Cancer biotherapy & radiopharmaceuticals最新文献

{"title":"Tumor Forkhead Box Q1 Is Elevated, Correlates with Increased Tumor Size, International Federation of Gynecology and Obstetrics Stage but Worse Overall Survival in Epithelial Ovarian Cancer Patients.","authors":"Xiaoyi Wang,&nbsp;Xiaowu Zhu","doi":"10.1089/cbr.2020.4444","DOIUrl":"https://doi.org/10.1089/cbr.2020.4444","url":null,"abstract":"<p><p><b><i>Background:</i></b> Forkhead box Q1 (FOXQ1) regulates epithelial ovarian cancer (EOC) cell proliferation, migration, and invasion; however, its prognostic effect in EOC patients is unclear. This study assessed FOXQ1 expression in EOC patients by immunohistochemical (IHC) staining and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and to analyze its correlation with EOC patients' clinical features and prognosis. <b><i>Materials and Methods:</i></b> FOXQ1 protein level in tumor and adjacent tissues from 173 EOC patients who underwent resection was detected by IHC staining and further scored by a semiquantitative scoring method; meanwhile, FOXQ1 mRNA level in tumor and adjacent tissues from 105 out of 173 EOC patients (whose fresh-frozen tissues were available) was detected by RT-qPCR. Besides, EOC patients' clinical features and survival data were collected. <b><i>Results:</i></b> Both FOXQ1 protein (<i>n</i> = 173) and mRNA (<i>n</i> = 105) levels were increased in tumor tissues compared with adjacent tissues (both <i>p</i> < 0.001) in EOC patients. Meanwhile, tumor FOXQ1 protein level was positively correlated with tumor size (<i>p</i> = 0.005) and International Federation of Gynecology and Obstetrics (FIGO) stage (<i>p</i> = 0.037), while <i>FOXQ1</i> tumor mRNA level was only positively correlated with tumor size (<i>p</i> = 0.015) in EOC patients; however, they were not correlated with other clinical features such as histological subtypes, tumor differentiation, peritoneal cytology, and so on (all <i>p</i> > 0.05). Moreover, FOXQ1 protein (<i>p</i> = 0.030) and mRNA (<i>p</i> = 0.011) levels in tumors were both correlated with worse overall survival (OS) in EOC patients. <b><i>Conclusion:</i></b> FOXQ1 is elevated in tumor tissues, and its high tumor expression correlates with increased tumor size, elevated FIGO stage, and worse OS in EOC patients.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"837-842"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25512458","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":"Metformin Affects Paclitaxel Sensitivity of Ovarian Cancer Cells Through Autophagy Mediated by Long Noncoding RNASNHG7/miR-3127-5p Axis.","authors":"Ze Yu,&nbsp;Yuezhen Wang,&nbsp;Bin Wang,&nbsp;Junwei Zhai","doi":"10.1089/cbr.2019.3390","DOIUrl":"https://doi.org/10.1089/cbr.2019.3390","url":null,"abstract":"<p><p><b><i>Background</i>:</b> Ovarian cancer is the public health issue worldwide. Paclitaxel is a first-line chemotherapy drug for ovarian cancer, but paclitaxel resistance weakens the therapeutic effect. Metformin (Met) improved the paclitaxel sensitivity in a mouse model of ovarian cancer. However, the mechanism of Met on paclitaxel sensitivity is still unclear in ovarian cancer. <b><i>Materials and Methods</i>:</b> Cell viability, apoptosis, migration, and invasion were measured by Cell Counting Kit-8 (CCK8), flow cytometry, and transwell assays severally. The expression of long noncoding RNA (lncRNA) small nucleolar RNA host gene 7 (SNHG7) and microRNA-3127-5p (miR-3127-5p) were detected by real-time quantitative polymerase chain reaction. The protein levels of poly (ADP-ribose) polymerase, microtubule-associated protein 1 light chain 3 (LC3)-I, LC3-II, and Beclin 1 were examined by Western blot assay. RNA immunoprecipitation assay detected the relationship between SNHG7 and miR-3127-5p. Then, the binding correlation between SNHG7 and miR-3127-5p was predicted by starBase and verified by the dual-luciferase reporter. The