FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2000476637> ?p ?o ?g. }

• W2000476637 abstract "The human genome encodes many long non-coding RNAs (lncRNAs). However, their biological functions, molecular mechanisms, and the prognostic value associated with pancreatic ductal adenocarcinoma (PDAC) remain to be elucidated. Here, we identify a fundamental role for the lncRNA HOXA transcript at the distal tip (HOTTIP) in the progression and chemoresistance of PDAC. High-throughput microarrays were performed to detect the expression profiles of lncRNAs and messenger RNAs in eight human PDAC tissues and four pancreatic tissues. Quantitative real-time PCR was used to determine the levels of HOTTIP and HOXA13 transcripts in PDAC cell lines and 90 PDAC samples from patients. HPDE6 cells (immortalized human pancreatic ductal epithelial cells) and corresponding adjacent non-neoplastic tissues were used as controls, respectively. The functions of HOTTIP and HOXA13 in cell proliferation, invasion, and epithelial-mesenchymal transition were evaluated by targeted knockdown in vitro. CCK-8 assays, colony formation assays, and xenografts in nude mice were used to investigate whether targeted silencing of HOTTIP could sensitize pancreatic cancer cells to gemcitabine. Immunohistochemistry was performed to investigate the relationship between HOXA13 expression and patient outcome. Microarray analyses revealed that HOTTIP was one of the most significantly upregulated lncRNAs in PDAC tissues compared with pancreatic tissues. Quantitative PCR further verified that HOTTIP levels were increased in PDAC cell lines and patient samples compared with controls. Functionally, HOTTIP silencing resulted in proliferation arrest by altering cell-cycle progression, and impaired cell invasion by inhibiting epithelial-mesenchymal transition in pancreatic cancer. Additionally, inhibition of HOTTIP potentiated the antitumor effects of gemcitabine in vitro and in vivo. Furthermore, knockdown of HOXA13 by RNA interference (siHOXA13) revealed that HOTTIP promoted PDAC cell proliferation, invasion, and chemoresistance, at least partly through regulating HOXA13. Immunohistochemistry results revealed that higher HOXA13 expression was correlated with lymph node metastasis, poor histological differentiation, and decreased overall survival in PDAC patients. As a crucial tumor promoter, HOTTIP promotes cell proliferation, invasion, and chemoresistance by modulating HOXA13. Therefore, the HOTTIP/HOXA13 axis is a potential therapeutic target and molecular biomarker for PDAC." @default.
• W2000476637 created "2016-06-24" @default.
• W2000476637 creator A5001720031 @default.
• W2000476637 creator A5006195312 @default.
• W2000476637 creator A5007026706 @default.
• W2000476637 creator A5010769195 @default.
• W2000476637 creator A5016120039 @default.
• W2000476637 creator A5021966040 @default.
• W2000476637 creator A5023091772 @default.
• W2000476637 creator A5026966273 @default.
• W2000476637 creator A5027334447 @default.
• W2000476637 creator A5030692575 @default.
• W2000476637 creator A5044932847 @default.
• W2000476637 creator A5048664845 @default.
• W2000476637 creator A5050209085 @default.
• W2000476637 creator A5051815365 @default.
• W2000476637 creator A5056649068 @default.
• W2000476637 creator A5063329944 @default.
• W2000476637 creator A5080257042 @default.
• W2000476637 creator A5083505888 @default.
• W2000476637 date "2015-03-12" @default.
• W2000476637 modified "2023-10-14" @default.
• W2000476637 title "The long non-coding RNA HOTTIP promotes progression and gemcitabine resistance by regulating HOXA13 in pancreatic cancer" @default.
• W2000476637 cites W1931508686 @default.
• W2000476637 cites W1949135884 @default.
• W2000476637 cites W1970741980 @default.
• W2000476637 cites W1976149758 @default.
• W2000476637 cites W1980877070 @default.
• W2000476637 cites W1982434780 @default.
