Cancer biotherapy & radiopharmaceuticals最新文献

{"title":"Theranostics: Timing is Everything.","authors":"J. H. Turner","doi":"10.1089/cbr.2024.0088","DOIUrl":"https://doi.org/10.1089/cbr.2024.0088","url":null,"abstract":"On stage, and in real life, timing is critical for success. Theranostic cancer care epitomizes the central role of timing in the evolution of efficacious molecular targeted radioligand therapy and its incorporation into routine clinical practice of oncology. Nuclear medicine has returned to its therapeutic roots, having been founded as a medical specialty, over three-quarters of a century ago, with radioiodine therapy of thyroid cancer. The very recent oncologist acceptance of 68Ga/177Lu/225Ac-PSMA effectiveness in treating prostate cancer has re-established the role of the physician in nuclear medicine. This article addresses various important issues in respect of timing related to this resurgence. Training of the required new workforce in technical -omics expertise and physicianly virtues is an urgent priority. Precision in radioligand therapy requires definition of individual radiation absorbed dose (Gy) to tumor and to critical normal organs, preferably prospectively. It is time to abandon one-size-fits-all administration of fixed activities (GBq) in arbitrary cycle intervals and duration. The time has also come to design combination sequenced theranostic-immuno-chemotherapeutic approaches to metastatic cancer to address unmet needs, particularly in pancreatic carcinoma; exploiting the potential of new fibroblast activation protein inhibitor radioligands targeting the tumor microenvironment. Public perception of all things \"nuclear,\" including nuclear medicine, has recently recovered from the general opprobrium and radiophobia of the last half-century. Nuclear is the new green. At last, there have arisen propitious circumstances for the future development of theranostics: The timing is right, now.","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":"58 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140964915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-Term Biological Toxicity Prediction of [177Lu]Lutetium-Oxodotreotide: An Original Retrospective Analysis.","authors":"Julien Dubois, Guillaume Tosato, P. Garrigue, David Taieb, Benjamin Guillet, V. Nail","doi":"10.1089/cbr.2023.0195","DOIUrl":"https://doi.org/10.1089/cbr.2023.0195","url":null,"abstract":"Introduction: [177Lu]Lutetium (Lu)-oxodotreotide is a radiopharmaceutical drug used as peptide receptor radionuclide therapy (PRRT) for somatostatin receptor-expressing neuroendocrine neoplasms. It provides an additional effective alternative treatment for these rare cancers. Although well tolerated, its safety profile must continue to be characterized to support its use as a first-line treatment or for additional cycles. This study aims to evaluate factors associated with the occurrence of [177Lu]Lu-oxodotreotide induced short-term toxicity. Materials and Methods: A retrospective observational monocentric study was carried out from July 2013 to October 2021. Inclusion criteria were defined as follows: patients who received at least four cycles of [177Lu]Lu-oxodotreotide and were followed up for 6 months after the last injection. Graduated toxicity was defined using the National Cancer Institute Common Terminology Criteria for Adverse Events 5.0. Cox regression was used in the analysis. Results: Forty patients were included. The most frequent toxicities occurred during the first cycle and were graded as G1 or G2. As expected, toxicities were predominantly hematological and hepatic, with incomplete reversibility after each cycle. The following factors were significantly related to the occurrence of hematological or hepatic toxicity during PRRT: gastrointestinal primary tumor diagnosis, bone metastases, peritoneal metastases, pancreatic metastases or pulmonary metastases, and high tumor grade. Conclusion: Knowledge and consideration of these factors in adjusting [177Lu]Lu-oxodotreotide treatment regimen could help prevent or reduce the severity of these toxicities. Further studies are still warranted to refine these results and improve treatment management.","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":"29 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140660918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA EBLN3P Accelerates Cell Proliferation and Invasion of Colon Cancer through Modulating the miR-519d-3p/ZFP91 Axis.","authors":"Xiaohui Wang, Yinzi Yue, Jinhua Tan, Fei Kou, Bude Su, Jin Xie, Shuai Yan","doi":"10.1089/cbr.2022.0089","DOIUrl":"https://doi.org/10.1089/cbr.2022.0089","url":null,"abstract":"Purpose: The study aims to explore the roles and underlying mechanisms of long noncoding RNAs endogenous bornavirus-like nucleoprotein (lncRNA EBLN3P) in colon cancer, emphasizing the potential impact of these insights on advancing colon cancer treatment strategies. By shedding light on lncRNA EBLN3P's involvement, this research could contribute to the development of novel therapeutic approaches, enhancing the efficacy of interventions for colon cancer patients. Methods: We employed quantitative reverse transcription polymerase chain reaction to assess the levels of lncRNA EBLN3P, zinc finger protein (ZFP91), and miR-519d-3p, alongside CCK-8 and EdU assays for cell proliferation, flow cytometry for apoptosis, and Transwell and wound healing assays for migration and invasion. The in vivo function of lncRNA EBLN3P was investigated through a xenograft model, and protein levels were evaluated via Western blot analysis. Results: LncRNA EBLN3P was found to be upregulated in colon cancer tissues and cells, promoting cell proliferation and metastasis while inhibiting apoptosis. Downregulation of lncRNA EBLN3P reduced tumor size, volume, and weight in a mouse model. MiR-519d-3p, which negatively interacts with lncRNA EBLN3P, was found to be downregulated in colon cancer tissues and cell lines. Its upregulation hindered cancer cell proliferation and metastasis while enhancing apoptosis. ZFP91, a binding partner of miR-519d-3p, was upregulated in colon cancer and inversely related to miR-519d-3p levels. Rescue experiments indicated that the effects of lncRNA EBLN3P silencing could be reversed by miR-519d-3p suppression, but were mitigated by ZFP91 downregulation. Conclusion: LncRNA EBLN3P facilitates colon cancer progression via the miR-519d-3p/ZFP91 axis, presenting a novel understanding of lncRNA EBLN3P's role and offering potential therapeutic insights for colon cancer treatment. This study fills a critical gap by linking lncRNA EBLN3P with the miR-519d-3p/ZFP91 axis in the context of colon cancer, thereby broadening our understanding of the molecular mechanisms underlying colon cancer progression.","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":"77 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140717900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acknowledgment of Reviewers 2023.","authors":"","doi":"10.1089/fpsam.2023.29027.ack","DOIUrl":"https://doi.org/10.1089/fpsam.2023.29027.ack","url":null,"abstract":"","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":"216 ","pages":"103"},"PeriodicalIF":0.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140528917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircEXOC6B Suppresses the Proliferation and Motility and Sensitizes Ovarian Cancer Cells to Paclitaxel Through miR-376c-3p/FOXO3 Axis.","authors":"Yingchun Zheng,&nbsp;Zhen Li,&nbsp;Shiying Yang,&nbsp;Yue Wang,&nbsp;Zhaohui Luan","doi":"10.1089/cbr.2020.3739","DOIUrl":"https://doi.org/10.1089/cbr.2020.3739","url":null,"abstract":"<p><p><b><i>Background:</i></b> Circular RNAs (circRNAs) are regarded as important regulators in the tumorigenesis of multiple cancers. However, the characterization of circRNA exocyst complex component 6B (circEXOC6B) in ovarian cancer is barely known. <b><i>Materials and Methods:</i></b> Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to detect the enrichment of circEXOC6B, microRNA-376c-3p (miR-376c-3p), and forkhead box O3 (FOXO3). Cell proliferation was examined by Cell Counting Kit-8 (CCK8) assay and colony formation assay. Cell metastasis was measured by transwell assays. Western blot assay was conducted to examine the expression of proliferation and metastasis-related proteins and FOXO3. The chemoresistance of ovarian cancer cells was analyzed by CCK8 assay. Flow cytometry was used to detect cell apoptosis. The activities of caspase3 and caspase9 were analyzed through using colorimetric assay kits. The direct interaction between miR-376c-3p and circEXOC6B or FOXO3 was predicted by StarBase software and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Murine