The novel role and function of LINC01235 in metastasis of gastric cancer cells by inducing epithelial-mesenchymal transition
| Autor: | Chun-Dong Zhang, Yong-Zhi Li, Dong-Qiu Dai, Cheng Zhang, Yu Liang, Kun-Zhe Wu, Jun-Peng Pei |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0106 biological sciences
Epithelial-Mesenchymal Transition Cell Biology medicine.disease_cause 01 natural sciences Metastasis 03 medical and health sciences Cell Movement Stomach Neoplasms Cell Line Tumor Genetics medicine Humans Gene silencing Neoplasm Invasiveness Epithelial–mesenchymal transition Cell Proliferation 030304 developmental biology 0303 health sciences Gene knockdown Cancer Prognosis medicine.disease Gene Expression Regulation Neoplastic medicine.anatomical_structure Cancer cell Cancer research RNA Long Noncoding Carcinogenesis 010606 plant biology & botany |
| Zdroj: | Genomics. 113:1504-1513 |
| ISSN: | 0888-7543 |
| Popis: | LncRNAs play a vital role in the tumorigenesis of gastric cancer (GC). This study determined that LINC01235 expression has greater fold changes by analyzing TCGA RNA-Seq data. The qRT-PCR assay confirmed that LINC01235 is significantly over-expressed in GC cells and tissues. Additionally, the overall survival analysis showed that patients with a higher LINC01235 expression had a poorer prognosis than those with a lower LINC01235 expression. Univariate Cox regression analysis indicated that high LINC01235 expression is positively correlated with poor prognosis. Moreover, LINC01235 was an independent poor prognostic marker for GC in multivariate Cox analysis. In vitro assays suggested that LINC01235 knockdown suppresses GC cell migration and invasion. GSEA revealed that high LINC01235 expression is strongly enriched in the EMT pathway. Western blotting results revealed that LINC01235 silencing decreases the expression of EMT-induced proteins. In conclusion, LINC01235 can promote GC cell metastasis via EMT and function as a prognostic biomarker. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect