Cancer Biomarkers最新文献

筛选
英文 中文
Glioma stem cells remodel immunotolerant microenvironment in GBM and are associated with therapeutic advancements. 胶质瘤干细胞重塑了胶质瘤的免疫耐受微环境,并与治疗进展有关。
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-230486
Xifeng Fei, Jie Wu, Haiyan Tian, Dongyi Jiang, Hanchun Chen, Ke Yan, Yuan Wang, Yaodong Zhao, Hua Chen, Xiangtong Xie, Zhimin Wang, Wenyu Zhu, Qiang Huang
{"title":"Glioma stem cells remodel immunotolerant microenvironment in GBM and are associated with therapeutic advancements.","authors":"Xifeng Fei, Jie Wu, Haiyan Tian, Dongyi Jiang, Hanchun Chen, Ke Yan, Yuan Wang, Yaodong Zhao, Hua Chen, Xiangtong Xie, Zhimin Wang, Wenyu Zhu, Qiang Huang","doi":"10.3233/CBM-230486","DOIUrl":"10.3233/CBM-230486","url":null,"abstract":"<p><p>Glioma is the most common primary tumor of the central nervous system (CNS). Glioblastoma (GBM) is incurable with current treatment strategies. Additionally, the treatment of recurrent GBM (rGBM) is often referred to as terminal treatment, necessitating hospice-level care and management. The presence of the blood-brain barrier (BBB) gives GBM a more challenging or \"cold\" tumor microenvironment (TME) than that of other cancers and gloma stem cells (GSCs) play an important role in the TME remodeling, occurrence, development and recurrence of giloma. In this review, our primary focus will be on discussing the following topics: niche-associated GSCs and macrophages, new theories regarding GSC and TME involving pyroptosis and ferroptosis in GBM, metabolic adaptations of GSCs, the influence of the cold environment in GBM on immunotherapy, potential strategies to transform the cold GBM TME into a hot one, and the advancement of GBM immunotherapy and GBM models.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11492047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142141868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
KIF18A promotes cervical squamous cell carcinoma progression by activating the PI3K/AKT pathway through upregulation of CENPE. KIF18A 通过上调 CENPE 激活 PI3K/AKT 通路,从而促进宫颈鳞状细胞癌的进展。
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-240074
Fengyi Sun, Tiantian Zhao
{"title":"KIF18A promotes cervical squamous cell carcinoma progression by activating the PI3K/AKT pathway through upregulation of CENPE.","authors":"Fengyi Sun, Tiantian Zhao","doi":"10.3233/CBM-240074","DOIUrl":"10.3233/CBM-240074","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer is a prevalent malignancy that significantly contributes to morbidity and mortality rates among women in developing nations. Although the association of KIF18A with various cancers has been established, its role in cervical squamous cell carcinoma (CESC) remains elusive.</p><p><strong>Methods: </strong>The KIF18A impact on the progression of CESC and its underlying mechanism were investigated through comprehensive bioinformatics analysis utilizing publicly available datasets. The levels of KIF18A and CENPE were assessed in clinical CESC samples through western blotting and qRT-PCR. To discover the role and molecular pathways of KIF18A in CESC, a combination of experimental approaches, including wound-healing, flow cytometry, CCK-8, and Transwell assay, were employed.</p><p><strong>Results: </strong>Our results demonstrate a significant KIF18A expression upregulation in CESC tissues in contrast to healthy tissues. In vitro, KIF18A upregulation was found to enhance cell growth, migration, and invasion and activate the PI3K/AKT signaling pathway while concurrently suppressing apoptosis. Conversely, downregulating KIF18A exhibited contrasting effects. Mechanistically, we observed a positive significant connection between KIF18A and CENPE in CESC cells.</p><p><strong>Conclusion: </strong>KIF18A promotes tumor growth in CESC by modulating the PI3K/AKT signaling pathway through regulation of CENPE, making it a potential biomarker for diagnosis and prognosis as well as a therapeutic target.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11492023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142333424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Serum aspartate aminotransferase, a novel potential biomarker of prognosis in extranodal natural killer/T cell lymphoma, nasal type. 血清天冬氨酸氨基转移酶--鼻型结节外自然杀伤/T细胞淋巴瘤预后的潜在新型生物标志物
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-230068
Ningning Yao, Qing Hou, Yu Liang, Xin Cao, Bochen Sun, Lijuan Wei, Ruifang Sun, Jianzhong Cao