effects of Met and SNHG7 on tumor growth were tested in ovarian cancer mice model. <b><i>Results</i>:</b> Met inhibited cell viability, migration, invasion, SNHG7 level, and autophagy and promoted apoptosis in paclitaxel-resistant ovarian cancer cells. Moreover, Met partly reversed SNHG7-mediated paclitaxel sensitivity and autophagy in ovarian cancer cells. SNHG7 directly bound to miR-3127-5p. Met abolished the promoting effect of SNHG7 overexpression on tumor growth and autophagy <i>in vivo</i>. <b><i>Conclusion</i>:</b> The authors' findings indicated that Met expedited paclitaxel sensitivity by regulating SNHG7/miR-3127-5p-mediated autophagy in ovarian cancer cells.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"792-801"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2019.3390","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38034635","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 Nuclear Enriched Autosomal Transcript 1 Facilitates Cell Proliferation, Migration Invasion, and Suppresses Apoptosis in Endometrial Cancer by Targeting MicroRNA-202-3p/T Cell Immunoglobulin and Mucin Domain 4 Axis.","authors":"Caiyan Xu,&nbsp;Jianjun Zhai,&nbsp;Yujing Fu","doi":"10.1089/cbr.2020.3902","DOIUrl":"https://doi.org/10.1089/cbr.2020.3902","url":null,"abstract":"<p><p><b><i>Background:</i></b> Endometrial cancer (EC) is an intractable gynecological cancer with increasing incidence and mortality worldwide. Accumulating studies indicated that long noncoding RNA nuclear enriched autosomal transcript 1 (<i>NEAT1</i>) was a novel oncogene implicated in a variety of cancers. However, whether <i>NEAT1</i> could accelerate cell growth in EC is unclear. <b><i>Materials and Methods:</i></b> <i>NEAT1</i>, microRNA (miR)-202-3p, and T cell immunoglobulin and mucin domain 4 (<i>TIMD4</i>) levels were detected by quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were examined by cell counting kit-8 and flow cytometry. Transwell assay was employed for the evaluation of cell migration and invasion. The relationship between miR-202-3p and <i>NEAT1</i> or <i>TIMD4</i> was determined by luciferase reporter system. TIMD4 protein expression was assessed by Western blot assay. <b><i>Results:</i></b> <i>NEAT1</i> was upregulated, whereas miR-202-3p was downregulated in EC tumors and cells. Depletion of <i>NEAT1</i> restrained EC cell proliferation, migration, invasion, and improved apoptosis. MiR-202-3p was targeted by <i>NEAT1</i> and could bind to <i>TIMD4</i>. Subsequently, it is observed that miR-202-3p inhibitor neutralized NEAT1 silencing mediated suppression on EC cell progression. Meanwhile, TIMD4 rescued miR-202-3p induced inhibition on cell progression in EC. Furthermore, it was obvious that <i>NEAT1</i> facilitated TIMD4 expression by absorbing miR-202-3p in EC. <b><i>Conclusions:</i></b> Upregulation of NEAT1 accelerated EC cell progression through sponging miR-202-3p to facilitate TIMD4 expression, providing potential novel treatment method for EC.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"815-823"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2020.3902","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38341101","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":"High APOBEC1 Complementation Factor Expression Positively Modulates the Proliferation, Invasion, and Migration of Endometrial Cancer Cells Through Regulating P53/P21 Signaling Pathway.","authors":"Qin Liu,&nbsp;Chun-Yan Chen,&nbsp;Gui-Lin Chen","doi":"10.1089/cbr.2020.3957","DOIUrl":"https://doi.org/10.1089/cbr.2020.3957","url":null,"abstract":"<p><p><b><i>Background:</i></b> APOBEC1 complementation factor (<i>A1CF</i>) is a component of the apolipoprotein-B messenger RNA editing complex that participates in various cellular processes and acts as an oncogene in many cancers. In this study, it was aimed to investigate the roles of <i>A1CF</i> and its potential mechanism