OncoTargets and therapy最新文献

{"title":"MicroRNA-126 Inhibit Viability of Colorectal Cancer Cell by Repressing mTOR Induced Apoptosis and Autophagy [Retraction]","authors":"Li Wei, Zhanhong Chen, Na Cheng, Xing Li, Jie Chen, Donghao Wu, Min Dong, Xiangyuan Wu","doi":"10.2147/ott.s464377","DOIUrl":"https://doi.org/10.2147/ott.s464377","url":null,"abstract":"Retraction for the article MicroRNA-126 Inhibit Viability of Colorectal Cancer Cell by Repressing mTOR Induced Apoptosis and Autophagy","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139917868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosome-Delivered EGFR Induced by Acidic Bile Salts Regulates Macrophage M2 Polarization to Promote Esophageal Adenocarcinoma Cell Proliferation","authors":"Chuangui Chen, Jinsheng Ding, Zhao Ma, Yongjie Xie, Linhua Zhang, Dunwan Zhu","doi":"10.2147/ott.s437560","DOIUrl":"https://doi.org/10.2147/ott.s437560","url":null,"abstract":"<strong>Purpose:</strong> Chronic gastroesophageal reflux disease (GERD) causes the abnormal reflux of acid and bile salts, which would induce Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC). EGFR, as one of main components of the exosome, plays an important role in cancer progression. Here, we investigated the role of acidic bile salts (ABS)-induced exosomal EGFR in EAC cell proliferation.<br/><strong>Methods:</strong> Electronic microscopic examination and Western blot were used to identify exosomes. Western blot, siRNA transfection, enzyme-linked immunosorbent assay, qRT-PCR, cell viability detection, mouse xenograft tumor models, and immunohistochemical staining were performed to study the function of ABS-induced exosomal EGFR in cell proliferation.<br/><strong>Results:</strong> We found that ABS improved the exosomal EGFR level of normal human esophageal epithelial cells, BE cells, and BE-associated adenocarcinoma cells. The results were confirmed in the serum-derived exosomes from healthy persons and patients suffering from GERD, BE with or without GERD, and EAC with or without GERD. Moreover, cell line-derived exosomal EGFR was found to promote macrophage M2 polarization through the PI3K-AKT pathway. The co-incubation medium of macrophages and exosomes improved cell proliferation and tumor growth, which depended on the exosomal EGFR level. CCL18 was identified as the most effective component of the co-incubation medium to promote EAC cell proliferation by binding to its receptor PITPNM3 in vitro and in vivo.<br/><strong>Conclusion:</strong> Our findings demonstrate that ABS-induced exosomal EGFR regulates macrophage M2 polarization to promote EAC proliferation. This study provides an important insight into the role of ABS in EAC development.<br/><br/><strong>Keywords:</strong> cancer progression, pro-oncogenic, PI3K/AKT pathway, CCL18, PITPNM3<br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139753581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-136 Targets MIEN1 and Involves the Metastasis of Colon Cancer by Suppressing Epithelial-to-Mesenchymal Transition [Retraction]","authors":"Haipeng Ren, Yuanling Qi, Xiaoyan Yin, Jianfeng Gao","doi":"10.2147/ott.s464003","DOIUrl":"https://doi.org/10.2147/ott.s464003","url":null,"abstract":"Retraction for the article miR-136 targets MIEN1 and involves the metastasis of colon cancer by suppressing epithelial-to-mesenchymal transition","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139753552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mst1-Hippo Pathway Triggers Breast Cancer Apoptosis via Inducing Mitochondrial Fragmentation in a Manner Dependent on JNK–Drp1 Axis [Retraction]","authors":"Hui Ouyang, Enxiang Zhou, Huan Wang","doi":"10.2147/ott.s464002","DOIUrl":"https://doi.org/10.2147/ott.s464002","url":null,"abstract":"Retraction for the article Mst1-Hippo pathway triggers breast cancer apoptosis via inducing mitochondrial fragmentation in a manner dependent on JNK&ndash;Drp1 axis","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139753549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thyroid Metastases from Triple-Negative Breast Cancer with High PD-L1 Expression – A Rare Presentation","authors":"Wenjuan Meng, Qingxia Guo, Gaoyan Tang, Guiyan Han, Guikai Ma, Qingyun Zhang, Rui Li, Shuzhen Liu, Guohua Yu","doi":"10.2147/ott.s428745","DOIUrl":"https://doi.org/10.2147/ott.s428745","url":null,"abstract":"<strong>Abstract:</strong> Thyroid metastases secondary to triple-negative breast cancer are sporadic. Diagnosis usually requires fine needle aspiration biopsy (FNAB) and immunohistochemistry. There are no treatment guidelines for this type of cancer, and to date, reports of chemotherapy combined with immunotherapy in thyroid metastases are very rare. Here, we first report the effectiveness of anti-PD-1 inhibitor in combination with chemotherapy for the treatment of metastatic thyroid cancer secondary to advanced triple-negative breast cancer with high expression of programmed cell death ligand 1 (PD-L1). Following six cycles of albumin paclitaxel (400mg d1/21 days) plus PD-1 antibody inhibitor (Sindilizumab 200mg d1/21 days), the patient experienced significant relief of neck swelling and obstructive feeding, both the thyroid metastases and the right breast lesion regressed completely following six cycles of treatment. Chemotherapy combined with immunotherapy may provide a new direction for unresectable advanced thyroid metastases.