{"title":"Serum aspartate aminotransferase, a novel potential biomarker of prognosis in extranodal natural killer/T cell lymphoma, nasal type.","authors":"Ningning Yao, Qing Hou, Yu Liang, Xin Cao, Bochen Sun, Lijuan Wei, Ruifang Sun, Jianzhong Cao","doi":"10.3233/CBM-230068","DOIUrl":"10.3233/CBM-230068","url":null,"abstract":"<p><strong>Background: </strong>Aspartate aminotransferase (AST), an indicator of liver cell damage, was related to the prognosis of certain malignant tumors.</p><p><strong>Objective: </strong>This study examined the predictive value of AST in patients with extranodal natural killer/T cell lymphoma (ENKTL).</p><p><strong>Methods: </strong>We reviewed 183 cases diagnosed with ENKTL and selected 26 U/L as the optimum cut-off value of AST. We used the univariate and multivariate Cox regression to compare the different AST groups' overall survival (OS) and progression-free survival (PFS).</p><p><strong>Results: </strong>Prior to propensity score matching (PSM), Kaplan-Meier analysis showed that patients in the low AST subgroup had better OS and PFS than the high AST subgroup. Multivariate analysis revealed that AST was an independent indicator for prognosis. After PSM, the low AST subgroup maintained a significantly better OS and PFS than the high AST subgroup.</p><p><strong>Conclusion: </strong>AST might represent a significant prognostic marker for ENKTL patients.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11191476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138813954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
GINS2 promotes the progression of human HNSCC by altering RRM2 expression. GINS2 通过改变 RRM2 的表达促进人类 HNSCC 的发展。
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-230337
Tianxiang Wang, Luxi Qian, Pingchuan Zhang, Mingyu Du, Jing Wu, Fanyu Peng, Chengyun Yao, Rong Yin, Li Yin, Xia He
{"title":"GINS2 promotes the progression of human HNSCC by altering RRM2 expression.","authors":"Tianxiang Wang, Luxi Qian, Pingchuan Zhang, Mingyu Du, Jing Wu, Fanyu Peng, Chengyun Yao, Rong Yin, Li Yin, Xia He","doi":"10.3233/CBM-230337","DOIUrl":"10.3233/CBM-230337","url":null,"abstract":"<p><strong>Introduction: </strong>GINS2 exerts a carcinogenic effect in multiple human malignancies, while it is still unclear that the potential roles and underlying mechanisms of GINS2 in HNSCC.</p><p><strong>Methods: </strong>TCGA database was used to screen out genes with significant differences in expression in HNSCC. Immunohistochemistry and qRT-PCR were used to measure the expression of GINS2 in HNSCC tissues and cells. GINS2 was detected by qRT-PCR or western blot after knockdown or overexpression. Celigo cell counting, MTT, colony formation, and flow cytometric assay were used to check the ability of proliferation and apoptosis. Bioinformatics and microarray were used to screen out the downstream genes of GINS2.</p><p><strong>Results: </strong>GINS2 in HNSCC tissues and cells was up-regulated, which was correlated with poor prognosis. GINS2 gene expression was successfully inhibited and overexpressed in HNSCC cells. Knockdown of GINS2 could inhibit proliferation and increase apoptosis of cells. Meanwhile, overexpression of GINS2 could enhance cell proliferation and colony formation. Knockdown of RRM2 may inhibit HNSCC cell proliferation, while overexpression of RRM2 rescued the effect of reducing GINS2 expression.</p><p><strong>Conclusion: </strong>Our study reported the role of GINS2 in HNSCC for the first time. The results demonstrated that in HNSCC cells, GINS2 promoted proliferation and inhibited apoptosis via altering RRM2 expression. Therefore, GINS2 might play a carcinogen in HNSCC, and become a specific promising therapeutic target.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11307040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140190468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Circ_0049271 targets the miR-1197/PTRF axis to attenuate the malignancy of osteosarcoma. Circ_0049271靶向miR-1197/PTRF轴,减轻骨肉瘤的恶性程度。
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-230191
Yixin Wen, Feng Xu, Hui Zhang
