表达及其与膀胱癌的临床病理特征、预后、转移和化疗耐药性的相关性。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-08-03 DOI: 10.1080/15384047.2024.2386753

Dan Xiong, Yafei Xu, Hongbo Wang, Yunlin Ye

{"title":"Amino-truncated NOV expression and its correlation with clinicopathologic features, prognosis, metastasis, and chemoresistance in bladder cancer.","authors":"Dan Xiong, Yafei Xu, Hongbo Wang, Yunlin Ye","doi":"10.1080/15384047.2024.2386753","DOIUrl":"10.1080/15384047.2024.2386753","url":null,"abstract":"Nephroblastoma, an overexpressed gene (NOV) protein, plays an important role in proliferation, differentiation, angiogenesis, adhesion, invasion and tumorigenesis, but the function of amino-truncated NOV is different. This study is to investigate the role of amino-truncated NOV in the progression of bladder cancer. Using immunohistochemistry and Western blot analysis, we detected the amino-truncated NOV in bladder cancer, and statistical analysis was performed to estimate the association between the expression of amino-truncated NOV and the patient's prognosis by SPSS 19.0. With transduction of amino-truncated NOV, we evaluated alteration for proliferation, migration, invasion and chemoresistance in bladder cancer cells, as well as some proteins related to Wnt/β-catenin pathway and epithelial-mesenchymal transition. The truncated variant of the NOV protein was located in a nucleus other than the cytoplasm and highly expressed in bladder cancer, which was also linked to higher pathological grade and positive lymph node metastasis as well as recurrence. The exact sequence of this truncated protein was confirmed, and it was a 26-kDa splicing. The truncated NOV protein found in bladder cancer was cut at the 187th amino acid of the full-length protein. It was also involved in bladder cancer progression and chemoresistance through a mechanism involving epithelial-mesenchymal transition (EMT) and the Wnt/β-catenin signaling pathway. Our findings provide experimental evidence that the nuclear NOV protein expression is a potential biomarker in the prognostic evaluation of bladder cancer and enhanced amino-truncated NOV expression is potentially important for bladder cancer cell invasion, metastasis and chemoresistance during progression.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11299625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888507","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

The relationship between long non-coding gene CASC21 polymorphisms and cervical cancer. 长非编码基因 CASC21 多态性与宫颈癌的关系

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-03-11 DOI: 10.1080/15384047.2024.2322207

Lili Han, Jing Liu, Mireayi Shataer, Chengyong Wu, Mayinuer Niyazi

{"title":"The relationship between long non-coding gene CASC21 polymorphisms and cervical cancer.","authors":"Lili Han, Jing Liu, Mireayi Shataer, Chengyong Wu, Mayinuer Niyazi","doi":"10.1080/15384047.2024.2322207","DOIUrl":"10.1080/15384047.2024.2322207","url":null,"abstract":"Background: CASC21 was reported to be a hotspot gene in cervical cancer. The relationship between CASC21 genetic polymorphisms and cervical cancer has not been reported. Genetic factors influence the occurrence of cervical cancer. Thus, we explored the correlation between CASC21 polymorphisms and cervical cancer.Methods: A total of 973 participants within 494 cervical cancer cases and 479 healthy controls were recruited. Five single nucleotide polymorphisms (SNPs) in the CASC21 gene were genotyped using the Agena MassARRAY platform. Chi-squared test, logistic regression analysis, odds ratio (OR), multifactor dimensionality reduction (MDR), and 95% confidence interval (95%CI) were used for data analysis.Results: In the overall analysis, rs16902094 (p = .014, OR = 1.86, 95% CI = 1.12-3.08) and rs16902104 (p = .014, OR = 1.86, 95% CI = 1.12-3.09) had the risk-increasing correlation with the occurrence of cervical cancer. Stratification analysis showed that rs16902094 and rs16902104 were still associated with cervical cancer risk in the subgroups with age > 51, BMI < 24 kg/m2, smokers, and patients with cervical squamous cell carcinoma. MDR analysis displayed that rs16902094 (.49%) and rs16902104 (.52%) were the main influential attribution factor for cervical cancer risk.Conclusion: Our finding firstly determined that two CASC21 SNPs (rs16902094, rs16902104) were associated with an increased risk of cervical cancer, which adds to our knowledge regarding the effect of CASC21 on cervical carcinogenesis.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140093448","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

Influence of genetic polymorphisms in vascular endothelial-related genes on the clinical outcome of axitinib in patients with metastatic renal cell carcinoma. 血管内皮相关基因的遗传多态性对转移性肾细胞癌患者服用阿西替尼的临床疗效的影响

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-07 DOI: 10.1080/15384047.2024.2312602

