Oncology reports最新文献_第3页

Progress of research on γδ T cells in colorectal cancer (Review). γδT细胞在结直肠癌中的研究进展（综述）。

IF 3.8 3区医学

Oncology reports Pub Date : 2024-12-01 Epub Date: 2024-10-04 DOI: 10.3892/or.2024.8819

Lijuan Pan, Yiru Zhou, Yeye Kuang, Chan Wang, Weimin Wang, Xiaotong Hu, Xiabin Chen

引用次数: 0

GOLPH3 inhibition overcomes cisplatin resistance by restoring the glutathione/reactive oxygen species balance in the A549 non‑small cell lung cancer cell line. 抑制 GOLPH3 可恢复 A549 非小细胞肺癌细胞系的谷胱甘肽/活性氧平衡，从而克服顺铂耐药性。

IF 3.8 3区医学

Oncology reports Pub Date : 2024-12-01 Epub Date: 2024-10-18 DOI: 10.3892/or.2024.8829

Qiongying Wei, Jinquan Lin, Zhuangbin Lin, Nanding Yu, Yingxiao Wu, Xuexue Tan, Dan Xue

{"title":"GOLPH3 inhibition overcomes cisplatin resistance by restoring the glutathione/reactive oxygen species balance in the A549 non‑small cell lung cancer cell line.","authors":"Qiongying Wei, Jinquan Lin, Zhuangbin Lin, Nanding Yu, Yingxiao Wu, Xuexue Tan, Dan Xue","doi":"10.3892/or.2024.8829","DOIUrl":"10.3892/or.2024.8829","url":null,"abstract":"Cisplatin resistance is common in non‑small cell lung cancer (NSCLC); however, the molecular mechanisms remain unclear. The present study aimed to identify a new function of Golgi phosphoprotein 3 (GOLPH3) in NSCLC‑associated cisplatin resistance. Using A549 human NSCLC cells and the cisplatin‑resistant variant, stable cell lines with GOLPH3 knockdown or overexpression were established using lentiviral vectors. Through Cell Counting Kit‑8 and EdU assays, it was revealed that knockdown of GOLPH3 significantly enhanced cisplatin sensitivity in NSCLC cells. Specifically, flow cytometric analysis showed that GOLPH3 knockdown promoted apoptosis and G2‑phase cell cycle arrest in A549 cells. Mechanistically, intracellular reactive oxygen species (ROS) and glutathione (GSH) levels were measured using assay kits, and it was demonstrated that GOLPH3 knockdown decreased intracellular GSH levels, and further attenuated intracellular cisplatin efflux and GSH/ROS imbalance. In addition, tumor‑sphere formation assays verified that GOLPH3 knockdown mitigated the stem cell‑like phenotype of NSCLC cells. In conclusion, the present findings indicated the relevance of GOLPH3 in NSCLC‑associated cisplatin resistance, and thus targeting GOLPH3 may be developed into a combination therapy to overcome cisplatin resistance.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11526445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

[Retracted] hsa‑miR‑212 modulates the radiosensitivity of glioma cells by targeting BRCA1. [撤稿】hsa-miR-212 通过靶向 BRCA1 调节胶质瘤细胞的放射敏感性。

IF 3.8 3区医学

Oncology reports Pub Date : 2024-12-01 Epub Date: 2024-10-04 DOI: 10.3892/or.2024.8818

Xin He, Saijun Fan

引用次数: 0

Oncogenic mechanisms of COL10A1 in cancer and clinical challenges (Review). COL10A1 在癌症中的致癌机制及临床挑战（综述）。

IF 3.8 3区医学

Oncology reports Pub Date : 2024-12-01 Epub Date: 2024-10-11 DOI: 10.3892/or.2024.8821

Qiang Yi, Gangfeng Zhu, Weijian Zhu, Jiaqi Wang, Xinting Ouyang, Kuan Yang, Jinghua Zhong