xenograft assay was conducted to verify the role of circEXOC6B on the paclitaxel (PTX) resistance of ovarian cancer cells <i>in vivo</i>. <b><i>Results:</i></b> The level of circEXOC6B was notably decreased in ovarian cancer tissues. Low level of circEXOC6B was associated with malignant pathological characteristics in ovarian cancer patients. CircEXOC6B suppressed the proliferation and motility and decreased the chemoresistance of ovarian cancer cells to PTX. CircEXOC6B functioned through directly targeting and downregulating miR-376c-3p. FOXO3 was a direct target of miR-376c-3p, and the abundance of FOXO3 was regulated by circEXOC6B/miR-376c-3p axis. CircEXOC6B accelerated the PTX sensitivity of ovarian cancer cells through acting as a decoy of miR-376c-3p to upregulate FOXO3 <i>in vivo</i>. <b><i>Conclusion:</i></b> CircEXOC6B suppressed the progression and PTX resistance of ovarian cancer cells through sequestering miR-376c-3p, thus enhancing FOXO3 level.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"802-814"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2020.3739","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38446700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Potential Usefulness of ^99mTc-HYNIC-(Ser)₃-LTVPWY Peptide for Predicting HER2 Status Alteration After Chemotherapy in Ovarian Tumor-Bearing Mice.","authors":"Zahra Avan,&nbsp;Javad Biabani Ardakani,&nbsp;Fereshteh Talebpour Amiri,&nbsp;Seyed Mohammad Abedi,&nbsp;Seyed Jalal Hosseinimehr","doi":"10.1089/cbr.2020.4004","DOIUrl":"https://doi.org/10.1089/cbr.2020.4004","url":null,"abstract":"<p><p><b><i>Purpose:</i></b> The assessment of HER2 expression has a significant impact on optimizing cancer treatment protocol in patients. The aim of this study was to evaluate the potential usefulness of ^99mTc-HYNIC-(Ser)₃-LTVPWY peptide for detecting HER2 alteration after paclitaxel therapy of ovarian tumor xenografts in nude mice. <b><i>Materials and Methods:</i></b> Mice bearing SKOV-3 tumors were treated with paclitaxel and saline. The antitumor efficacy of paclitaxel was compared with the control group in tumor size and histopathological examinations. In biodistribution and imaging studies, the tumor uptakes of radiolabeled peptide were evaluated in mice-bearing ovarian tumors in both groups. The HER2 expressions in transplanted tumors were analyzed by immunohistochemistry (IHC). <b><i>Results:</i></b> Tumor size gradually increased in all mice during the treatment, whereas tumors had considerably faster growth in the saline group compared to those in the paclitaxel-treated mice. Paclitaxel could suppress ovarian tumor growth and prevent vascular and cell proliferation in the tumoral mass. Biodistribution and imaging results demonstrated nonsignificant radionuclide accumulations in transplanted tumors in the paclitaxel- and saline-treated groups. IHC staining confirmed the HER2 status that was similar in both groups. <b><i>Conclusions:</i></b> The response of HER2 status to paclitaxel in mice bearing HER2-expression tumors was profitably monitored by HER2 targeted ^99mTc-HYNIC-(Ser)₃-LTVPWY peptide that was agreement with IHC. The utilization of this radiolabeled peptide may be a valuable probe in evaluating HER2 status after chemotherapy.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"862-869"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2020.4004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38450723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-205 Promotes the Viability, Migration, and Tube Formation of Cervical Cancer Cells <i>In Vitro</i> by Targeting <i>GATA3</i>.","authors":"Hua Han,&nbsp;Xiaofeng Xu","doi":"10.1089/cbr.2020.4184","DOIUrl":"https://doi.org/10.1089/cbr.2020.4184","url":null,"abstract":"<p><p><b><i>Background:</i></b> Both microRNA (miR)-205 and GATA Binding Protein 3 (<i>GATA3</i>) were involved in cervical cancer (CC), yet their correlation remained poorly understood. The authors' study aimed to unveil their correlation in CC. <b><i>Materials and Methods:</i></b> Clinical cervical tissue samples were collected. Survival rates of CC patients with high or low miR-205 and <i>GATA3</i> expressions were analyzed using Kaplan-Meier curve. CC cell viability, migration, and tube formation were measured by cell counting kit-8 assay, scratch assay, and tube formation