<br/><br/><strong>Keywords:</strong> thyroid metastases, triple-negative breast cancer, albumin paclitaxel, anti-PD-1 inhibitor, effectiveness<br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139753443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-182 Promotes Tumor Growth and Increases Chemoresistance of Human Anaplastic Thyroid Cancer by Targeting Tripartite Motif 8 [Retraction]","authors":"Yao Liu, Bing Zhang, Tiefeng Shi, Huadong Qin","doi":"10.2147/ott.s463642","DOIUrl":"https://doi.org/10.2147/ott.s463642","url":null,"abstract":"Retraction for the article miR-182 promotes tumor growth and increases chemoresistance&nbsp;of human anaplastic thyroid cancer by targeting tripartite motif 8","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139753447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kanglaite Reverses Multidrug Resistance of HCC by Inducing Apoptosis and Cell Cycle Arrest via PI3K/AKT Pathway [Retraction]","authors":"Chendong Yang, Aihua Hou, Chunfeng Yu, Lingling Dai, Wen Wang, Kangle Zhang, Hongmin Shao, Jinghua Ma, Wenjuan Xu","doi":"10.2147/ott.s463641","DOIUrl":"https://doi.org/10.2147/ott.s463641","url":null,"abstract":"Retraction for the article Kanglaite reverses multidrug resistance of HCC by inducing apoptosis and cell cycle arrest via PI3K/AKT pathway","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139753615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3/<i>MALAT1</i>/ELAVL1 Axis Promotes Tumor Growth in Ovarian Cancer.","authors":"Jian Xiong, Wenqin Lian, Rui Zhao, Kefei Gao","doi":"10.2147/OTT.S431810","DOIUrl":"10.2147/OTT.S431810","url":null,"abstract":"<p><strong>Background: </strong>Studies increasingly recognize the role of N6-methyladenosine (<i>m6A</i>) modification in cancer occurrence and development. METTL3 is a core catalytic subunit of m6A-modified methyltransferases complex, but its regulatory mechanism in ovarian cancer (OC) is not clear.</p><p><strong>Methods: </strong>In this study, GEPIA 2.0 database was applied for expression analysis, survival analysis and correlation analysis for OC. Additionally, in vitro and in vivo assays were conducted to explore regulatory mechanisms of METTL3 in OC.</p><p><strong>Results: </strong>We found that METTL3 and <i>MALAT1</i> were significantly overexpressed in OC tissues and cells compared to normal ovarian tissues and cells. The proliferation rate of OC cells was reduced significantly after knocking down the expression of <i>METTL3</i> or <i>MALAT1</i>. Subsequently, <i>MALAT1</i> as oncogene was found to interact with METTL3 and was upregulated in OC tissues and cells. Silencing <i>MALAT1</i> inhibited OC cell proliferation. Further studies indicated that METTL3 enhanced the stability of <i>MALAT1</i> by promoting the m6A modification of <i>MALAT1</i> and that ELAVL1 as a downstream binding protein significantly up-regulated <i>MALAT1</i> expression.</p><p><strong>Conclusion: </strong>In conclusion, METTL3 was a carcinogenic molecule that promoted the occurrence of OC. The potential mechanism of the carcinogenic effect of METTL3 was realized by enhancing the m6A modification of <i>MALAT1</i> mRNA through RNA binding protein ELAVL1.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10860502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139723552","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}

{"title":"Response to Savolitinib in a Patient with Advanced Poorly Differentiated Lung Carcinoma Positive for a Novel EML4-MET Gene Fusion","authors":"Ganlu Ouyang, Pei Shu, Yinyin Xue, Feng Luo, Yan Li","doi":"10.2147/ott.s442685","DOIUrl":"https://doi.org/10.2147/ott.s442685","url":null,"abstract":"<strong>Background:</strong> Cellular-mesenchymal to epithelial transition factor (c-MET) alterations have significant therapeutic implications in non-small cell lung cancer (NSCLC). Although MET fusion is a rare genomic event, advances in detection technologies have enabled the identification of various MET fusion partner genes. However, standard therapeutic options for MET fusion in NSCLC cases remain undefined. This report presents a novel fusion variant, EML4-MET, encompassing exons 1 to 13 of EML4 and exons 15 to 21 of MET, including the entire MET kinase domain, and discusses the response of this case to savolitinib treatment.