{"title":"Oncogenic mechanisms of COL10A1 in cancer and clinical challenges (Review).","authors":"Qiang Yi, Gangfeng Zhu, Weijian Zhu, Jiaqi Wang, Xinting Ouyang, Kuan Yang, Jinghua Zhong","doi":"10.3892/or.2024.8821","DOIUrl":"10.3892/or.2024.8821","url":null,"abstract":"Collagen type X α1 chain (COL10A1), a gene encoding the α‑1 chain of type X collagen, serves a key role in conferring tensile strength and structural integrity to tissues. Upregulation of COL10A1 expression has been observed in different malignancies, including lung, gastric and pancreatic cancer, and is associated with poor prognosis. The present review provides an updated synthesis of the evolving biological understanding of COL10A1, with a particular focus on its mechanisms of action and regulatory functions within the context of tumorigenesis. For example, it has been established that increased COL10A1 expression promotes cancer progression by activating multiple signaling pathways, including the TGF‑β1/Smad, MEK/ERK and focal adhesion kinase signaling pathways, thereby inducing proliferation, invasion and migration. Additionally, COL10A1 has been demonstrated to induce epithelial‑mesenchymal transition and reshapes the extracellular matrix within tumor tissues. Furthermore, on the basis of methyltransferase‑like 3‑mediated N6‑methyladenosine methylation, COL10A1 intricately regulates the epitranscriptomic machinery, thereby augmenting its oncogenic role. However, although COL10A1 serves a pivotal role in gene transcription and the orchestration of tumor growth, the question of whether COL10A1 would serve as a viable therapeutic target remains a subject of scientific hypothesis requiring rigorous examination. Variables such as distinct tumor microenvironments and treatment associations necessitate further experimental validation. Therefore, a comprehensive assessment and understanding of the functional and mechanistic roles of COL10A1 in cancer may pave the way for the development of innovative cancer treatment strategies.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11487528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Flavonoids as modulators of metabolic reprogramming in renal cell carcinoma (Review). 类黄酮作为肾细胞癌代谢重编程的调节剂（综述）。

IF 3.8 3区医学

Oncology reports Pub Date : 2024-12-01 Epub Date: 2024-10-18 DOI: 10.3892/or.2024.8826

Asif Shahzad, Wenjing Liu, Yijian Sun, Xiangjie Liu, Jiaojiao Xia, Kun Cui, Buqing Sai, Yuechun Zhu, Zhe Yang, Qiao Zhang

{"title":"Flavonoids as modulators of metabolic reprogramming in renal cell carcinoma (Review).","authors":"Asif Shahzad, Wenjing Liu, Yijian Sun, Xiangjie Liu, Jiaojiao Xia, Kun Cui, Buqing Sai, Yuechun Zhu, Zhe Yang, Qiao Zhang","doi":"10.3892/or.2024.8826","DOIUrl":"10.3892/or.2024.8826","url":null,"abstract":"Renal cell carcinoma (RCC) is distinguished by its varied metabolic reprogramming driven by tumor suppressor gene dysregulation and oncogene activation. Tumors can adapt nutrient uptake and metabolism pathways to meet the altered biosynthetic, bioenergetic and redox demands of cancer cells, whereas conventional chemotherapeutics and molecular inhibitors predominantly target individual metabolic pathways without addressing this adaptability. Flavonoids, which are well‑known for their antioxidant and anti‑inflammatory properties, offer a unique approach by influencing multiple metabolic targets. The present comprehensive review reveals the intricate processes of RCC metabolic reprogramming, encompassing glycolysis, mitochondrial oxidative phosphorylation and fatty acid biosynthesis. The insights derived from the present review may contribute to the understanding of the specific anticancer mechanisms of flavonoids, potentially paving the way for the development of natural antitumor drugs focused on the metabolic reprogramming of RCC.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11526433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Repurposing the antipsychotic drug penfluridol for cancer treatment (Review). 将抗精神病药物五氟利多重新用于癌症治疗（综述）。

IF 4.3 3区医学

Oncology reports Pub Date : 2024-12-01 Epub Date: 2024-11-08 DOI: 10.3892/or.2024.8833