in endometrial cancer (EC). <b><i>Materials and Methods:</i></b> Gene expression prolife was downloaded from The Cancer Genome Atlas database. Then Kaplan-Meier and Cox regression analyses were conducted to assess the prognostic value of <i>A1CF</i> in EC. Cell Counting Kit-8, plate clone formation, and transwell assays were used to estimate the functions of <i>A1CF</i> on the proliferation, invasion, and migration of EC cell. The gene set enrichment analysis was used to analyze the pathway that is enriched by <i>A1CF</i>, whereas quantitative real-time polymerase chain reaction and Western blot analyses were utilized to detect the mRNA and protein expression involved. <b><i>Results:</i></b> It was detected that the upregulated <i>A1CF</i> was enriched in P53/P21 signaling pathway and tightly associated with patients' age, stage, and death. Besides, high <i>A1CF</i> expression led to a shorter overall survival of patients and predicted a poor prognosis in EC. The overexpression of <i>A1CF</i> promoted the proliferation, invasion, and migration of EC cells, whereas the depletion of <i>A1CF</i> suppressed these processes. Moreover, P21 and P53 were reduced whereas cyclin D1 and proliferating cell nuclear antigen were induced along with the increasing of <i>A1CF</i>. However, the effects of silencing <i>A1CF</i> on these protein expressions were on the contrary. <b><i>Conclusion:</i></b> <i>A1CF</i> was highly expressed and closely related to the prognosis and progression of EC through the regulation of P53/P21 signaling pathway, providing a possible new therapy target site for EC.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"750-758"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2020.3957","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38282168","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 circRNA circFAT1 in Endometrial Cancer Cells Increases Their Stemness by Upregulating miR-21 Through Methylation.","authors":"Weiwei Wu,&nbsp;Jianqing Zhou,&nbsp;Yan Wu,&nbsp;Xuedong Tang,&nbsp;Weili Zhu","doi":"10.1089/cbr.2020.4506","DOIUrl":"https://doi.org/10.1089/cbr.2020.4506","url":null,"abstract":"<p><p><b><i>Background:</i></b> Circular (Circ)RNA circFAT1 play tumor-suppressive or oncogenic roles in different cancers. Microarray analysis observed altered expression of circFAT1 in endometrial cancer (EC) and its inverse correlation with miR-21. <b><i>Materials and Methods:</i></b> Expression of circFAT1 and miR-21 in EC and paired nontumor tissues collected from 62 EC patients was analyzed by quantitative reverse transcription PCR (RT-qPCR). An experiment was conducted to evaluate the expression and interaction between circFAT1 and miR-21, followed by RT-qPCR and methylation-specific PCR. The role of circFAT1 and miR-21 in regulating the stemness was assessed by cell stemness assay. Heml 1.0 software was used to show differential gene expression. ANOVA Tukey's test and Pearson's correlation coefficient was used. <b><i>Results:</i></b> CircFAT1 was upregulated in EC and positively correlated with miR-21 across EC tissues. In RL95-2 and HEC-1-A cells, overexpression of circFAT1 increased the expression levels of miR-21 and decreased the methylation of miR-21 gene, whereas overexpression of miR-21 did not alter the expression of circFAT1. Cell stemness analysis showed that overexpression of circFAT1 and miR-21 increased cell stemness, and miR-21 inhibition decreased cell stemness. Moreover, inhibitor of miR-21 suppressed the role of circFAT1. <b><i>Conclusions:</i></b> In conclusion, circFAT1 is upregulated in EC and it may increase cancer cell stemness by upregulating miR-21.