Oncology Research最新文献

IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway. IL13RA2通过激活糖酵解和Wnt/β-catenin信号通路促进婴儿血管瘤的进展。

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.048315

Ziyong Liu, Tao Ma, Jinfang Li, Wei Ren, Zhixin Zhang

{"title":"IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway.","authors":"Ziyong Liu, Tao Ma, Jinfang Li, Wei Ren, Zhixin Zhang","doi":"10.32604/or.2024.048315","DOIUrl":"10.32604/or.2024.048315","url":null,"abstract":"Background: Interleukin 13 receptor subunit alpha 2 (IL13RA2) plays an essential role in the progression of many cancers. However, the role of IL13RA2 in infantile haemangioma (IH) is still unknown.Materials and methods: IL13RA2 expression in IH tissues was analyzed using western blot, qRT-PCR, and immunofluorescence. The role of IL13RA2 in haemangioma-derived endothelial cells (HemECs) was determined following knockdown or overexpression of IL13RA2 using CCK-8, colony formation, apoptosis, wound healing, tubule formation, Transwell, and western blot.Results: IL13RA2 expression was upregulated in IH tissues. IL13RA2 overexpression promoted proliferation, migration, and invasion of HemECs and induced glycolysis, which was confirmed with a glycolysis inhibitor. Specifically, IL13RA2 interacted with β-catenin and activated the Wnt/β-catenin pathway in HemECs, which were involved in the above-mentioned effects of IL13RA2.Conclusions: These findings revealed that targeting IL13RA2 is a potential therapeutic approach for IH.","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110371","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

Retraction: Knockdown of Long Noncoding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Inhibits Proliferation, Migration, and Invasion and Promotes Apoptosis by Targeting miR-124 in Retinoblastoma. 撤回：敲除长非编码 RNA (lncRNA) 转移相关肺腺癌转录本 1 (MALAT1) 通过靶向 miR-124 抑制视网膜母细胞瘤的增殖、迁移和侵袭并促进凋亡

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056121

引用次数: 0

Correction: Long non-coding RNA LINC02163 accelerates malignant tumor behaviors in breast cancer by regulating the microRNA-511-3p/HMGA2 axis as a competing endogenous RNA. 更正：长非编码 RNA LINC02163 作为竞争性内源性 RNA，通过调节 microRNA-511-3p/HMGA2 轴，加速乳腺癌的恶性肿瘤行为。

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.051893

Chenglin Qin, Linfang Jin, Jia Li, Wenzhang Zha, Huiming Ding, Xiaorong Liu, Xun Zhu

引用次数: 0

Retraction: miR-181a-5p Promotes Proliferation and Invasion and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). 撤稿：miR-181a-5p 通过调节肌醇多磷酸-5-磷酸酶 A (INPP5A) 促进宫颈癌细胞的增殖和侵袭并抑制其凋亡

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056126

引用次数: 0

Retraction: miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway. 撤稿：miR-3188 通过靶向 TUSC5 和调节 p38 MAPK 信号通路调控乳腺癌的细胞增殖、凋亡和迁移。

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056118

引用次数: 0

Retraction: miR-940 Upregulation Suppresses Cell Proliferation and Induces Apoptosis by Targeting PKC-δ in Ovarian Cancer OVCAR3 Cells. 撤稿：miR-940 上调通过靶向 PKC-δ 抑制卵巢癌 OVCAR3 细胞增殖并诱导其凋亡

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056127

引用次数: 0

Immunomodulatory and chemopreventive effects of resveratrol on the digestive system cancers. 白藜芦醇对消化系统癌症的免疫调节和化学预防作用。

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.049745

Meir Djaldetti

{"title":"Immunomodulatory and chemopreventive effects of resveratrol on the digestive system cancers.","authors":"Meir Djaldetti","doi":"10.32604/or.2024.049745","DOIUrl":"10.32604/or.2024.049745","url":null,"abstract":"Resveratrol (RSV), the primary polyphenol found in grapes, has been revealed to have anti-inflammatory properties by reducing the capacity of the peripheral blood mononuclear cells to produce pro-inflammatory cytokines, including IL-1β, IL-6, IL-1ra and TNFα. Considering the close association between chronic inflammation and cancer development, RSV's immunomodulatory properties are one way by which the polyphenol may inhibit cancer initiation, proliferation, neovascularization, and migration. Resveratrol influences the generation of microtumor environment which is one of the key factors in cancer progress. In addition to immunomodulation, RSV inhibits cancer development by expressing anti-oxidant effects, causing cell cycle arrest, stimulating the function of certain enzymes, and activating cell signaling pathways. The end outcome is one of the various forms of cell death, including apoptosis, pyroptosis, necroptosis, and more, as it has been observed in vitro. RSV has been shown to act against cancer in practically every organ, while its effects on colon cancer have been documented more frequently. It is remarkable that longer-term clinical studies that may have established the potential for this natural substance to serve as a therapeutic adjuvant to traditional anti-cancer medications were not prompted by the encouraging outcomes seen with cancer cells treated with non-toxic doses of resveratrol. The current review aims to assess the recent findings about the immunological and anti-cancer characteristics of RSV, with a particular emphasis on cancers of the digestive tract, as a challenge for future clinical research that may contribute to the better prognosis of cancer.","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110372","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

