Assuntos
Imageamento Tridimensional , Laparoscopia , Humanos , Colo , Artérias , Laparoscopia/métodos , TomografiaAssuntos
Procedimentos Cirúrgicos do Sistema Digestório , Laparoscopia , Neoplasias Retais , Humanos , Procedimentos Cirúrgicos do Sistema Digestório/efeitos adversos , Laparoscopia/efeitos adversos , Anastomose Cirúrgica/efeitos adversos , Neoplasias Retais/cirurgia , Neoplasias Retais/complicações , Fístula Anastomótica/etiologia , Fístula Anastomótica/prevenção & controle , Fístula Anastomótica/cirurgia , Estudos Retrospectivos , Complicações Pós-Operatórias/etiologia , Complicações Pós-Operatórias/prevenção & controle , Complicações Pós-Operatórias/cirurgiaRESUMO
The great importance of long non-coding RNAs (lncRNAs) in tumorigenesis has been acknowledged gradually. LINC01857 is previously reported to be highly expressed in gastric cancer (GC), while the regulatory mechanism of LINC01857 in GC is largely unknown. In this study, we detected high expression of LINC01857 from the GC microarray GSE109476. Additionally, LINC01857 expression is remarkably upregulated in GC cell lines (AGS, MKN-45, HGC-27, and SGC-7901) compared with the normal gastric mucosal cell line GES-1. Functionally, LINC01857 knockdown suppressed the proliferation, migration, invasion, and epithelial-mesenchymal transformation (EMT) of GC cells, while LINC01857 overexpression promoted the proliferation, migration, invasion, and EMT of GC cells. Furthermore, our data demonstrate that LINC01857 targeted miR-4731-5p and subsequently increased the expression of HOXC6 in GC. Rescue experiments showed that miR-4731-5p inhibition and HOXC6 overexpression could reverse the biological behavior of GC cells induced by LINC01857 knockdown. In conclusion, we demonstrated that LINC01857 sponged miR-4731-5p to promote the expression of HOXC6 and eventually acts as an oncogene in GC.
Assuntos
MicroRNAs , Neoplasias Gástricas , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , Proteínas de Homeodomínio/metabolismo , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , Invasividade Neoplásica/genética , Neoplasias Gástricas/genéticaRESUMO
BACKGROUND lncRNA HCP5 plays a cancer-promoting role in a variety of cancers. This study was the first to explore the mechanism of HCP5 in gastric carcinoma (GC). MATERIAL AND METHODS The differences in HCP5 between GC patients and healthy people were revealed in the TCGA database. The expression of HCP5 in GC tissues and adjacent tissues was compared by qRT-PCR. At the same time, the clinic pathological features of the patients were counted. Starbase and luciferase assay predicted and verified that miR-27b-3p is a targeted miRNA for HCP5. The expression of HCP5 and miR-27b-3p in various GC cells was detected by qRT-PCR. Cell viability and metastasis in different treatment groups were assessed by use of Cell Couting Kit-8 assay and clone formation assay, wound-healing assay, and transwell assay. Finally, expression of epithelial-mesenchymal transition (EMT)-associated markers was detected by Western blot. RESULTS We found that HCP5 was overexpressed in GC tissues. Patients with higher expression of HCP5 had larger tumors, were more likely to have lymph node metastasis, and had higher TNM stage. HCP5 was overexpressed in GC cells, but this was reversed by miR-27b-3p. Silencing HCP5 inhibited GC cell viability and metastasis by downregulating Vimentin and N-cadherin and up-regulating E-cadherin, but this effect was partially reversed by miR-27b-3p inhibitor. CONCLUSIONS The effect of silencing HCP5 on repressing GC cells viability and metastasis by regulating EMT-associated markers can be partially reversed by miR-27b-3p inhibitor.