Cancer Biotherapy and Radiopharmaceuticals最新文献

{"title":"Same-Day Positron Emission Tomography/Computed Tomography with ⁶⁸Ga-Radiolabeled Fibroblast Activation Protein Inhibitors and ¹⁸F-Fluorodeoxyglucose Imaging for Gastrointestinal Cancers.","authors":"Xiaoshan Chen, Yunuan Liu, Xinming Zhao, Fenglian Jing, Bin Wang, Xiaolin Chen, Xiao Pang, Jingmian Zhang, Jianfang Wang, Zhaoqi Zhang, Jingya Han, Mengjiao Wang","doi":"10.1089/cbr.2024.0182","DOIUrl":"10.1089/cbr.2024.0182","url":null,"abstract":"<p><p><b><i>Objective:</i></b> We investigated the clinical practicability of same-day ⁶⁸Ga-radiolabeled fibroblast activation protein inhibitors (⁶⁸Ga-FAPI)-first and ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) imaging and compared it with same-day ¹⁸F-FDG-first or 2-day procedures in diagnosing gastrointestinal cancers. <b><i>Materials and Methods:</i></b> Sixty-five patients with confirmed gastrointestinal cancers were divided into same-day ⁶⁸Ga-FAPI-first group (Group A), same-day ¹⁸F-FDG-first group (Group B), and 2-day group (Group C). Low-dose CT and low injection activity were performed on ⁶⁸Ga-FAPI positron emission tomography/computed tomography (PET/CT). Interval times, radiation dose, diagnostic performance, and detectability were assessed among groups. Additionally, the uptake, tumor-to-liver ratio (TLR), diagnostic efficacy, and TNM stage were compared between the two modalities. <b><i>Results:</i></b> The total waiting time for Group C was significantly longer than that for Group A or B (both <i>p</i> < 0.001). The total dose-length product and effective dose decreased in all groups. There were comparable detectability and diagnostic performance among groups (all <i>p</i> > 0.05). The within-group analysis in Group B indicated that ⁶⁸Ga-FAPI PET/CT had higher uptake in the primary and recurrent lesions than ¹⁸F-FDG without differences in TLR, due to higher liver background on ⁶⁸Ga-FAPI PET than Group A or C (both <i>p</i> < 0.001).⁶⁸Ga-FAPI PET/CT possessed higher accuracy than ¹⁸F-FDG and changed staging in 14 patients (14/65, 21.54%). <b><i>Conclusions:</i></b> The same-day ⁶⁸Ga-FAPI-first and ¹⁸F-FDG imaging reduced examination waiting time without increased radiation dose, simultaneously achieving excellent diagnostic performance and improving clinical staging in diagnosing gastrointestinal cancers.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"130-138"},"PeriodicalIF":2.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142513374","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":"Stratification of Lung Adenocarcinoma Patients Based on <i>In Silico</i> and Immunohistochemistry Analyses of Oxidative Stress-Related Genes.","authors":"Chongrong Qiu, Yuming Zhou, Xiaoliu Xiao, Tianjun Song, Dongyun Zeng, Jingliang Peng","doi":"10.1089/cbr.2024.0094","DOIUrl":"10.1089/cbr.2024.0094","url":null,"abstract":"<p><p><b><i>Background:</i></b> Lung adenocarcinoma (LUAD) remains heterogeneous in the prognosis of patients; oxidative stress (OS) has been widely linked to cancer progression. Therefore, it is necessary to explore the prognostic value of the OS-associated genes in LUAD. <b><i>Methods:</i></b> An OS-associated prognostic signature was developed using the Cox regression and random forest model in The Cancer Genome Atlas-LUAD dataset. Kaplan-Meier <b>(K-M)</b> survival curve and time-dependent receiver operating characteristic (tROC) curves were applied to evaluate and validate the predictive accuracy of this signature among the training and testing cohorts. A nomogram was constructed and also verified by the concordance index (C-index), calibration curves, and tROC curves, respectively. ESTIMATE algorithm and CIBERSORT algorithms were conducted to explore the signature's immune characteristics. Core target genes of the prognostic signature were identified in the protein-protein interaction network. <b><i>Results:</i></b> A six OS-associated prognostic gene signature (<i>CDC25C, ERO1A, GRIA1, TERT, CAV1, BDNF</i>) was developed. The tROC and K-M survival curves in the training and testing cohorts revealed that the signature had good and robust predictive capability to predict the overall survival of LUAD patients. Meanwhile, the risk score was an independent prognostic