Kazuyuki Numakura, Ryoma Igarashi, Makoto Takahashi, Taketoshi Nara, Sohei Kanda, Mitsuru Saito, Shintaro Narita, Takamitsu Inoue, Takenori Niioka, Masatomo Miura, Tomonori Habuchi

{"title":"Influence of genetic polymorphisms in vascular endothelial-related genes on the clinical outcome of axitinib in patients with metastatic renal cell carcinoma.","authors":"Kazuyuki Numakura, Ryoma Igarashi, Makoto Takahashi, Taketoshi Nara, Sohei Kanda, Mitsuru Saito, Shintaro Narita, Takamitsu Inoue, Takenori Niioka, Masatomo Miura, Tomonori Habuchi","doi":"10.1080/15384047.2024.2312602","DOIUrl":"10.1080/15384047.2024.2312602","url":null,"abstract":"Objective: Axitinib is an oral multi-target tyrosine kinase inhibitor used for the treatment of renal cell carcinoma (RCC). Because of the severe adverse events (AEs) associated with axitinib, patients often need dose reductions or discontinue its use, highlighting the need for effective biomarkers to assess efficacy and/or AEs. The aim of this study was to investigate the relationship between single nucleotide polymorphisms (SNPs) in genes involved in the pharmacodynamic action of axitinib and clinical prognosis and AEs in metastatic RCC (mRCC) patients.Methods: This study included 80 mRCC patients treated with first-, second-, or third-line axitinib (5 mg orally twice daily). Clinical parameters and genetic polymorphisms were examined in 75 cases (53 males and 22 females). We assessed three SNPs in each of three candidate genes namely, angiotensin-converting enzyme (ACE), nitric oxide synthase 3 (NOS3), and angiotensin II receptor type 1 (AT1R), all of which are involved in axitinib effects on vascular endothelial function.Results: Axitinib-treated patients carrying the ACE deletion allele suffered more frequently from hand-foot syndrome and a deterioration in kidney function (p = .045 and p = 0.005, respectively) whereas those carrying the NOS3 G allele suffered more frequently from proteinuria and multiple AEs (p = .025 and p = 0.036, respectively).Conclusions: Our study found that the ACE deletion allele and the NOS3 G allele are associated with increased AEs.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10857686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139701965","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

Role of transforming growth factor-β1 pathway in angiogenesis induced by chronic stress in colorectal cancer. 转化生长因子-β1通路在慢性应激诱导结直肠癌血管生成中的作用

IF 3.6 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-06-10 DOI: 10.1080/15384047.2024.2366451

Jie Zhang, Yao-Tiao Deng, Jie Liu, Lu Gan, Yu Jiang

{"title":"Role of transforming growth factor-β1 pathway in angiogenesis induced by chronic stress in colorectal cancer.","authors":"Jie Zhang, Yao-Tiao Deng, Jie Liu, Lu Gan, Yu Jiang","doi":"10.1080/15384047.2024.2366451","DOIUrl":"10.1080/15384047.2024.2366451","url":null,"abstract":"Background: Chronic stress can induce stress-related hormones; norepinephrine (NE) is considered to have the highest potential in cancer. NE can stimulate the expression of hypoxia-inducible factor-1α (HIF-1α), which is associated with vascular endothelial growth factor (VEGF) secretion and tumor angiogenesis. However, the underlying mechanisms are poorly understood.Methods: Tumor-bearing mice were subjected to chronic restraint stress and treated with normal saline, human monoclonal VEGF-A neutralizing antibody bevacizumab, or β-adrenergic receptor (β-AR) antagonist (propranolol). Tumor growth and vessel density were also evaluated. Human colorectal adenocarcinoma cells were treated with NE, propranolol, or the inhibitor of transforming growth factor-β (TGF-β) receptor Type I kinase (Ly2157299) in vitro. TGF-β1 in mouse serum and cell culture supernatants was quantified using ELISA. The expression of HIF-1α was measured using Real time-PCR and western blotting. Cell migration and invasion were tested.Results: Chronic restraint stress attenuated the efficacy of bevacizumab and promoted tumor growth and angiogenesis in a colorectal tumor model. Propranolol blocked this effect and inhibited TGF-β1 elevation caused by chronic restraint stress or NE. NE upregulated HIF-1α expression, which was reversed by propranolol or Ly2157299. Propranolol and Ly2157199 blocked NE-stimulated cancer cell migration and invasion.Conclusions: Our results demonstrate the effect of NE on tumor angiogenesis and the critical role of TGF-β1 signaling during this process. In addition, β-AR/TGF-β1 signaling/HIF-1α/VEGF is a potential signaling pathway. This study also indicates that psychosocial stress might be a risk factor which weakens the efficacy of anti-angiogenic therapy.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11168221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141295595","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

