FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2901472288> ?p ?o ?g. }

• W2901472288 abstract "Metastasis is the primary cause of death in renal cell carcinoma (RCC). Loss of cell-to-cell adhesion, including tight junctions (TJs) is the initial step in the process of metastasis. Claudin-7 (CLDN7) is a major component of TJs. However, the clinical significance and its regulation of kidney tumorigenesis remain poorly understood.A total of 120 fresh clear cell RCC (ccRCC) specimens and 144 primary RCC and adjacent nonmalignant renal paraffin specimens were obtained from Department of Urology, Peking University First Hospital. Expression of CLDN7 in ccRCC tissues and cell lines were determined using bioinformatic data mining, quantitative real-time PCR (qRT-PCR), Western blotting and immunostaining. The clinical significance of CLDN7 expression and promoter DNA methylation status was analyzed in ccRCC patients from Peking University First Hospital and The Cancer Genome Atlas. Additionally, the methylation specific-PCR, bisulfite genomic sequencing and demethylation analysis of CLDN7 were performed. Biological functions of CLDN7 were investigated by examining cell proliferation using MTS assays and EdU incorporation assays, cell migration by in vitro wound healing assays and transwell migration assays, cell invasion by transwell invasion assays, and cell apoptosis by flow cytometry. Mouse model experiments were performed to confirm the effects of CLDN7 on tumor growth and metastasis in vivo. The molecular mechanism of CLDN7 function was investigated using gene-set enrichment analysis (GSEA) and high-throughput cDNA sequencing (RNA-Seq) and confirmed by qRT-PCR, Western blot and immunostaining in vitro and in vivo.Our findings revealed that CLDN7 is frequently downregulated via hypermethylation of its promoter in ccRCC. CLDN7 can help predict aggressive tumor status and poor prognosis in ccRCC patients. Interestingly, hypermethylation of the CLDN7 promoter was related to advanced ccRCC status and poor prognosis. Moreover, overexpression of CLDN7 induced cell apoptosis, suppressed proliferation, migration and invasion abilities of ccRCC cells both in vitro and in vivo. Additionally, GSEA and RNA-Seq results showed that CLDN7 had negative effects in cancer-associated signaling pathways and (epithelial-mesenchymal transition) EMT-related pathways. These results were validated by qRT-PCR, Western blot and immunostaining.We have demonstrated a previously undescribed role of CLDN7 as a ccRCC suppressor and suggest that loss of CLDN7 potentiates EMT and tumor progression. CLDN7 may serve as a functional tumor suppressor in tumor progression and a potential biomarker and target in patients with ccRCC." @default.
• W2901472288 created "2018-11-29" @default.
• W2901472288 creator A5015545772 @default.
• W2901472288 creator A5017371998 @default.
• W2901472288 creator A5032269255 @default.
• W2901472288 creator A5067301238 @default.
• W2901472288 creator A5071679893 @default.
• W2901472288 creator A5076246947 @default.
• W2901472288 creator A5078658507 @default.
• W2901472288 creator A5081938339 @default.
• W2901472288 creator A5085943063 @default.
• W2901472288 creator A5088309123 @default.
• W2901472288 date "2018-11-14" @default.
• W2901472288 modified "2023-10-17" @default.
• W2901472288 title "Downregulation of CLDN7 due to promoter hypermethylation is associated with human clear cell renal cell carcinoma progression and poor prognosis" @default.
• W2901472288 cites W1554042779 @default.
• W2901472288 cites W1847856285 @default.
• W2901472288 cites W1971460862 @default.
• W2901472288 cites W1977267259 @default.
• W2901472288 cites W1985544363 @default.
• W2901472288 cites W1992933063 @default.
• W2901472288 cites W1994242106 @default.
• W2901472288 cites W2028593825 @default.
• W2901472288 cites W2039021968 @default.
• W2901472288 cites W2041845183 @default.
• W2901472288 cites W2062572623 @default.
• W2901472288 cites W2070640824 @default.
• W2901472288 cites W2075304876 @default.
• W2901472288 cites W2083887116 @default.
• W2901472288 cites W2091882758 @default.