factor influencing patients' overall survival. The results of the C-index (0.714), calibration curves, and the 1-, 2-, and 3-year tROC curves (area under the curve = 0.703, 0.737, and 0.723, respectively) suggested that the nomogram had good predictive efficacy and prognostic value for LUAD. Then, the authors found that the high-risk group may be depletion or loss of antitumor function of immune cells. Finally, 10 core genes of the signature were predicted. <b><i>Conclusion:</i></b> Their study may provide a novel understanding for the identification of prognostic stratification in LUAD patients, as well as the regulation of OS-associated genes in LUAD progression.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"11-21"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141478034","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":"Unlocking Clinical Insights: Lymphocyte-Specific Protein Tyrosine Kinase Candidates as Promising Therapeutic Targets for Pancreatic Cancer Risk Stratification.","authors":"Huan Zhang, Paul Winter, Thomas Wartmann, Luca Simioni, Sara Al-Madhi, Aris Perrakis, Roland S Croner, Wenjie Shi, Quan Yu, Ulf D Kahlert","doi":"10.1089/cbr.2024.0056","DOIUrl":"10.1089/cbr.2024.0056","url":null,"abstract":"<p><p><b><i>Background:</i></b> Uncover the pivotal link between lymphocyte-specific protein tyrosine kinase (Lck)-related genes and clinical risk stratification in pancreatic cancer. <b><i>Methods:</i></b> This study identifies shared genes between differentially expressed genes (DEGs) and Lck-related genes in pancreatic cancer using a methodological framework rooted in The Cancer Genome Atlas database. Feature gene selection is accomplished and a signature model is constructed. Statistical significant clinical endpoints such as overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI) were defined. <b><i>Results:</i></b> After performing random survival forest, Lasso regression, and multivariate Cox regression model, 7 trait genes out of 272 Lck-associated DEGs are selected to create a signature model that is independent of other clinical factors and can predict OS and DSS. It appears that high-risk patients have activated the TP53 signaling pathway and the cell cycle signaling pathway. <i>LAMA3</i> turned out to be the hub gene of the signature with high expression in pancreatic cancer. Patients with increased expression of <i>LAMA3</i> had a short OS, DSS, and PFI in comparison. The candidate competing endogenous RNA network of <i>LAMA3</i> turned out to be OPI5-AS1/hsa-miR-186-5p/<i>LAMA3</i> axis. <b><i>Conclusions:</i></b> A characteristic signature of seven Lck-related genes, especially <i>LAMA3</i>, has been shown to be a key factor in clinical risk stratification for pancreatic cancer.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"1-10"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141263640","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":"Raddeanin A Inhibits Colorectal Cancer Growth and Ameliorates Oxaliplatin Resistance Through the WNT/β-Catenin Signaling Pathway.","authors":"Junguo Chen, Yanhong Zhang, Xijie Chen, Dandong Luo, Danlin Liu, Zhaoliang Yu, Yanyun Lin, Xiaosheng He, Juanni Huang, Lei Lian","doi":"10.1089/cbr.2024.0061","DOIUrl":"10.1089/cbr.2024.0061","url":null,"abstract":"<p><p><b><i>Background:</i></b> Chemotherapy based on oxaliplatin (OXA) is the first-line treatment for advanced colorectal cancer (CRC), and acquired resistance to OXA is the main reason for clinical treatment failure in CRC. <b><i>Methods:</i></b> To search for compounds that can reverse OXA resistance, we screened a small molecule inhibitor drug library and identified a drug, Raddeanin A (RA), that enhanced the anticancer effect of OXA. Using human CRC cell lines, CRC organoid models, and <i>in vivo</i> subcutaneous tumorigenic studies, we determined that RA inhibits the proliferation of CRC cells by promoting apoptosis and inducing cell cycle arrest. <b><i>Results:</i></b> We constructed OXA-resistant CRC cell lines and demonstrated that RA enhances the sensitivity of these cells to OXA. Further experiments showed that the mechanism by which RA enhanced the anticancer effects of OXA in CRC was by inhibiting the activation of the WNT/β-catenin signaling pathway. <b><i>Conclusions:</i></b> Because RA has been shown to be biocompatible in animal models, there is a possibility that RA could be developed as a sensitizer for resistant cancer cells or as a novel lead compound to enhance the therapeutic efficacy of OXA in resistant CRCs.