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"843-849"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39226345","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":"PARP1 Is Targeted by miR-519a-3p and Promotes the Migration, Invasion, and Tube Formation of Ovarian Cancer Cells.","authors":"Hua Chang,&nbsp;Xue Zhang,&nbsp;Baixue Li,&nbsp;Xiangkai Meng","doi":"10.1089/cbr.2020.4394","DOIUrl":"https://doi.org/10.1089/cbr.2020.4394","url":null,"abstract":"Background: Poly ADP-ribose polymerase 1 (PARP1) has been discovered to be implicated in ovarian cancer (OC), but its interaction with microRNA (miR)-519a-3p remained poorly understood. This study aimed to uncover their roles and interactions in OC. Materials and Methods: Clinical tissue from OC patients and adjacent normal tissue were collected, and the survival rates of OC patients with high or low PARP1 expression were analyzed by Kaplan-Meier curve. After transfection, OC cell viability, migration, and tube formation were detected with cell counting kit-8 (CCK-8) assay, scratch assay, and tube formation assay, respectively. Target gene of miR-519a-3p and potential binding sites between them were predicted with TargetScan and confirmed using dual-luciferase reporter assay. Relative expressions of miR-519a-3p, PARP1, E-cadherin, N-cadherin, SNAIL, vascular endothelial growth factor (VEGF), and p53 were measured by quantitative real-time polymerase chain reaction and Western blot as needed. Results: PARP1 expression was upregulated in OC, which was related to poor prognosis of OC patients. Silencing PARP1 decreased PARP1 expression and suppressed viability, migration, invasion, and tube formation in OC cells, while overexpressed PARP1 did the opposite. PARP1 was the target gene of miR-519a-3p, and it reversed the effects of miR-519a-3p on the migration, invasion, and tube formation of OC cells by upregulating the expressions of PAR, PARP1, N-cadherin, SNAIL, and VEGF and downregulating those of E-cadherin and p53. Conclusion: PARP1, a target gene of miR-519a-3p, promoted the migration, invasion, and tube formation of OC cells, providing a possible therapeutic target for treatment of OC patients.","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"824-836"},"PeriodicalIF":3.4,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38915265","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":"A Risk Score System Based on the Methylation Levels of 15 RNAs in Breast Cancer.","authors":"Ying Sun,&nbsp;Rengui Wang","doi":"10.1089/cbr.2020.4074","DOIUrl":"https://doi.org/10.1089/cbr.2020.4074","url":null,"abstract":"<p><p><b><i>Background:</i></b> Breast cancer (BC) occurs in the epithelial tissues of the breast gland, which is the most common cancer in women. This study is implemented to construct a risk score system for BC. <b><i>Materials and Methods:</i></b> The methylation data of BC from The Cancer Genome Atlas database (the training set) and GSE37754 from Gene Expression Omnibus database (the validation set) were downloaded. The differentially methylated RNAs (DMRs) between BC and normal samples were screened by limma package, and the correlations between the expression levels and methylation levels of the DMRs were analyzed to calculate their Pearson correlation coefficients (PCCs) using the cor.test function. To build the risk score system, the optimal RNAs were identified by penalized package. Subsequently, the nomogram survival model was established using the rms package. The lncRNA-mRNA comethylation network was constructed by Cytoscape software, and then enrichment analysis was performed using DAVID tool. <b><i>Results:</i></b> From the 1170 DMRs between BC and normal samples, 800 DMRs with significant negative PCCs were screened. For building the risk score system, the 15 optimal RNAs were selected. Afterward, the nomogram survival model based on four independent clinical prognostic factors (including age, radiation therapy, tumor recurrence, and RS model status) was constructed. In the comethylation network, the long noncoding RNA (lncRNA) <i>PRNT</i> was comethylated with <i>FAM19A5</i> and <i>RBM24</i>. For the mRNAs in the comethylation network, angiogenesis and pathways in cancer were enriched. <b><i>Conclusion:</i></b> The risk score system and the nomogram survival model might be of great importance for the prognosis prediction of BC patients.