Asma Ali Ibrahim Mze, Amirah Abdul Rahman

{"title":"Repurposing the antipsychotic drug penfluridol for cancer treatment (Review).","authors":"Asma Ali Ibrahim Mze, Amirah Abdul Rahman","doi":"10.3892/or.2024.8833","DOIUrl":"10.3892/or.2024.8833","url":null,"abstract":"Cancer is one of the most prevalent diseases and the leading cause of death worldwide. Despite the improved survival rates of cancer in recent years, the current available treatments often face resistance and side effects. Drug repurposing represents a cost‑effective and efficient alternative to cancer treatment. Recent studies revealed that penfluridol (PF), an antipsychotic drug, is a promising anticancer agent. In the present study, a scoping review was conducted to ascertain the anticancer properties of PF. For this, a literature search was performed using the Scopus, PubMed and Web of Science databases with the search string 'penfluridol' AND 'cancer'. A total of 23 original articles with in vivo and/or in vitro studies on the effect of PF on cancer were included in the scoping review. The outcome of the analysis demonstrated the anticancer potential of PF. PF significantly inhibited cell proliferation, metastasis and invasion while inducing apoptosis and autophagy in vivo and across a spectrum of cancer cell lines, including breast, lung, pancreatic, glioblastoma, gallbladder, bladder, oesophageal, leukaemia and renal cancers. However, research on PF derivatives with high anticancer activities and reduced neurological side effects may be necessary.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

[Corrigendum] BMP‑6 inhibits the metastasis of MDA‑MB‑231 breast cancer cells by regulating MMP‑1 expression. [更正] BMP-6 通过调节 MMP-1 的表达抑制 MDA-MB-231 乳腺癌细胞的转移。

IF 3.8 3区医学

Oncology reports Pub Date : 2024-12-01 Epub Date: 2024-10-11 DOI: 10.3892/or.2024.8822

Fen Hu, Yunfeng Zhang, Mi Li, Lina Zhao, Jing Chen, Shuang Yang, Xiujun Zhang

引用次数: 0

HOXD1 inhibits lung adenocarcinoma progression and is regulated by DNA methylation. HOXD1 可抑制肺腺癌的发展，并受 DNA 甲基化的调控。

IF 3.8 3区医学

Oncology reports Pub Date : 2024-12-01 Epub Date: 2024-10-25 DOI: 10.3892/or.2024.8832

Xin Hu, Sijia Zhang, Xiaoyu Zhang, Hongyan Liu, Yutao Diao, Lianlian Li

{"title":"HOXD1 inhibits lung adenocarcinoma progression and is regulated by DNA methylation.","authors":"Xin Hu, Sijia Zhang, Xiaoyu Zhang, Hongyan Liu, Yutao Diao, Lianlian Li","doi":"10.3892/or.2024.8832","DOIUrl":"10.3892/or.2024.8832","url":null,"abstract":"The homeobox (HOX) gene family encodes a number of highly conserved transcription factors and serves a crucial role in embryonic development and tumorigenesis. Homeobox D1 (HOXD1) is a member of the HOX family, whose biological functions in lung cancer are currently unclear. The University of Alabama at Birmingham Cancer data analysis Portal of HOXD1 expression patterns demonstrated that HOXD1 was downregulated in lung adenocarcinoma (LUAD) patient samples compared with adjacent normal tissue. Western blotting analysis demonstrated low HOXD1 protein expression levels in lung LUAD cell lines. The Kaplan‑Meier plotter database demonstrated that reduced HOXD1 expression levels in LUAD correlated with poorer overall survival. Meanwhile, an in vitro study showed that HOXD1 overexpression suppressed LUAD cell proliferation, migration and invasion. In a mouse tumor model, upregulated HOXD1 was demonstrated to inhibit tumor growth. In addition, targeted bisulfite sequencing and chromatin immunoprecipitation assays demonstrated that DNA hypermethylation occurred in the promoter region of the HOXD1 gene and was associated with the action of DNA methyltransferases. Moreover, upregulated HOXD1 served as a transcriptional factor and increased the transcriptional expression of bone morphogenic protein (BMP)2 and BMP6. Taken together, the dysregulation of HOXD1 mediated by DNA methylation inhibited the initiation and progression of LUAD by regulating the expression of BMP2/BMP6.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11526444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Effect of colony‑stimulating factor in the mechanism of bone metastasis development (Review). 集落刺激因子在骨转移发生机制中的作用（综述）。