• W2901472288 cites W2096330673 @default.
• W2901472288 cites W2130737451 @default.
• W2901472288 cites W2145078624 @default.
• W2901472288 cites W2146364391 @default.
• W2901472288 cites W2155619409 @default.
• W2901472288 cites W2161609794 @default.
• W2901472288 cites W2164422245 @default.
• W2901472288 cites W2165798775 @default.
• W2901472288 cites W2283885217 @default.
• W2901472288 cites W2342466465 @default.
• W2901472288 cites W2409001986 @default.
• W2901472288 cites W2416081551 @default.
• W2901472288 cites W2478110905 @default.
• W2901472288 cites W2570618306 @default.
• W2901472288 cites W2614480329 @default.
• W2901472288 cites W2746233794 @default.
• W2901472288 cites W432417060 @default.
• W2901472288 doi "https://doi.org/10.1186/s13046-018-0924-y" @default.
• W2901472288 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6234584" @default.
• W2901472288 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30428910" @default.
• W2901472288 hasPublicationYear "2018" @default.
• W2901472288 type Work @default.
• W2901472288 sameAs 2901472288 @default.
• W2901472288 citedByCount "38" @default.
• W2901472288 countsByYear W29014722882019 @default.
• W2901472288 countsByYear W29014722882020 @default.
• W2901472288 countsByYear W29014722882021 @default.
• W2901472288 countsByYear W29014722882022 @default.
• W2901472288 countsByYear W29014722882023 @default.
• W2901472288 crossrefType "journal-article" @default.
• W2901472288 hasAuthorship W2901472288A5015545772 @default.
• W2901472288 hasAuthorship W2901472288A5017371998 @default.
• W2901472288 hasAuthorship W2901472288A5032269255 @default.
• W2901472288 hasAuthorship W2901472288A5067301238 @default.
• W2901472288 hasAuthorship W2901472288A5071679893 @default.
• W2901472288 hasAuthorship W2901472288A5076246947 @default.
• W2901472288 hasAuthorship W2901472288A5078658507 @default.
• W2901472288 hasAuthorship W2901472288A5081938339 @default.
• W2901472288 hasAuthorship W2901472288A5085943063 @default.
• W2901472288 hasAuthorship W2901472288A5088309123 @default.
• W2901472288 hasBestOaLocation W29014722881 @default.
• W2901472288 hasConcept C104317684 @default.
• W2901472288 hasConcept C121608353 @default.
• W2901472288 hasConcept C142724271 @default.
• W2901472288 hasConcept C150194340 @default.
• W2901472288 hasConcept C190727270 @default.
• W2901472288 hasConcept C2777472916 @default.
• W2901472288 hasConcept C2779013556 @default.
• W2901472288 hasConcept C2781278892 @default.
• W2901472288 hasConcept C29537977 @default.
• W2901472288 hasConcept C502942594 @default.
• W2901472288 hasConcept C54355233 @default.
• W2901472288 hasConcept C555283112 @default.
• W2901472288 hasConcept C71924100 @default.
• W2901472288 hasConcept C86803240 @default.
• W2901472288 hasConceptScore W2901472288C104317684 @default.
• W2901472288 hasConceptScore W2901472288C121608353 @default.
• W2901472288 hasConceptScore W2901472288C142724271 @default.
• W2901472288 hasConceptScore W2901472288C150194340 @default.
• W2901472288 hasConceptScore W2901472288C190727270 @default.
• W2901472288 hasConceptScore W2901472288C2777472916 @default.
• W2901472288 hasConceptScore W2901472288C2779013556 @default.
• W2901472288 hasConceptScore W2901472288C2781278892 @default.
• W2901472288 hasConceptScore W2901472288C29537977 @default.
• W2901472288 hasConceptScore W2901472288C502942594 @default.
• W2901472288 hasConceptScore W2901472288C54355233 @default.
• W2901472288 hasConceptScore W2901472288C555283112 @default.
• W2901472288 hasConceptScore W2901472288C71924100 @default.
• W2901472288 hasConceptScore W2901472288C86803240 @default.
• W2901472288 hasIssue "1" @default.

• next