<br/><strong>Case Presentation:</strong> A 65-year-old woman was diagnosed with advanced poorly differentiated lung carcinoma. Molecular profiling of circulating tumor DNA (ctDNA), carried out by next-generation sequencing (NGS), identified a novel EML4-MET fusion. The patient was administered the MET receptor tyrosine kinase inhibitor savolitinib at 400 mg daily. One month later, computed tomography (CT) revealed some lesions with volume reduction. However, COVID-19 diminished the efficacy of savolitinib. Regrettably, the patient succumbed to respiratory and circulatory failure due to disease progression in March 2023.<br/><strong>Conclusion:</strong> This case uncovers a new type of MET fusion and expands the range of potential MET fusion targets in NSCLC. The patient responded to savolitinib, suggesting a reference basis for the treatment of similar cases with EML4-MET fusion in the future. Additional research is warranted to assess the biological significance of the EML4-MET fusion in NSCLC.<br/><br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139579732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amplifying Curcumin’s Antitumor Potential: A Heat-Driven Approach for Colorectal Cancer Treatment","authors":"Janviere Kabagwira, Ryan N Fuller, Paul A Vallejos, Chase S Sugiono, Vola-Masoandro Andrianarijaona, Jazmine Brianna Chism, Michael P O'Leary, David Caba Molina, William Langridge, Maheswari Senthil, Nathan R Wall","doi":"10.2147/ott.s448024","DOIUrl":"https://doi.org/10.2147/ott.s448024","url":null,"abstract":"<strong>Introduction:</strong> Peritoneal metastases from colorectal cancer (CRC) present a significant clinical challenge with poor prognosis, often unresponsive to systemic chemotherapy. Cytoreductive surgery (CRS) combined with hyperthermic intraperitoneal chemotherapy (HIPEC) is a treatment approach for select patients. The use of curcumin, a natural compound with antitumor properties, in HIPEC is of interest due to its lower side effects compared to conventional drugs and potential for increased efficacy through direct delivery to the peritoneal cavity.<br/><strong>Methods:</strong> An in vitro hyperthermic model was developed to simulate clinical HIPEC conditions. Three colon cancer cell lines (SK-CO-1, COLO205, SNU-C1) representing different genetic mutations (p53, KRAS, BRAF) were treated with either curcumin (25 μM) or mitomycin-C (1 μM) for 1, 2, or 3 hours. Post-treatment, cells were incubated at 37°C (normothermia) or 42°C (hyperthermia). Cell viability and proliferation were assessed at 24, 48 and 72 hours post-treatment using Annexin V/PI, MTT assay, trypan blue exclusion, and Hoffman microscopy.<br/><strong>Results:</strong> Hyperthermia significantly enhanced the antitumor efficacy of curcumin, evidenced by a two-fold reduction in cell viability compared to normothermia across all cell lines. In the SNU-C1 cell line, which harbors a p53 mutation, mitomycin-C failed to significantly impact cell viability, unlike curcumin, suggesting mutation-specific differences in treatment response.<br/><strong>Discussion:</strong> The findings indicate that hyperthermia augments the antitumor effects of curcumin in vitro, supporting the hypothesis that curcumin could be a more effective HIPEC agent than traditional drugs like mitomycin-C. Mutation-associated differences in response to treatments were observed, particularly in p53 mutant cells. While further studies are needed, these preliminary results suggest that curcumin in HIPEC could represent a novel therapeutic strategy for CRC patients with peritoneal metastases. This approach may offer improved outcomes with fewer side effects, particularly in genetically distinct CRC subtypes.<br/><br/><strong>Plain Language Summary:</strong> In this study, we aimed to improve treatments for peritoneal carcinomatosis (PC), a challenging form of colorectal cancer (CRC) that does not respond well to regular chemotherapy. We explored an approach called hyperthermic intraperitoneal chemotherapy (HIPEC), which involves delivering potent chemotherapy directly to the abdominal area at an elevated temperature. Our innovative idea was to enhance HIPEC’s effectiveness by using curcumin, a natural compound with fewer side effects than conventional HIPEC drugs. To test our theory, we conducted experiments on colon cancer cells under high-temperature conditions, mimicking what occurs during HIPEC treatments. We also compared curcumin with the standard drug, mitomycin-C (MMC). We discovered that curcumin, when deliv","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139579867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}