Basic Information
LncRNA/CircRNA Name | circ_006100 |
Synonyms | |
Region | |
Ensemble | |
Refseq |
Classification Information
Regulatory Mechanism | Biological Function | Clinical Application | |||
---|---|---|---|---|---|
TF | Immune | Survival | |||
Enhancer | Apoptosis | apoptosis | Drug | ||
Variant | Cell Growth | Circulating | |||
MiRNA | EMT | Metastasis | |||
Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
Cancer Name | gastric cancer |
ICD-0-3 | C16 |
Methods | qRT-PCR , luciferase reporter assay , western blot , CCK?? assay , colony formation assay , hoechst staining , transwell assay , Immunohistochemistry |
Sample | GC tissues and adjacent non??umour tissues ,GC cell lines (KN??5, MGC??03, AGS and SGC??901) and human gastric epithelial cell line (GES????)? |
Expression Pattern | up-regulated |
Function Description | Patients with a high hsa_circ_006100 level or low miR-195 level had tumours with a high TNM stage, poor cellular differentiation and lymph node metastasis. miR-195 was targeted and inhibited by hsa_circ_006100. Overexpression of hsa_circ_006100 enhanced cellular viability and proliferation, while miR-195 suppressed hsa_circ_006100-enhanced cell growth and induced apoptosis in MGC-803 and AGS cells.Forced hsa_circ_006100 expression promoted the migration and invasion of MGC-803 and AGS cells, while those activities were inhibited by miR-195. Mechanistically, GPRC5A was predicted as a target of miR-195 and was upregulated in gastric cancer.In vivo studies showed that knockdown of hsa_circ_006100 delayed tumour growth, reduced PCNA expression and upregulated miR-195 and BCL-2 expression which was restored by miR-195 inhibition due to GPRC5A/EGFR signalling, and changed the EMT phenotype in vivo. |
Pubmed ID | 31318114 |
Year | 2019 |
Title | Elevated Levels of hsa_circ_006100 in Gastric Cancer Promote Cell Growth and Metastasis via miR-195/GPRC5A Signalling |
External Links
Links for circ_006100 | GenBank HGNC NONCODE |
Links for gastric cancer | OMIM COSMIC |