Proliferation, Metastasis, and Radiosensitivity of Nasopharyngeal Carcinoma Cells in the Expression and Effect of Kiwifruit Extract through the Regulation of miR-205-5p

Abstract

Background. Radix Actinidiae extract (RAE) has been shown to inhibit cancer in many studies, but its potential mechanism in nasopharyngeal cancer (NPC) progression remains unclear. Methods. NPC cells (SUNE1) were treated with different doses of RAE. For transfection, SUNE1 cells were transfected with the microRNA (miR)-205-5p inhibitor (anti-miR-205-5p) or mimic followed by treatment with 200 μg/mL RAE for 24 h. The MTT assay and colony formation assay were used to detect cell proliferation and radiosensitivity. The transwell assay was used to detect cell migration and invasion. The expression of miR-205-5p was detected by quantitative real-time PCR. The protein expression levels of matrix metalloproteinase-2 (MMP2) and matrix metalloproteinase-9 (MMP9) were detected by western blot analysis. Results. RAE inhibited NPC cell proliferation, migration, and invasion, while it enhanced radiosensitivity ( P < 0.05 ). Also, RAE treatment decreased miR-205-5p expression, as well as MMP2 and MMP9 protein levels ( P < 0.05 ). Anti-miR-205-5p transfection enhanced the effects of RAE on NPC cell proliferation, migration, invasion, and radiosensitivity ( P < 0.05 ), while miR-205-5p mimic transfection had an opposite effect ( P < 0.05 ). Conclusion. RAE might decrease miR-205-5p, thereby it inhibited NPC cell proliferation and metastasis and enhanced radiosensitivity.

Curcumin Increases Radiosensitivity of Radioresistant Nasopharyngeal Cancer

“…For instance, miR-29c [35], miR-22 [36], miR-142-3p [37], and PD-L1 [38] can predict the prognosis and tumor-free survival rate of NPC patients; miR-23a, DAKP1, GRP78, and 14-3-3 sigma can assess the sensitivity of radiotherapy [39]. Kiwi fruit extract has been found to regulate miR-205-5p, resulting in the modulation of proliferation, metastasis, and radiosensitivity of nasopharyngeal carcinoma cells [40]. Our study found that miR-205-5p and TP53INP1 were involved in curcumin-mediated effects on the biological functions of C6661-IR, and the former directly targeted the latter.…”