Basic Information
LncRNA/CircRNA Name | LINC00173 |
Synonyms | NA |
Region | GRCh38_12:116533422-116536518 |
Ensemble | ENSG00000196668 |
Refseq | NR_027345 |
Classification Information
Regulatory Mechanism | Biological Function | Clinical Application | |||
---|---|---|---|---|---|
TF | Immune | Survival | |||
Enhancer | Apoptosis | Drug | Cisplatin | ||
Variant | Cell Growth | Circulating | |||
MiRNA | EMT | Metastasis | |||
Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
Cancer Name | small cell lung cancer |
ICD-0-3 | C56.9 |
Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP, etc. |
Sample | SCLC tissues, SCLC cell lines NCI-H69, NCI-H446, and the drugresistant H69AR, Cisplatin-resistant NCIH446DDP |
Expression Pattern | up-regulated |
Function Description | Linc00173 was highly expressed in SCLC chemoresistant cell lines, and promoted SCLC cells chemoresistance, proliferation, and migrationinvasion. Animal studies validated that Linc00173 induced tumor chemoresistance and growth of SCLC in vivo. Moreover, Linc00173 upregulated Etk through functioning as a competitive endogenous RNA (ceRNA) by sponging miRNA-218 and led to the upregulation of GSKIP and NDRG1, resulting in the translocation of ?-catenin. Importantly, expression analysis revealed that both Linc00173 and Etk were upregulated in SCLC patient samples and exhibiting positive Linc00173/Etk correlation. High expression of Linc00173 closely correlated with chemoresistance, extensive stage, and shorter survival in SCLC patients. Collectively, our study illustrated a Linc00173-mediated process that facilitated chemoresistance and progression in SCLC, which might provide treatment strategy against SCLC. |
Pubmed ID | 31477834 |
Year | 2019 |
Title | Linc00173 promotes chemoresistance and progression of small cell lung cancer by sponging miR-218 to regulate Etk expression |
External Links
Links for LINC00173 | GenBank HGNC NONCODE |
Links for small cell lung cancer | OMIM COSMIC |