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Upregulation of lncRNA ADAMTS9-AS2 promotes salivary adenoid cystic carcinoma (SACC) metastasis via miR-143-3p-mediated regulation of PI3K/Akt and MEK/Erk signaling

ABSTRACT: Upregulation of lncRNA ADAMTS9-AS2 promotes salivary adenoid cystic carcinoma (SACC) metastasis via miR-143-3p-mediated regulation of PI3K/Akt and MEK/Erk signaling

PROVIDER: PRJNA482556 | ENA |

REPOSITORIES: ENA

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Upregulation of lncRNA ADAMTS9-AS2 promotes salivary adenoid cystic carcinoma (SACC) metastasis via miR-143-3p-mediated regulation of PI3K/Akt and MEK/Erk signaling

Project description:Neurotropic infiltrative growth and distant metastasis are the main causes of death in salivary adenoid cystic carcinoma (SACC) patients. Long noncoding RNAs (lncRNAs) are involved in many human neoplasms, however their potential roles in SACC are unclear. In our study, we found that ADAMTS9-AS2 was significantly upregulated in SACC patients with metastasis and SACC -LM cells. Moreover, ADAMTS9-AS2 expression was closely associated with the prognosis and distant metastasis in SACC patients. Next, we found that c-myc could specifically bind to the promoter of ADAMTS9-AS2 and activated its transcription. Knockdown of ADAMTS9-AS2 significantly inhibited migration and invasion of SACC cells in vitro and distant lung metastasis in vivo. Furthermore, ADAMTS9-AS2 which mainly expressed in the cytoplasm shared miRNA response elements with ITGA6. Overexpression of ADAMTS9-AS2 competitively bound to miR-143-3p that inhibited ITGA6 from miRNA-mediated degradation, thus activated the activity of PI3K/Akt and MEK/Erk signaling and facilitated SACC metastasis. In summary, ADAMTS9-AS2 promotes migration and invasion in SACC by competing with miR-143-3p. This sheds a new insight into the regulation mechanism of ADAMTS9-AS2 and provides a possible application for the SACC treatment.

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Micronome profiling in 3 pairs of salivary adenoid cystic carcinoma(SACC) and the corresponding nomal salivary gland tissues

Project description:To screen miRNAs for potential NDRG2 regulation, we performed micronome profiling in 3 pairs of SACC samples and the corresponding normal salivary glands. The sequencing analysis generated approximately 1,000,000 clean reads per sample. All reads were mapped to annotated miRNAs in the miRBase database (version 22), whereas approximately 45% of the clean reads were mapped to mature miRNAs in the database. After applying a stringent filtering criterion to compare the results from SACC tumor tissue and the adjacent normal salivary glands (log2 fold change >1, FDR<0.05), we identified 176 dysregulated miRNAs.

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Upregulation of lncRNA ADAMTS9-AS2 Promotes Salivary Adenoid Cystic Carcinoma Metastasis via PI3K/Akt and MEK/Erk Signaling.

Project description:Neurotropic infiltrative growth and distant metastasis are the main causes of death in salivary adenoid cystic carcinoma (SACC) patients. Long noncoding RNAs (lncRNAs) are involved in many human neoplasms, however, their potential roles in SACC are unclear. In our study, we found that ADAM metallopeptidase with thrombospondin type 1 motif, 9 (ADAMTS9) antisense RNA 2 (ADAMTS9-AS2) was significantly upregulated in SACC patients with metastasis and SACC-lung metastasis (LM) cells. Moreover, ADAMTS9-AS2 expression was closely associated with the prognosis and distant metastasis in SACC patients. Next, we found that c-myc could specifically bind to the promoter of ADAMTS9-AS2 and activated its transcription. Knockdown of ADAMTS9-AS2 significantly inhibited migration and invasion of SACC cells in vitro and distant lung metastasis in vivo. Furthermore, ADAMTS9-AS2, which mainly expressed in the cytoplasm, shared microRNA (miRNA) response elements with Integrin α6 (ITGA6). Overexpression of ADAMTS9-AS2 competitively bound to miR-143-3p that inhibited ITGA6 from miRNA-mediated degradation, and thus it activated the activity of PI3K/Akt and MEK/Erk signaling and facilitated SACC metastasis. In summary, ADAMTS9-AS2 promotes migration and invasion in SACC by competing with miR-143-3p. This sheds a new insight into the regulation mechanism of ADAMTS9-AS2, and it provides a possible application for the SACC treatment.

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