IF 3.8 3区医学

Oncology reports Pub Date : 2024-12-01 Epub Date: 2024-10-18 DOI: 10.3892/or.2024.8824

Yukun Han, Yiling Wang, Tongtong Lv, Qing Yang, Dezhou Cheng, Jinxin Li, Wei Wang, Jinbai Huang, Xiaochun Peng

{"title":"Effect of colony‑stimulating factor in the mechanism of bone metastasis development (Review).","authors":"Yukun Han, Yiling Wang, Tongtong Lv, Qing Yang, Dezhou Cheng, Jinxin Li, Wei Wang, Jinbai Huang, Xiaochun Peng","doi":"10.3892/or.2024.8824","DOIUrl":"10.3892/or.2024.8824","url":null,"abstract":"Bone metastasis (BM) is a common complication of cancer and contributes to a higher mortality rate in patients with cancer. The treatment of BM remains a significant challenge for oncologists worldwide. The colony‑stimulating factor (CSF) has an important effect on the metastasis of multiple cancers. In vitro studies have shown that CSF acts as a cytokine, promoting the colony formation of hematopoietic cells by activating granulocytes and macrophages. Other studies have shown that CSF not only promotes cancer aggressiveness but also correlates with the development and prognosis of various types of cancer. In recent years, the effect of CSF on BM has been primarily investigated using cellular and animal models, with limited clinical studies available. The present review discussed the composition and function of CSF, as well as its role in the progression of BM across various types of cancer. The mechanisms by which osteoclast‑ and osteoblast‑mediated BM occur are comprehensively described. In addition, the mechanisms of action of emerging therapeutic agents are explored for their potential clinical applications. However, further clinical studies are required to validate these findings.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 6","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Repurposing propofol for breast cancer therapy through promoting apoptosis and arresting cell cycle. 通过促进细胞凋亡和抑制细胞周期，将异丙酚重新用于乳腺癌治疗。

IF 3.8 3区医学

Oncology reports Pub Date : 2024-11-01 Epub Date: 2024-10-04 DOI: 10.3892/or.2024.8814

Peng Sun, Hanqing Huang, Jian-Chao Ma, Binyang Feng, Yiqing Zhang, Genggeng Qin, Weian Zeng, Zhong-Kai Cui

{"title":"Repurposing propofol for breast cancer therapy through promoting apoptosis and arresting cell cycle.","authors":"Peng Sun, Hanqing Huang, Jian-Chao Ma, Binyang Feng, Yiqing Zhang, Genggeng Qin, Weian Zeng, Zhong-Kai Cui","doi":"10.3892/or.2024.8814","DOIUrl":"10.3892/or.2024.8814","url":null,"abstract":"Breast cancer is the most prevalent cancer among women worldwide, characterized by a high mortality rate and propensity for metastasis. Although surgery is the standard treatment for breast cancer, there is still no effective method to inhibit tumor metastasis and improve the prognosis of patients with breast cancer after surgery. Propofol, one of the most widely used intravenous anesthetics in surgery, has exhibited a positive association with improved survival outcomes in patients with breast cancer post‑surgery. However, the underlying molecular mechanism remains to be elucidated. The present study revealed that triple negative breast cancer cells, MDA‑MB‑231 and 4T1, exposed to propofol exhibited a significant decrease in cell viability. Notably, propofol exhibited minimal cytotoxic effects on HUVECs under the same conditions. Furthermore, propofol significantly inhibited the migration and invasion ability of MDA‑MB‑231 and 4T1 cells. Propofol promoted apoptosis in 4T1 cells through upregulation of Bax and cleaved caspase 3, while downregulating B‑cell lymphoma‑extra large. Concomitantly, propofol induced cell cycle arrest of 4T1 cells by downregulating cyclin E2 and phosphorylated cell division cycle 6. Furthermore, propofol exhibited excellent anticancer efficacy in a 4T1 breast cancer allograft mouse model. The present study sheds light on the potential of propofol as an old medicine with a novel use for breast cancer treatment.","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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