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"41-53"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711869","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":"<i>SERPINH1</i> as a Novel Biomarker for Colon Cancer Bone Metastasis with Machine Learning and Immunohistochemistry Validation.","authors":"Guoping Zhao, Tianjun Song, Qingfa Qing, Huaifu Cheng, Jinmin Zhao","doi":"10.1089/cbr.2024.0162","DOIUrl":"10.1089/cbr.2024.0162","url":null,"abstract":"<p><p><b><i>Background:</i></b> Bone metastasis (BM) is a serious clinical symptom of advanced colorectal cancer. However, there is a lack of effective biomarkers for early diagnosis and treatment. <b><i>Method:</i></b> RNA-seq data from public databases (GSE49355, GSE101607) were collected and normalized and batch effects were removed using the combat package. Differential expression analysis was performed to identify significant genes. Robust Rank Aggregation and machine learning algorithms were used to pinpoint candidate biomarkers. These biomarkers were validated using immunohistochemistry and further analyzed for survival rates. Enrichment analysis was conducted to explore biological mechanisms. Additionally, drug sensitivity and immune infiltration analyses were performed to provide insights into potential therapeutic targets. <b><i>Results:</i></b> Analysis results revealed 386 genes elevated in primary versus normal tissues and 26 genes varying between primary and BM. Serpin Protease Inhibitor Clade H1 (<i>SERPINH1)</i> as a novel biomarker for colon cancer metastasis. High <i>SERPINH1</i> expression correlates with poor survival outcomes and is linked to high lymphatic invasion and advanced cancer stages. Additionally, <i>SERPINH1</i> expression influences immune infiltration and is not predictive of chemotherapy response, but potential new drugs are suggested for high-expression cases. The gene also enriches classical cancer pathways such as Hedgehog and transforming growth factor-β. <b><i>Conclusions:</i></b> We identified novel colon cancer BM markers, including <i>SERPINH1</i>, using machine learning algorithms combined with traditional transcriptomic data and validated their expression through immunohistochemistry. This biomarker could significantly assist clinicians in making more precise treatment decisions.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"31-40"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142481429","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":"IL-21 and IL-33 May Be Effective Biomarkers to Predict the Efficacy of PD-1 Monoclonal Antibody for Advanced Cholangiocarcinoma.","authors":"Haijiao Yan, Qian Deng, Yu Meng, Ye Zhang, Jun Wu, Wensong Liu","doi":"10.1089/cbr.2024.0149","DOIUrl":"10.1089/cbr.2024.0149","url":null,"abstract":"<p><p><b><i>Background and Objective:</i></b> Treatment options for patients with advanced biliary tract cancer (BTC) are limited. The programmed cell death protein-1 (PD-1) inhibitors may have synergistic effects with chemotherapy. Therefore, the aim of our study was to provide real-world data on treatment outcomes in BTC patients receiving chemotherapy alone versus a combination of chemotherapy and PD-1 inhibitors. Additionally, we explored potential markers predictive of PD-1 inhibitor efficacy in this combined therapy. <b><i>Methods:</i></b> We conducted a review of patients at Changzhou First People's Hospital who received PD-1 inhibitors in combination with chemotherapy or chemotherapy alone as first-line treatment for advanced BTC. The primary endpoints of the study were progression-free survival (PFS) and overall survival (OS). Kaplan-Meier survival curves and the log-rank test were used to analyze the data. Immunohistochemistry showed the expression of interleukin-21 (IL-21), interleukin-33 (IL-33), and Eomes in the tumor tissue of patients who received PD-1 inhibitors in combination with chemotherapy. <b><i>Results:</i></b> The study enrolled 61 patients receiving PD-1 inhibitors