DLAT promotes triple-negative breast cancer progression via YAP1 activation. DLAT 通过激活 YAP1 促进三阴性乳腺癌的进展。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-10-26 DOI: 10.1080/15384047.2024.2421578

Diya Liu, Xuehui Wang, Fengyuan Qian, Danrong Ye, Xiaochong Deng, Lin Fang

{"title":"DLAT promotes triple-negative breast cancer progression via YAP1 activation.","authors":"Diya Liu, Xuehui Wang, Fengyuan Qian, Danrong Ye, Xiaochong Deng, Lin Fang","doi":"10.1080/15384047.2024.2421578","DOIUrl":"10.1080/15384047.2024.2421578","url":null,"abstract":"Background: Breast cancer (BC) is the most prevalent malignant tumor in women globally. Triple-negative breast cancer (TNBC) represents the most malignant and invasive subtype of BC. New therapeutic targets are urgently needed for TNBC owing to its receptor expression characteristics, which render it insensitive to traditional targeted and endocrine therapies for BC. The role and mechanisms of dihydrolipoamide S-acetyltransferase (DLAT) as a crucial molecule in glycometabolism and cuproptosis-related biological processes in tumors remain to be explored.Methods: DLAT expression was investigated using bioinformatics methods and quantitative real-time polymerase chain reaction. Subsequently, the MTT assay, colony formation assay, and migration-invasion assay were performed to validate the effect of DLAT on TNBC cell viability, proliferation, and migration. Cytoplasmic-nuclear separation experiments, western blot analysis, and co-immunoprecipitation assays were performed to elucidate the underlying molecular mechanisms.Results: This study revealed a robust correlation between elevated DLAT expression in BC and unfavorable prognosis in patients, with higher expression of DLAT compared to other subtypes in TNBC. Functional cytology experiments indicated that DLAT plays a tumor-promoting role in TNBC. Mechanistic studies showed that DLAT directly interacts with YAP1, leading to the dephosphorylation and activation of YAP1 and its increased nuclear translocation, thereby transcriptionally activating and regulating downstream oncogenes, promoting the malignant phenotype of TNBC. Rescue experiments indicated that DLAT promotes the malignant behavior of TNBC through a YAP1-dependent pathway.Conclusions: Our research unveiled the significant involvement of DLAT in TNBC, along with the potential for modulating DLAT/YAP1 activity as a targeted treatment strategy for TNBC.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495690","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

Extracellular vesicle-packaged miR-4253 secreted by cancer-associated fibroblasts facilitates cell proliferation in gastric cancer by inducing macrophage M2 polarization. 癌相关成纤维细胞分泌的胞外囊泡包装 miR-4253 通过诱导巨噬细胞 M2 极化促进胃癌细胞增殖

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-11-06 DOI: 10.1080/15384047.2024.2424490

Xinxing Duan, Xiong Yu, Jin Gan

{"title":"Extracellular vesicle-packaged miR-4253 secreted by cancer-associated fibroblasts facilitates cell proliferation in gastric cancer by inducing macrophage M2 polarization.","authors":"Xinxing Duan, Xiong Yu, Jin Gan","doi":"10.1080/15384047.2024.2424490","DOIUrl":"10.1080/15384047.2024.2424490","url":null,"abstract":"Cancer-associated fibroblasts (CAFs) can interact with macrophages in the tumor microenvironment by secreting extracellular vesicles (EVs), thereby affecting tumor progression. However, the mechanisms of CAF-secreted EVs in gastric cancer (GC) remain not well understood. Here, we investigated the effect of CAF-EVs on macrophage polarization in GC and the underlying mechanisms. Macrophage polarization was evaluated using flow cytometry and quantitative real-time polymerase chain reaction. GC cell proliferation was determined using cell counting kit-8, EdU, and colony formation assays. The molecular mechanism was explored using microarray analysis, dual-luciferase reporter assay, and RNA pull-down analysis. The results showed that CAFs secreted EVs that inhibit macrophage M1 polarization and promote M2 polarization. Moreover, miR-4253 expression was increased in CAF-EVs, and inhibition of miR-4253 reversed the macrophage polarization induced by EVs. IL6R was identified as the target of miR-4253. Additionally, macrophages treated with EVs that encapsulated miR-4253 promote GC cell proliferation. In conclusion, CAF-secreted EVs packaging miR-4253 facilitate macrophage polarization from M1 to M2 phenotype by targeting IL6R, thereby accelerating GC cell proliferation. The findings suggest that EV-encapsulated miR-4253 may be a promising therapeutic target of GC.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11542604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589521","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

Immunotherapy resistance in solid tumors: mechanisms and potential solutions. 实体瘤的免疫疗法抗药性：机制与潜在解决方案。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-02-22 DOI: 10.1080/15384047.2024.2315655

Daniel S Lefler, Steven A Manobianco, Babar Bashir

引用次数: 0