| [1] PubMed ID: | 30015867 |
| Disease Name: | Thyroid Carcinoma, Anaplastic |
| Sample: | ATC cell lines and tissues |
| Dysfunction Pattern: | interaction[miR-135a-mediated c-myc activation] |
| Validated Method: | Western Blot//CCK8//qRT-PCR//Luciferase Report Assay//Colony Formation Assay//Transwell Assay |
| Description: | The present study identified that the expression levels of UCA1, in ATC cell lines and tissues, were significantly upregulated compared with normal human thyroid cell line and adjacent non?cancerous tissues, respectively. In addition, using luciferase assays, it was confirmed that miR‑135a directly bound to UCA1 and the 3' untranslated region of c‑myc, and UCA1 competed with c‑myc for miR‑135a binding. miR‑135a inhibition may upregulate c‑myc expression, however, the upregulation of c‑myc may be partially reduced by short hairpin UCA1. |
| Causality: | Yes |
| Causal Description: | UCA1 knockdown significantly inhibited ATC cell viability, proliferation, migration and invasion and the expression level of c?myc proto?oncogene (c?myc) in vitro, and suppressed ATC tumor growth in vivo. |
| Clinical-realted Application: | |
| [2] PubMed ID: | 33486611 |
| Disease Name: | Thyroid Carcinoma, Anaplastic |
| Sample: | ATC tissues and cells |
| Dysfunction Pattern: | Interaction(miR-148a/PD-L1 pathway) |
| Validated Method: | In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//Luciferase Report Assay |
| Description: | UCA1 and PD-L1 expression levels were elevated in ATC tissues and cells. UCA1 negatively regulated the expression of miR-148a, and miR-148a targeted PD-L1 to down-regulate its expression. Besides, we found that UCA1 attenuated the killing effect of cytotoxic CD8 + T cells and reduced cytokine secretion through PD-L1 and miR-148a. |
| Causality: | Yes |
| Causal Description: | . Silencing UCA1 and PD-L1 enhanced the killing effect of cytotoxic CD8 + T cells on ATC cells. Finally, silencing UCA1 or PD-L1 in ATC cells restored the suppression of the killing effect of CD8 + T cells in vivo. |
| Clinical-realted Application: | |
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