| Expression pattern: |
DN |
| Associated gene: |
RNF180, SOCS5, HK2, PFKM, E-cadherin, Vimentin |
| Associated microRNA: |
hsa-miR-4299 |
| Biological function: |
Tumor-suppressive; inhibits proliferation and migration, promotes apoptosis, suppresses glycolysis, and reverses EMT, thereby attenuating cisplatin resistance in NSCLC. |
| Molecular mechanism: |
Bioinformatics suggests potential interaction with hsa-miR-4299 and downstream RNF180/SOCS5; authors propose a non-classical mechanism possibly stabilizing hsa-miR-4299 rather than classical miRNA sponging; direct binding not experimentally validated. |
| Biological pathway or process: |
glycolysis (inhibits); EMT (inhibits); proliferation (inhibits); migration (inhibits); apoptosis (promotes); drug resistance (inhibits) |
| Detected method: |
Q
S
|
| Validation methods: |
RNA-seq; RNase R Treatment; RT-qPCR; Clinical Sample Validation; Survival Analysis; Transfection; CCK8; Wound Healing Assay; Annexin V/PI Flow Cytometry; Western Blot; IHC (Immunohistochemistry); In Vivo Animal Model; Bioinformatics Analysis |
| Clinical significance: |
Low hsa_circ_0135681 expression is associated with poorer overall survival in NSCLC patients; proposed as a prognostic marker and potential diagnostic biomarker/therapeutic target. |
| Description: |
This study identifies hsa_circ_0135681 as significantly downregulated in NSCLC tissues and links its low expression to worse patient overall survival. Forced overexpression suppresses cisplatin-resistant NSCLC cell growth and migration while promoting apoptosis, and inhibits tumor growth in a xenograft model. Mechanistically, it reduces glycolysis (lower glucose consumption/lactate production and decreased HK2/PFKM) and inhibits EMT; a putative hsa-miR-4299-RNF180/SOCS5 regulatory network is proposed mainly from bioinformatics and expression changes. |
| Confidence score: |
0.7628 |