{"title":"Circ_0049271 targets the miR-1197/PTRF axis to attenuate the malignancy of osteosarcoma.","authors":"Yixin Wen, Feng Xu, Hui Zhang","doi":"10.3233/CBM-230191","DOIUrl":"10.3233/CBM-230191","url":null,"abstract":"<p><strong>Background: </strong>Circular RNAs (circRNAs) perform key regulatory functions in osteosarcoma (OS) tumorigenesis. In this study, we aimed to explore the detailed action mechanisms of circ_0049271 in OS progression.</p><p><strong>Methods: </strong>Cell colony formation, cell counting kit-8, and transwell assays were performed to assess the proliferation and invasion of OS cells. Quantitative reverse transcription-polymerase chain reaction and western blotting were used to determine the expression levels of polymerase 1 and transcript release factor (PTRF), microRNA (miR)-1197, and circ_0049271 in OS cells. Furthermore, RNA immunoprecipitation and dual luciferase assays were conducted to explore the targeted relationships among PTRF, miR-1197, and circ_0049271. Finally, a tumor formation assay was conducted to determine the effects of circ_0049271 on in vivo tumor growth in mice.</p><p><strong>Results: </strong>High expression levels of miR-1197 and low levels of circ_0049271 and PTRF were observed in OS cells. circ _0049271 targeted miR-1197 to mediate PTRF expression. Moreover, the proliferation and invasion of OS cells were repressed by circ_0049271 or PTRF overexpression and increased by miR-1197 upregulation. Enforced circ_0049271 also impeded tumor growth in vivo. Upregulation of miR-1197 reversed the antitumor effects of circ_0049271 on OS progression in vitro; however, PTRF overexpression attenuated the cancer-promoting effects of miR-1197 on OS in vitro.</p><p><strong>Conclusions: </strong>Our findings revealed that circ_0049271 targeted the miR-1197/PTRF axis to attenuate the malignancy of OS, suggesting a potential target for its clinical treatment.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11321495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140869425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Regulation of cagA-Helicobacter on gastric PIM2 expression in gastric cancer. cagA-Helicobacter 对胃癌中胃 PIM2 表达的调控。
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-230351
Wenjuan Liang, Haiyan Wang, Lijuan Hong, Wenting Cao, Shuaiyin Chen, Rongguang Zhang
{"title":"Regulation of cagA-Helicobacter on gastric PIM2 expression in gastric cancer.","authors":"Wenjuan Liang, Haiyan Wang, Lijuan Hong, Wenting Cao, Shuaiyin Chen, Rongguang Zhang","doi":"10.3233/CBM-230351","DOIUrl":"10.3233/CBM-230351","url":null,"abstract":"<p><strong>Background: </strong>The association between infection with cagA-positive H. pylori and an elevated susceptibility to gastric cancer has been firmly established. PIM2 is known to be overexpressed in various types of cancers; however, the specific mechanism by which cagA influences the regulation of PIM2 expression in gastric cancer remains unidentified at present.</p><p><strong>Materials and methods: </strong>A mutant NCTC11637ΔcagA strain of H. pylori and the eukaryotic expression vector pcDNA-cagA were constructed for evaluating PIM2 expression levels in gastric cancer cells (HGC27, SGC7901, and AG) co-cultured with the NCTC11637 and NCTC11637ΔcagA strain, as well as pcDNA-cagA and the empty vector pcDNA3.1 (+).</p><p><strong>Results: </strong>Co-culturing gastric cancer cells with NCTC11637 significantly increased PIM2 expression levels (P< 0.001) compared to the negative control group. Additionally, the expression of PIM2 in cells co-cultured with NCTC11637 was higher than that co-cultured with NCTC11637ΔcagA (P< 0.001). Furthermore, successful construction of the eukaryotic expression vector pcDNA-cagA resulted in a significant increase in PIM2 mRNA expression levels after its transfection into gastric cancer cells compared to the control group after 48 hours.</p><p><strong>Conclusions: </strong>The findings indicate that H. pylori/cagA A could be one of the key factors in regulating PIM2 expression levels, potentially influencing the progression of H. pylori-related Gastric Cancer.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11491992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142333425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
HNRNPA2B1 induces cell proliferation and acts as biomarker in breast cancer. HNRNPA2B1 可诱导细胞增殖并作为乳腺癌的生物标志物。
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-230576
Yi Yang, Yi Zhang, Tongbao Feng, Chunfu Zhu