NCAPD2 serves as a potential prognostic biomarker for lung adenocarcinoma and promotes cell proliferation, migration, invasion and cell cycle in vitro. NCAPD2 是肺腺癌的潜在预后生物标志物，在体外促进细胞增殖、迁移、侵袭和细胞周期。

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.047490

Peiling Wu, Lifang Zhao, Hongyan Zhang, Yueyan Lou, Dongfang Chen, Shan Xue, Xueqing Liu, Handong Jiang

{"title":"NCAPD2 serves as a potential prognostic biomarker for lung adenocarcinoma and promotes cell proliferation, migration, invasion and cell cycle in vitro.","authors":"Peiling Wu, Lifang Zhao, Hongyan Zhang, Yueyan Lou, Dongfang Chen, Shan Xue, Xueqing Liu, Handong Jiang","doi":"10.32604/or.2024.047490","DOIUrl":"10.32604/or.2024.047490","url":null,"abstract":"Objectives: The pro-oncogenic effects of NCAPD2 have been extensively studied across various tumor types; however, its precise role within the context of lung adenocarcinoma (LUAD) remains elusive. This study aims to elucidate the biological functions of NCAPD2 in LUAD and unravel the underlying mechanistic pathways.Methods: Utilizing bioinformatics methodologies, we explored the differential expression of NCAPD2 between normal and tumor samples, along with its correlations with clinical-pathological characteristics, survival prognosis, and immune infiltration.Results: In the TCGA-LUAD dataset, tumor samples demonstrated significantly elevated levels of NCAPD2 expression compared to normal samples (p < 0.001). Clinically, higher NCAPD2 expression was notably associated with advanced T, N, and M stages, pathologic stage, gender, smoking status, and diminished overall survival (OS). Moreover, differentially expressed genes (DEGs) associated with NCAPD2 were predominantly enriched in pathways related to cell division. Immune infiltration analysis revealed that NCAPD2 expression levels were linked to the infiltration of memory B cells, naïve CD4+ T cells, activated memory CD4+ T cells, and M1 macrophages. In vitro experiments demonstrated that silencing NCAPD2 suppressed LUAD cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and cell cycle progression.Conclusions: In summary, NCAPD2 may represent a promising prognostic biomarker and novel therapeutic target for LUAD.","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110374","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

Retraction: Gamma Irradiation Upregulates B-cell Translocation Gene 2 to Attenuate Cell Proliferation of Lung Cancer Cells Through the JNK and NF-κB Pathways. 撤回：γ射线通过JNK和NF-κB途径上调B细胞转座基因2以抑制肺癌细胞的增殖

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.056120

引用次数: 0

COL4A2 enhances thyroid cancer cell proliferation through the AKT pathway. COL4A2 通过 AKT 通路促进甲状腺癌细胞增殖

IF 2 4区医学

Oncology Research Pub Date : 2024-08-23 eCollection Date: 2024-01-01 DOI: 10.32604/or.2024.047382

Liang He, Wei Han, Kai Yue, Xudong Wang

{"title":"COL4A2 enhances thyroid cancer cell proliferation through the AKT pathway.","authors":"Liang He, Wei Han, Kai Yue, Xudong Wang","doi":"10.32604/or.2024.047382","DOIUrl":"10.32604/or.2024.047382","url":null,"abstract":"Objectives: Thyroid cancer (THCA) is the most common malignant tumor in endocrine system and the incidence has been increasing worldwide. And the number of patients dying from THCA has also gradually risen because the incidence continues to increase, so the mechanisms related to effective targets is necessary to improve the survival. This study was to preliminarily investigate the effects of the COL4A2 gene on the regulation of thyroid cancer (THCA) cell proliferation and the associated pathways.Methods: Bioinformatics analysis revealed that COL4A2 was closely associated with cancer development. COL4A2 expression in THCA tissues was analyzed using immunohistochemistry, and survival information was determined via Kaplan‒Meier curves. The expression of COL4A2 and AKT pathway-related genes were analyzed using qPCR and western blot analyses. Colony formation as well as CCK-8 assays exhibited the cell proliferation level and cell activity, respectively. Downstream of COL4A2 was identified by Gene set enrichment analysis (GSEA). The effects of the COL4A2 and AKT pathways on THCA tumor growth in vivo were determined using a mouse model.Results: Bioinformatics analysis exhibited that COL4A2 plays a significant role in cancer and that the AKT pathway is downstream of COL4A2. THCA patients with high COL4A2 expression had shorter recurrence-free survival. Upregulation of COL4A2 gene expression in 2 THCA cell lines promoted tumor cell growth and activity. The use of AKT pathway blockers also restrained the growth and activity of the 2 THCA cell lines. The use of AKT pathway blockers reduced tumor volume and mass and prolonged mouse survival.Conclusions: COL4A2 can promote the growth as well as development of THCA through the AKT pathway and COL4A2 could be used as a target for THCA.","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110367","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