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"697-707"},"PeriodicalIF":3.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25356932","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-146a Enhances the Sensitivity of Breast Cancer Cells to Paclitaxel by Downregulating IRAK1.","authors":"Yalun Li,&nbsp;Weilong Li,&nbsp;Jun Lin,&nbsp;Chunjing Lv,&nbsp;Guangdong Qiao","doi":"10.1089/cbr.2020.3873","DOIUrl":"https://doi.org/10.1089/cbr.2020.3873","url":null,"abstract":"<p><p><b><i>Objective:</i></b> To investigate the effect of miR-146a on the sensitivity of breast cancer cells to paclitaxel (PTX). <b><i>Materials and Methods:</i></b> The mRNA expressions of miR-146a in normal breast cancer cells, MCF-7, and PTX-resistant breast cancer cells, MCF-7/PTX, were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). MTS was used to analyze the cytotoxicity treated with different concentrations of PTX. Overexpressed and silenced cell lines of miR-146a and interleukin-1 receptor-associated kinase 1 (IRAK1) were constructed, respectively. Cells were treated with PTX and observed the changes of cell morphology. Proliferation was detected by clone formation assay. Invasion and migration were measured by transwell. RT-PCR was applied to detect the expression of IRAK1 gene. Dual luciferase report was performed to validate the target relationship between miR-146a and IRAK1. Salvage experiments were used to further verify the relationship between miR-146a and IRAK1. <b><i>Results:</i></b> PTX reduces the viability of MCF-7 and MCF-7/PTX cells in a dose-dependent manner. The IC₅₀ of PTX in MCF-7 cells was significantly lower compared with MCF-7/PTX cells (<i>p</i> < 0.05). Compared with MCF-7/PTX cells, the expression of miR-146a gene in MCF-7 cells was significantly increased, while the expression of IRAK1 gene was significantly reduced (<i>p</i> < 0.05). Cell proliferation, invasion, and migration were decreased after miR-146a overexpression or IRAK1 silencing. Whereas, miR-146a silencing and IRAK1 overexpression can increase cell proliferation, invasion, and migration ability. Salvage experiments further verify that IRAK1 can weaken the role of miR-146a. <b><i>Conclusion:</i></b> miR-146a can enhance the sensitivity of breast cancer cells to PTX; the mechanism may be related to the downregulation of IRAK1.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"624-635"},"PeriodicalIF":3.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2020.3873","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38661301","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 AFAP1-AS1 Knockdown Represses Cell Proliferation, Migration, and Induced Apoptosis in Breast Cancer by Downregulating <i>SEPT2</i> Via Sponging miR-497-5p.","authors":"Bo Cai,&nbsp;Xichao Wang,&nbsp;Qing'ao Bu,&nbsp;Peng Li,&nbsp;Qingze Xue,&nbsp;Jun Zhang,&nbsp;Pengpeng Ding,&nbsp;Diwen Sun","doi":"10.1089/cbr.2020.3688","DOIUrl":"https://doi.org/10.1089/cbr.2020.3688","url":null,"abstract":"<p><p><b><i>Background:</i></b> Long non-coding RNA actin filament-associated protein1-antisense RNA 1 (AFAP1-AS1) was confirmed to be associated with tumorigenesis. However, the role of AFAP1-AS1 in breast cancer was little known. <b><i>Materials and Methods:</i></b> Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the levels of AFAP1-AS1, microRNA-497-5p (miR-497-5p), and Septin 2 (<i>SEPT2</i>) in breast cancer tissues and cells. The cell proliferation, migration, and apoptosis were tested by Methylthiazolyldiphenyl-tetrazolium bromide (MTT), Transwell and Flow cytometry assays, respectively. The targeting relationship between genes was predicted by StarBase v.3.0 and confirmed by dual-luciferase reporter