{"title":"HNRNPA2B1 induces cell proliferation and acts as biomarker in breast cancer.","authors":"Yi Yang, Yi Zhang, Tongbao Feng, Chunfu Zhu","doi":"10.3233/CBM-230576","DOIUrl":"10.3233/CBM-230576","url":null,"abstract":"<p><strong>Background: </strong>Numerous studies have shown that m6A plays an important regulatory role in the development of tumors. HNRNPA2B1, one of the m6A RNA methylation reading proteins, has been proven to be elevated in human cancers.</p><p><strong>Objective: </strong>In this study, we aimed to identify the role of HNRNPA2B1 in breast cancer.</p><p><strong>Methods: </strong>HNRNPA2B1 expression was investigated via RT-qPCR and TCGA database in breast cancer. Then, the function of HNRNPA2B1 on cancer cell was measured by CCK8 assays, colony formation and scratch assays. In addition, HNRNPA2B1 expression in BRCA was explored via the Wilcoxon signed-rank test, KruskalWallis test and logistic regression. The association with HNRNPA2B1 expression and survival were considered by KaplanMeier and Cox regression analyses. The biological function of HNRNPA2B1 was analyzed via gene set enrichment analysis (GSEA) and the cluster Profiler R software package.</p><p><strong>Results: </strong>We found that HNRNPA2B1 was highly expressed and induced cell proliferation and migration in breast cancer. Moreover, we observed HNRNPA2B1 induced tumor growth in vivo. In addition, we also found HNRNPA2B1 expression was associated with characteristics and prognosis in breast cancer patients.</p><p><strong>Conclusion: </strong>Our findings suggested that HNRNPA2B1 promoted tumor growth and could function as a new potential molecular marker in breast cancer.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11380248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142037849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
PRDM1 rs2185379, unlike BRCA1, is not a prognostic marker in patients with advanced ovarian cancer. PRDM1 rs2185379 与 BRCA1 不同,不是晚期卵巢癌患者的预后标志物。
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-230358
Klara Horackova, Michal Vocka, Sarka Lopatova, Petra Zemankova, Zdenek Kleibl, Jana Soukupova
{"title":"PRDM1 rs2185379, unlike BRCA1, is not a prognostic marker in patients with advanced ovarian cancer.","authors":"Klara Horackova, Michal Vocka, Sarka Lopatova, Petra Zemankova, Zdenek Kleibl, Jana Soukupova","doi":"10.3233/CBM-230358","DOIUrl":"10.3233/CBM-230358","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer (OC) is mostly diagnosed in advanced stages with high incidence-to-mortality rate. Nevertheless, some patients achieve long-term disease-free survival. However, the prognostic markers have not been well established.</p><p><strong>Objective: </strong>The primary objective of this study was to analyse the association of the suggested prognostic marker rs2185379 in PRDM1 with long-term survival in a large independent cohort of advanced OC patients.</p><p><strong>Methods: </strong>We genotyped 545 well-characterized advanced OC patients. All patients were tested for OC predisposition. The effect of PRDM1 rs2185379 and other monitored clinicopathological and genetic variables on survival were analysed.</p><p><strong>Results: </strong>The univariate analysis revealed no significant effect of PRDM1 rs2185379 on survival whereas significantly worse prognosis was observed in postmenopausal patients (HR = 2.49; 95%CI 1.90-3.26; p= 4.14 × 10 - 11) with mortality linearly increasing with age (HR = 1.05 per year; 95%CI 1.04-1.07; p= 2 × 10 - 6), in patients diagnosed with non-high-grade serous OC (HR = 0.44; 95%CI 0.32-0.60; p= 1.95 × 10 - 7) and in patients carrying a gBRCA1 pathogenic variant (HR = 0.65; 95%CI 0.48-0.87; p= 4.53 × 10 - 3). The multivariate analysis interrogating the effect of PRDM1 rs2185379 with other significant prognostic factors revealed marginal association of PRDM1 rs2185379 with worse survival in postmenopausal women (HR = 1.54; 95%CI 1.01-2.38; p= 0.046).</p><p><strong>Conclusions: </strong>Unlike age at diagnosis, OC histology or gBRCA1 status, rs2185379 in PRDM1 is unlikely a marker of long-term survival in patients with advance OC.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11321493/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140860745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
KLF5 inhibits the migration and invasion in cervical cancer cell lines by regulating SNAI1. KLF5 通过调节 SNAI1 抑制宫颈癌细胞株的迁移和侵袭。
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-230175
Xinjian Qu, Chang Xu, Wenbo Yang, Qianqian Li, Simei Tu, Chenghai Gao
