| Shuyan Li,Jian Zhang,Zhengming Wang,Wenjun Li. Downregulated lncRNA DRAIC enhances the radiotherapy sensitivity of human HCC cell line HepG2 by targeting miR-223-3p. Oncol Transl Med, 2022, 8: 293-300. |
| Downregulated lncRNA DRAIC enhances the radiotherapy sensitivity of human HCC cell line HepG2 by targeting miR-223-3p |
| Received:June 22, 2022 Revised:January 12, 2023 |
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| KeyWord:the long noncoding RNA (lncRNA) DRAIC; miR-223-3p; hepatocellular carcinoma (HCC); radiosensitivity medium classification |
| Author Name | Affiliation | E-mail | | Shuyan Li | Department of Radiotherapy, PLA Rocket Force Characteristic Medical Center | queyun175837@163.com | | Jian Zhang | Department of Radiotherapy, PLA Rocket Force Characteristic Medical Center | | | Zhengming Wang | Department of Radiotherapy, PLA Rocket Force Characteristic Medical Center | | | Wenjun Li | Department of Radiotherapy, PLA Rocket Force Characteristic Medical Center | queyun175837@163.com |
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| Abstract: |
| Objective This study aims to investigate the effects of the long noncoding RNA (lncRNA) DRAIC on the
proliferation, apoptosis, and radiosensitivity of hepatocellular carcinoma (HCC) cells and the molecular
mechanisms involved.
Methods Cancer tissues and their corresponding adjacent tissues from 30 patients with HCC were
collected, and the expression levels of DRAIC and miR-223-3p were detected via RT-qPCR. DRAIC
interference and miR-223-3p overexpression vectors were transfected into HepG2 cells. In addition, DRAIC
and miR-223-3p interference vectors were co-transfected into HepG2 cells. The constructed cells were
irradiated at 4 Gy. Cell colony formation assay, MTT assay, and flow cytometry were performed to detect the
radiosensitivity, proliferation inhibition rate, and apoptosis rate of HepG2 cells, respectively. Dual luciferase
reporter gene assay was performed to detect the targeted regulation of DRAIC on miR-223-3p expression.
Results The expression level of DRAIC in HCC tissues was higher than that in paracancer tissues,
whereas the expression level of miR-223-3p was lower in HCC tissues than that in paracancer tissues
(P < 0.05). Inhibition of DRAIC expression or overexpression of miR-223-3p increased the proliferation
inhibition and apoptosis rates of HepG2 cells (P < 0.05). After irradiation, cell survival fraction decreased
and cell proliferation inhibition and apoptosis rates increased (P < 0.05). DRAIC targeted the regulation of
miR-223-3p expression, and interference of miR-223-3p expression reversed the effects of inhibiting DRAIC
expression on the proliferation, apoptosis, and radiosensitivity of HepG2 cells.
Conclusion Inhibition of DRAIC expression can inhibit the proliferation of HepG2 cells, promote cell
apoptosis, and enhance the radiosensitivity of cells via upregulation of miR-223-3p. |
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