combined with chemotherapy and 65 receiving chemotherapy alone. The median OS and PFS for patients receiving PD-1 inhibitors in combination with chemotherapy were 11.7 and 6.7 months, respectively. These durations were significantly longer than those for chemotherapy alone: OS of 10.3 months (95% CI: 0.16-0.21, <i>p</i> = 0.031) and PFS of 5.3 months (95% Confidence interval (CI) 0.25-0.32, <i>p</i> = 0.018). High IL-21 expression or low IL-33 expression in tumor tissue correlated with better response rates to chemotherapy combined with PD-1 inhibitors. <b><i>Conclusions:</i></b> Combining PD-1 inhibitors with chemotherapy shows good antitumor activity, making it an effective way to treat BTC. The expression profiles of IL-21 and IL-33 hold promise as potential markers for guiding the chemotherapy combined with immunotherapy in BTC patients.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"78-88"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016811","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":"Human Biodistribution and Radiation Dosimetry of the Targeting Fibroblast Growth Factor Receptor 1-Positive Tumors Tracer [⁶⁸Ga]Ga-DOTA-FGFR1-Peptide.","authors":"Huiqing Yuan, Xiaoshan Chen, Mengmeng Zhao, Xinming Zhao, Xiaolin Chen, Jingya Han, Zhaoqi Zhang, Jingmian Zhang, Jianfang Wang, Meng Dai, Yunuan Liu","doi":"10.1089/cbr.2024.0073","DOIUrl":"10.1089/cbr.2024.0073","url":null,"abstract":"<p><p><b><i>Objective:</i></b> [⁶⁸Ga]Ga-DOTA-FGFR1-peptide is a novel positron emission tomography (PET) radiotracer targeting fibroblast growth factor receptor 1 (FGFR1). This study evaluated the safety, biodistribution, radiation dosimetry, and imaging potential of [⁶⁸Ga]Ga-DOTA-FGFR1-peptide. <b><i>Methods:</i></b> The FGFR1-targeting peptide DOTA-(PEG2)-KAEWKSLGEEAWHSK was synthesized by manual solid-phase peptide synthesis with high-performance liquid chromatography purification, and labeled with ⁶⁸Ga with DOTA as chelating agent. We recruited 14 participants and calculated the radiation dose of 4 of these pathologically confirmed nontumor subjects using OLINDA/EXM 2.2.0 software. At the same time, the imaging potential in 10 of these lung cancer patients was evaluated. <b><i>Results:</i></b> The biodistribution of [⁶⁸Ga]Ga-DOTA-FGFR1-peptide in 4 subjects showed the highest uptake in the bladder and kidney. Dosimetry analysis indicated that the bladder wall received the highest effective dose (3.73E-02 mSv/MBq), followed by the lungs (2.36E-03 mSv/MBq) and red bone marrow (2.09E-03 mSv/MBq). No normal organs were found to have excess specific absorbed doses. The average systemic effective dose was 4.97E-02 mSv/MBq. The primary and metastatic tumor lesions were clearly visible on PET/computed tomography (CT) images in 10 patients. <b><i>Conclusion:</i></b> Our results indicate that [⁶⁸Ga]Ga-DOTA-FGFR1-peptide has a good dosimetry profile and can be used safely in humans, and it has significant potential value for clinical PET/CT imaging.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"712-720"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141635862","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":"GRHPR, Targeted by miR-138-5p, Inhibits the Proliferation and Metastasis of Hepatocellular Carcinoma Through PI3K/AKT Signaling Pathway.","authors":"Shuangshuang Yang, Yixian Liu, Bushi Zhang, Jinxia Li, Fang Xu, Mengdan Yu, Ying Chen, Chenglong Li, Ting Liu, Ying Zhao, Qianwei Zhao, Jintao Zhang","doi":"10.1089/cbr.2023.0018","DOIUrl":"10.1089/cbr.2023.0018","url":null,"abstract":"<p><p><b><i>Background:</i></b> Hepatocellular carcinoma (HCC) is a highly aggressive cancer. This study elucidates the role of Glyoxylate reductase/hydroxypyruvate reductase (GRHPR) in HCC proliferation and metastasis, along with its molecular mechanism, and identifies miRNAs targeting GRHPR. <b><i>Materials and Methods:</i></b> Expression levels of GRHPR and miR-138-5p were assessed using real-time fluorescent quantitative polymerase chain reaction and Western blot techniques. Bioinformatic analysis was employed to identify miRNAs targeting GRHPR, and the results were confirmed via dual-luciferase reporter assays. HCC cell lines overexpressing GRHPR were established to investigate its roles in cell