Circular RNA hsa_circ_0011946 promotes the malignant process of salivary adenoid cystic carcinoma by downregulating miR‑1205 expression
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- Published online on: February 18, 2022 https://doi.org/10.3892/etm.2022.11224
- Article Number: 295
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Copyright: © Wei et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Circular RNA (circRNA/circ) hsa_circ_0011946 has been reported to serve an important role in a number of cancer types; however, to the best of our knowledge, its role in salivary adenoid cystic carcinoma (SACC) has not been reported. In the present study, the primary focus was the effects of hsa_circ_0011946 on the invasion, migration and epithelial‑mesenchymal transformation (EMT) of SACC cells, and the specific mechanisms involved. The expression levels of hsa_circ_0011946 and microRNA (miR)‑1205 in cancer tissues and paracancerous tissues of patients with SACC were analyzed using reverse transcription‑quantitative (RT‑q)PCR. The cell proliferation rate was determined using a Cell Counting Kit‑8 assay. Wound healing assays were performed to analyze the cell migratory ability, while a transwell assay was used to measure the cell invasion ability. Western blotting was used to analyze the expression levels of EMT‑related proteins. Cell transfection was used to knockdown hsa_circ_0011946 and knockdown or overexpress miR‑1205. Subcellular localization assays for hsa_circ_0011946 were performed using RT‑qPCR. A dual‑luciferase reporter gene assay was used to verify the binding between hsa_circ_0011946 and miR‑1205. The results of the present study revealed that the expression levels of hsa_circ_0011946 were significantly upregulated in cancer tissues from patients with SACC. The knockdown of hsa_circ_0011946 expression inhibited the proliferation, invasion and migration of SACC cells, thereby inhibiting the EMT process, which was achieved by downregulating miR‑1205 expression. In conclusion, circRNA hsa_circ_0011946 was discovered to promote the malignant process of SACC by downregulating miR‑1205 expression.