{"title":"KLF5 inhibits the migration and invasion in cervical cancer cell lines by regulating SNAI1.","authors":"Xinjian Qu, Chang Xu, Wenbo Yang, Qianqian Li, Simei Tu, Chenghai Gao","doi":"10.3233/CBM-230175","DOIUrl":"10.3233/CBM-230175","url":null,"abstract":"<p><strong>Background: </strong>Epithelial-mesenchymal transition (EMT) is an important biological process by which malignant tumor cells to acquire migration and invasion abilities. This study explored the role of KLF5 in the EMT process of in cervical cancer cell lines.</p><p><strong>Objective: </strong>Krüpple-like factor 5 (KLF5) is a basic transcriptional factor that plays a key role in cell-cycle arrest and inhibition of apoptosis. However, the molecular mechanism by which KLF5 mediates the biological functions of cervical cancer cell lines has not been elucidated. Here, we focus on the potential function of ELF5 in regulating the EMT process in in vitro model of cervical cancer cell lines.</p><p><strong>Method: </strong>Western-blot and real-time quantitative PCR were used to detect the expression of EMT-related genes in HeLa cells. MTT assays, cell scratch and Transwell assays were used to assess HeLa cells proliferation and invasion capability. Using the bioinformatics tool JASPAR, we identified a high-scoring KLF5-like binding sequence in the SNAI1 gene promoter. Luciferase reporter assays was used to detect transcriptional activity for different SNAI1 promoter truncates.</p><p><strong>Result: </strong>After overexpressing the KLF5 gene in HeLa cells, KLF5 not only significantly inhibited the invasion and migration of HeLa cells, but also increased the expression of E-cadherin and decreased the expression of N-cadherin and MMP9. In addition, the mRNA expression of upstream regulators of E-cadherin, such as SNAI1, SLUG, ZEB1/2 and TWIST1 was also decreased. Furthermore, KLF5 inhibiting the expression of the SNAI1 gene via binding its promoter region, and the EMT of Hela cells was promoted after overexpression of the SNAI1 gene.</p><p><strong>Conclusion: </strong>These results indicate that KLF5 can downregulate the EMT process of HeLa cells by decreasing the expression of the SNAI1 gene, thereby inhibiting the migration and invasion of HeLa cervical cancer cells.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11191462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139466614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Identification of key genes and signalling pathways in clear cell renal cell carcinoma: An integrated bioinformatics approach. 鉴定透明细胞肾细胞癌的关键基因和信号通路:一种综合生物信息学方法。
IF 2.2 4区 医学
Cancer Biomarkers Pub Date : 2024-01-01 DOI: 10.3233/CBM-230271
Vinoth S, Satheeswaran Balasubramanian, Ekambaram Perumal, Kirankumar Santhakumar
{"title":"Identification of key genes and signalling pathways in clear cell renal cell carcinoma: An integrated bioinformatics approach.","authors":"Vinoth S, Satheeswaran Balasubramanian, Ekambaram Perumal, Kirankumar Santhakumar","doi":"10.3233/CBM-230271","DOIUrl":"10.3233/CBM-230271","url":null,"abstract":"<p><strong>Background: </strong>Clear cell Renal Cell Carcinoma (ccRCC) is one of the most prevalent types of kidney cancer. Unravelling the genes responsible for driving cellular changes and the transformation of cells in ccRCC pathogenesis is a complex process.</p><p><strong>Objective: </strong>In this study, twelve microarray ccRCC datasets were chosen from the gene expression omnibus (GEO) database and subjected to integrated analysis.</p><p><strong>Methods: </strong>Through GEO2R analysis, 179 common differentially expressed genes (DEGs) were identified among the datasets. The common DEGs were subjected to functional enrichment analysis using ToppFun followed by construction of protein-protein interaction network (PPIN) using Cytoscape. Clusters within the DEGs PPIN were identified using the Molecular Complex Detection (MCODE) Cytoscape plugin. To identify the hub genes, the centrality parameters degree, betweenness, and closeness scores were calculated for each DEGs in the PPIN. Additionally, Gene Expression Profiling Interactive Analysis (GEPIA) was utilized to validate the relative expression levels of hub genes in the normal and ccRCC tissues.</p><p><strong>Results: </strong>The common DEGs were highly enriched in Hypoxia-inducible factor (HIF) signalling and metabolic reprogramming pathways. VEGFA, CAV1, LOX, CCND1, PLG, EGF, SLC2A1, and ENO2 were identified as hub genes.</p><p><strong>Conclusion: </strong>Among 8 hub genes, only the expression levels of VEGFA, LOX, CCND1, and EGF showed a unique expression pattern exclusively in ccRCC on compared to other type of cancers.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11191544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140013815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信