• W2000476637 cites W1985535740 @default.
• W2000476637 cites W1990956955 @default.
• W2000476637 cites W1994867502 @default.
• W2000476637 cites W1996994627 @default.
• W2000476637 cites W2009851083 @default.
• W2000476637 cites W2015704257 @default.
• W2000476637 cites W2016066165 @default.
• W2000476637 cites W2016112105 @default.
• W2000476637 cites W2030048096 @default.
• W2000476637 cites W2048249977 @default.
• W2000476637 cites W2051911149 @default.
• W2000476637 cites W2060772907 @default.
• W2000476637 cites W2071271349 @default.
• W2000476637 cites W2076458597 @default.
• W2000476637 cites W2077497255 @default.
• W2000476637 cites W2091161969 @default.
• W2000476637 cites W2093909277 @default.
• W2000476637 cites W2100932663 @default.
• W2000476637 cites W2107716254 @default.
• W2000476637 cites W2110957978 @default.
• W2000476637 cites W2112474929 @default.
• W2000476637 cites W2116236561 @default.
• W2000476637 cites W2124050695 @default.
• W2000476637 cites W2126820358 @default.
• W2000476637 cites W2140060911 @default.
• W2000476637 cites W2142344706 @default.
• W2000476637 cites W2143047857 @default.
• W2000476637 cites W2144137532 @default.
• W2000476637 cites W2146573461 @default.
• W2000476637 cites W2147835141 @default.
• W2000476637 cites W2147900600 @default.
• W2000476637 cites W2150098952 @default.
• W2000476637 cites W2150695488 @default.
• W2000476637 cites W2155637224 @default.
• W2000476637 cites W2157761630 @default.
• W2000476637 cites W2166884280 @default.
• W2000476637 cites W4247785462 @default.
• W2000476637 cites W2412697121 @default.
• W2000476637 doi "https://doi.org/10.1186/s12967-015-0442-z" @default.
• W2000476637 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4372045" @default.
• W2000476637 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25889214" @default.
• W2000476637 hasPublicationYear "2015" @default.
• W2000476637 type Work @default.
• W2000476637 sameAs 2000476637 @default.
• W2000476637 citedByCount "206" @default.
• W2000476637 countsByYear W20004766372015 @default.
• W2000476637 countsByYear W20004766372016 @default.
• W2000476637 countsByYear W20004766372017 @default.
• W2000476637 countsByYear W20004766372018 @default.
• W2000476637 countsByYear W20004766372019 @default.
• W2000476637 countsByYear W20004766372020 @default.
• W2000476637 countsByYear W20004766372021 @default.
• W2000476637 countsByYear W20004766372022 @default.
• W2000476637 countsByYear W20004766372023 @default.
• W2000476637 crossrefType "journal-article" @default.
• W2000476637 hasAuthorship W2000476637A5001720031 @default.
• W2000476637 hasAuthorship W2000476637A5006195312 @default.
• W2000476637 hasAuthorship W2000476637A5007026706 @default.
• W2000476637 hasAuthorship W2000476637A5010769195 @default.
• W2000476637 hasAuthorship W2000476637A5016120039 @default.
• W2000476637 hasAuthorship W2000476637A5021966040 @default.
• W2000476637 hasAuthorship W2000476637A5023091772 @default.
• W2000476637 hasAuthorship W2000476637A5026966273 @default.
• W2000476637 hasAuthorship W2000476637A5027334447 @default.
• W2000476637 hasAuthorship W2000476637A5030692575 @default.
• W2000476637 hasAuthorship W2000476637A5044932847 @default.
• W2000476637 hasAuthorship W2000476637A5048664845 @default.
• W2000476637 hasAuthorship W2000476637A5050209085 @default.
• W2000476637 hasAuthorship W2000476637A5051815365 @default.
• W2000476637 hasAuthorship W2000476637A5056649068 @default.
• W2000476637 hasAuthorship W2000476637A5063329944 @default.

• next