Abstract
BackgroundAs indoleamine-2,3-dioxygenase 1 (IDO1) is critical in tumor immune escape, we determined to study the regulatory mechanism of miR-218 on IDO1 in cervical cancer.MethodsReal-time PCR (RT-qPCR) was carried out to measure the expression of miR-218. RT-qPCR and Western blot were performed to detect the expression of IDO1 in cervical cancer. Dual-luciferase reporter assay was used to determine the binding of miR-218 on the IDO1 3′UTR. Cell viability, apoptosis, and related factors were determined using cell counting kit-8 (CCK-8), Annexin-V/PI (propidium) assay, enzyme-linked immunosorbnent assay (ELISA), RT-qPCR, and Western blot assays after miR-218 mimics has been transfected to HeLa cervical cancer cells.ResultsMiR-218 was downregulated in cervical cancer. The expression of miR-218 was negatively correlated with IDO1 in cervical cancer tissues and cells. IDO1 is a direct target of miR-218. MiR-218 overexpression was found to inhibit cell viability and promoted apoptosis via activating the expression of Cleaved-Caspase-3 and to inhibit the expression of Survivin, immune factors (TGF-β, VEGF, IL-6, PGE2, COX-2), and JAK2/STAT3 pathway.ConclusionMiR-218 inhibits immune escape of cervical cancer cells by direct downregulating IDO1.
Highlights
As indoleamine-2,3-dioxygenase 1 (IDO1) is critical in tumor immune escape, we determined to study the regulatory mechanism of miR-218 on IDO1 in cervical cancer
The results demonstrated that miR-218 levels were largely downregulated in cervical cancer tissues and that the survival rate of patients in the miR-218 low-expression group was lower than that in the miR-218 high-expression group within 2 years (Fig. 1a, b)
The clinical pathological features were determined, and our results indicated that high IDO1 levels were correlated to advanced Federation of Gynecology and Obstetrics (FIGO) stages and low differentiated histological features of cervical cancer; it was not correlated with ages (Table 1)
Summary
As indoleamine-2,3-dioxygenase 1 (IDO1) is critical in tumor immune escape, we determined to study the regulatory mechanism of miR-218 on IDO1 in cervical cancer. Cervical cancer is one of the most common malignancies in the female reproductive system. Studies have shown that tumor occurrence is closely related to the immune system, which has immune surveillance functions [7, 8]. The immune system can recognize and eliminate “non-self” cells through immune mechanisms to resist the occurrence and development of tumors [9]. In some cases, via tumor immune escape process, malignant cells could result in occurrence, development, metastasis, and recurrence of tumors [10]. As the tumor grows, it can form a microenvironment that helps the tumor escape immune surveillance [11].
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