assay. Pearson's correlation coefficient was applied to examine the correlation between the two groups. SEPT2 protein expression was evaluated by Western blot. Xenograft models were established to investigate the role of AFAP1-AS1 knockdown <i>in vivo</i>. <b><i>Results:</i></b> AFAP1-AS1 was upregulated in breast cancer tissues and cells, and AFAP1-AS1 knockdown could hinder proliferation and migration of breast cancer cells, and contribute to cell apoptosis. MiR-497-5p, which was downregulated in breast cancer, was verified to be a target of AFAP1-AS1 and inversely correlated with AFAP1-AS1 expression. <i>SEPT2</i>, as a target gene of miR-497-5p, was negatively regulated by miR-497-5p and positively correlated with AFAP1-AS1 expression. Importantly, AFAP1-AS1 could upregulate <i>SEPT2</i> expression by sponging miR-497-5p, and modulate cell progression by regulation of the miR-497-5p/<i>SEPT2</i> axis in breast cancer. <b><i>Conclusion:</i></b> AFAP1-AS1 knockdown repressed the progression of breast cancer cells by sponging miR-497-5p and downregulating <i>SEPT2</i>.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"662-672"},"PeriodicalIF":3.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2020.3688","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38404672","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":"Coexpression Module Construction by Weighted Gene Coexpression Network Analysis and Identify Potential Prognostic Markers of Breast Cancer.","authors":"Yanyan Wang,&nbsp;Kang Cui,&nbsp;Mingzhi Zhu,&nbsp;Yuanting Gu","doi":"10.1089/cbr.2020.3821","DOIUrl":"https://doi.org/10.1089/cbr.2020.3821","url":null,"abstract":"<p><p><b><i>Background:</i></b> Breast cancer (BC) is a malignant tumor with the highest morbidity among women, disrupting millions of their lives worldwide each year. However, the molecular mechanisms underlying remain unclear. <b><i>Materials and Methods:</i></b> The RNA-Sequencing and clinical data of BC patients from The Cancer Genome Atlas (TCGA) database were analyzed by weighted gene coexpression network analysis (WGCNA). Additionally, coexpressed modules were used to detect their correlation with the clinical traits of BC. Next, nodes of the most significant coexpression modules were used for Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, mRNA-lncRNA coexpression network and survival analyses. <b><i>Results:</i></b> In total, 2056 differentially expressed mRNAs (DEmRNAs) and 297 differentially expressed lncRNAs (DElncRNAs) were identified and subjected to WGCNA analysis, and 12 coexpression modules were generated. The top five significant modules (turquoise, green, red, brown, and blue modules) were related to one or more clinical traits of BC. In particular, the turquoise and green modules were chosen for further analysis. Next, by lncRNA-mRNA coexpression analysis of the turquoise and green modules, 12 DEmRNAs and 2 DElncRNAs were identified as hub nodes. The lncRNA-associated mRNAs of the networks were commonly related to several cancer-related pathways. Moreover, these networks also revealed central roles for <i>RP11-389C8.2</i> and <i>TGFBR2</i> in the turquoise module and <i>MYLK</i>, <i>KIT</i>, and <i>RP11-394O4.5</i> in the green module. Furthermore, 16 DEmRNAs and 3 DElncRNAs in these two modules were significantly correlated with the overall survival of BC patients. <b><i>Conclusions:</i></b> The authors' study identified some prognostic biomarkers that might play important roles in the development and treatment of BC. In particular, lncRNAs <i>AC016995.3</i>, <i>RP1-193H18.2</i>, and <i>RP11-166D19.1</i> were novel biomarkers for BC.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"612-623"},"PeriodicalIF":3.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cbr.2020.3821","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38581306","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}