assay, respectively. The potential binding sites between miR-205 and <i>GATA3</i> were predicted by TargetScan, and confirmed with dual-luciferase reporter assay. Relative expressions of miR-205, <i>GATA3</i>, vascular endothelial growth factor, E-cadherin, N-cadherin, and vimentin were quantified with quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. <b><i>Results:</i></b> MiR-205 was increased, yet <i>GATA3</i> was decreased in CC, indicating that they were negatively correlated. Upregulating miR-205 increased miR-205 expression and CC cell viability and promoted migration and tube formation, yet decreased <i>GATA3</i> expression, while downregulating miR-205 exerted the opposite effects. <i>GATA3</i> was the target gene of miR-205, and reversed the effect of miR-205 on <i>GATA3</i> expression and cell viability, migration, and tube formation in CC cells by reversing the effects of miR-205 on migration- and tube formation-related protein expressions. <b><i>Conclusion:</i></b> MiR-205 promotes CC cell viability, migration, and tube formation <i>in vitro</i> by targeting <i>GATA3</i>, providing new evidence for the implication of miR-205 in CC and a possible therapeutic method for CC. Clinical Trial Registration number: ZLK-20181103-01.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"779-791"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25530949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of N6-Methyladenosine Methylation in the Progression of Endometrial Cancer.","authors":"Kewei Song,&nbsp;Hongxia Xu,&nbsp;Changhe Wang","doi":"10.1089/cbr.2020.3912","DOIUrl":"https://doi.org/10.1089/cbr.2020.3912","url":null,"abstract":"<p><p><b><i>Purpose:</i></b> N6-methyladenosine (m6A) methylation was the most abundant internal modification on messenger RNAs in eukaryotes. This study intended to explore the role of m6A methylation in endometrial cancer (EC). <b><i>Materials and Methods:</i></b> The m6A-sequencing data \"GSE93911\" of human EC were downloaded from Gene Expression Omnibus database. Hisat2 software and MACS2 were used to perform the alignment of reads and m6A methylation peak calling, and the peaks were annotated using Chipseeker. Then, differential m6A methylation peaks between normal and tumor samples were analyzed, followed by the functional enrichment analysis of the differentially methylated genes in promoter and 3' untranslated region (UTR) using Clusterprofiler. Based on the 450K methylated chip data, gene expression and clinical data in The Cancer Genome Atlas, the differentially methylated genes were verified, followed by Cox univariate/multivariate regression analysis and survival analysis. Finally, a risk prognosis model was constructed. <b><i>Results:</i></b> The m6A peak number was decreased in EC. The distribution of m6A peaks was highly enriched near transcriptional start site, in promoter, UTR, intron and exon, followed by distal intergenic. A total of 581 differentially methylated genes (361 hyper- and 220 hypomethylated genes) were identified in promoter and UTR regions that were enriched in insulin resistance (IR) and extracellular matrix (ECM). A total of 181 genes with significant differential expressions and differential methylation site in EC were selected. Of which, 31 genes were correlated with survival, and an 11-gene risk prognosis model was identified, including GDF7, BNC2, SLC8A1, B4GALNT3, DHCR24, ESRP1, HOXB9, IGSF9, KIAA1324, MSnX1, and PHGDH. <b><i>Conclusion:</i></b> The m6A methylation regulated EC progression by targeting the genes related to IR and ECM. A 11-gene risk prognosis model was identified to predict survival of patients with EC.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"737-749"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2020.3912","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38587978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0000745 Promotes the Progression of Cervical Cancer by Regulating miR-409-3p/ATF1 Axis.","authors":"Xia Cui,&nbsp;Jiming Chen,&nbsp;Yafeng Zheng,&nbsp;Huaji Shen","doi":"10.1089/cbr.2019.3392","DOIUrl":"https://doi.org/10.1089/cbr.2019.3392","url":null,"abstract":"<p><p><b><i>Background:</i></b> Cervical cancer (CC) is a common gynecological malignancy with a high risk of recurrence and death. Circular RNAs play a crucial role in the occurrence and development of