proliferation, migration, and invasion. The biological function of miR-138-5p targeting GRHPR in HCC cells was also evaluated. Furthermore, a xenograft mouse model was utilized to examine the <i>in vivo</i> functions of GRHPR. <b><i>Results:</i></b> GRHPR expression was downregulated in HCC, whereas miR-138-5p was upregulated. Overexpression of GRHPR suppressed HCC cell proliferation, migration, and invasion. Conversely, inhibition of GRHPR by miR-138-5p promoted HCC cell proliferation and invasive properties. MiR-138-5p was found to regulate Phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) phosphorylation levels by inhibiting GRHPR expression. <b><i>Conclusion:</i></b> This study highlights GRHPR's role as a tumor suppressor in HCC, with its function being regulated by miR-138-5p.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"733-744"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141460903","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":"Theranostics, Advanced Cancer, and The Meaning of Life.","authors":"J Harvey Turner","doi":"10.1089/cbr.2024.0176","DOIUrl":"10.1089/cbr.2024.0176","url":null,"abstract":"<p><p>There is an unmet need to recognize and address the psychosocial and spiritual support of the rapidly growing population of cancer survivors living with advanced metastatic disease which is essentially incurable. Palliative chemotherapy may do more harm than good. The role of the physician in the provision of a supportive, compassionate relationship of mutual trust is critical in the exploration of spirituality and the meaning of life for each individual patient. The objective must be to enhance quality of life rather than prolong it at any cost. Nuclear physicians are now equipped to offer effective control of advanced metastatic cancer of prostate and neuroendocrine neoplasms without clinically evident toxicity. They also now have the potential to practice phronesis, and in so doing, to significantly ameliorate the quality of life of patients afflicted with these specific advanced cancers. During the time of prolonged symptom-free survival, these patients may be encouraged to find life's meaning and a peaceful acceptance of their inevitable demise.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"707-711"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142513375","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":"Long Noncoding RNA CRNDE Promotes Gastric Cancer Progression through Targeting miR-136-5p/MIEN1.","authors":"Yingchao Gu, Chaoyu Li, Xiankun Ren, Xiaodong Hu, Yuwen Huang, Lin Xia","doi":"10.1089/cbr.2023.0179","DOIUrl":"10.1089/cbr.2023.0179","url":null,"abstract":"<p><p><b><i>Background:</i></b> Long noncoding RNAs (lncRNAs) contribute to the initiation and progression of gastric cancer (GC). This study examined the potential role of lncRNA colorectal neoplasia differentially expressed (CRNDE) in modulating the expression of migration and invasion enhancer 1 (MIEN1) through the suppression of miR-136-5p in GC. <b><i>Methods:</i></b> The biological roles of CRNDE, miR-136-5p, and MIEN1 in GC were assessed both in laboratory settings and through the examination of clinical samples. <b><i>Results:</i></b> CRNDE was found to be significantly increased in GC tissues, and this upregulation was associated with an unfavorable prognosis of GC patients. <i>In vitro</i> experiments showed that inhibiting cell growth and migration, along with promoting apoptosis in GC cells, could be achieved by either disabling CRNDE or MIEN1, or by increasing the expression of miR-136-5p. MIEN1 is a specific recipient of miR-136-5p, and the anticancer effects of miR-136-5p can be counteracted by the increased expression of MIEN1. Through the examination of clinical specimens, it has been observed that there is a significant positive correlation between the expression of MIEN1 and CRNDE. In contrast, miR-136-5p expression in GC tissues shows a negative correlation. <b><i>Conclusion:</i></b> A previously unexplored therapeutic target for GC involves the CRNDE/miR-136-5p/MIEN1 signal transduction cascade.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"770-781"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141536063","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}