tumors. This study aimed to investigate the function and mechanism of circ_0000745 in CC. <b><i>Materials and Methods:</i></b> The levels of circ_0000745, miR-409-3p, and activating transcription factor 1 (ATF1) were determined by quantitative real-time polymerase chain reaction or Western blot assay. Cell proliferation was assessed by colony formation assay. Cell migration and invasion were evaluated by transwell assay. Glycolysis was analyzed by measuring extracellular acidification rate, glucose uptake, and lactate production. Also, the protein levels of glucose transporter 1 and lactate dehydrogenase A were detected using Western blot. The relationship among circ_0000745, miR-409-3p, and ATF1 were confirmed by dual-luciferase reporter assay. Moreover, xenograft assay was performed to analyze tumor growth <i>in vivo</i>. <b><i>Results:</i></b> Circ_0000745 and ATF1 were upregulated, whereas miR-409-3p was downregulated in CC tissues and cells. Knockdown of circ_0000745 repressed proliferation, migration, invasion, and glycolysis of CC cells. Circ_0000745 regulated CC progression by targeting miR-409-3p. Circ_0000745 modulated ATF1 expression through sponging miR-409-3p. MiR-409-3p hindered CC progression by targeting ATF1. Furthermore, depletion of circ_0000745 impeded tumor growth <i>in vivo</i>. <b><i>Conclusion:</i></b> Circ_0000745 promoted the progression of CC through modulating miR-409-3p/ATF1 axis, indicating a promising biomarker for CC therapy.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"766-778"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2019.3392","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38141692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of Epithelial Splicing Regulatory Protein 1 in Metastatic Lesions of Serous Ovarian Carcinoma Correlates with Poor Patient Prognosis.","authors":"Xinxin Lu,&nbsp;Runzhou Li,&nbsp;Xingshuang Wang,&nbsp;Qixuan Guo,&nbsp;Ling Wang,&nbsp;Xin Zhou","doi":"10.1089/cbr.2021.0215","DOIUrl":"https://doi.org/10.1089/cbr.2021.0215","url":null,"abstract":"Background: Epithelial splicing regulatory proteins (ESRPs) can regulate alternative splicing of RNA and play roles in tumorigenesis and development of various malignancies. In this study, bioinformatic analyses and immunohistochemistry (IHC) were used to investigate the function of ESPRs in serous ovarian carcinoma (SOC) oncogenesis and metastasis. Materials and Methods: The mRNA levels of ESRPs were analyzed by Oncomine and gene expression profiling interactive analysis (GEPIA). Prognostic values of ESRPs were analyzed by GEPIA and the UALCAN website. Genetic variations of ESRPs were analyzed by cBioPortal. ESRP1 was selected for further research. The relationship between ESRP1 and immunoregulatory molecules was studied by using the TISIDB database. ESRP1 protein expression in OC was investigated via IHC assays. Results: ESRP1 and ESRP2 mRNA were significantly upregulated in SOC (p < 0.05). The prognostic value of ESRP1 mRNA in SOC was inconsistent, and ESRP2 mRNA level did not relate to prognosis for OC patients. The IHC results showed higher ESRP1 expression in OC tissues than in normal ovarian tissues (p = 0.002), and ESRP1 expression in metastatic lesions of OC patients was higher than in paired primary OC tissues (p = 0.035). The ESRP1 expression was related to FIGO stage, differentiation, and peritoneal metastasis (p = 0.016; 0.031; 0.038, respectively). The ESRP1 switch (the differential expression of ESRP1 between metastatic and primary tumor of ovarian carcinoma) was significantly associated with E-cadherin expression in metastatic OC tumors (p = 0.012). The ESRP1 expression in both metastasis and ESRP1 switch significantly correlated with poor prognosis of OC patients (p = 0.045; 0.038, respectively), and ESRP1 switch and FIGO stage were independent risk factors for OC patient prognosis (p = 0.033; 0.009, respectively). Conclusions: The ESRP1 may promote OC metastasis by promoting OC cell colonization via the mesenchymal-epithelial transition (MET) process. The ESRP1 expression in metastatic lesions of OC patients may be a biomarker for predicting prognosis and a potential therapeutic target in OC.","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"850-861"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39394937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}