| 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. |
| LncRNA DRAIC下调可通过靶向miR-223-3p增强人肝癌细胞HepG2的放疗敏感性 |
| 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 |
| DOI：10.1007/s10330-022-0584-4 |
| 中文关键词: LncRNA DRAIC;mir-223-3-p;hepato-cellular癌;辐射敏感度介质分类 |
| 英文关键词: the long noncoding RNA (lncRNA) DRAIC; miR-223-3p; hepatocellular carcinoma (HCC); radiosensitivity medium classification |
| 基金项目: |
| 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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| 中文摘要: |
| 摘要目的探讨LncRNA DRAIC对肝细胞癌(HCC)细胞增殖、凋亡及放射敏感性的影响及其分子机制。方法收集30例HCC患者的癌组织及相应癌旁组织，采用RT-QPCR检测LncRNA DRAIC和miR-223-3p的表达水平。将LncRNA DRAIC干扰载体和miR-223-3p过表达载体转染HepG2细胞。另外，Lnc DRAIC和miR-223-3p干扰载体共转染HepG2细胞。构建的细胞用4Gy射线照射。采用细胞集落形成法检测细胞的放射敏感性。MTT法检测HepG2细胞增殖抑制率。流式细胞术检测HepG2细胞凋亡情况。采用双荧光素酶报告基因法检测Lnc DRAIC和miR-223-3p的靶向调控。结果Lnc DRAIC在HCC组织中的表达水平高于癌旁组织，miR-223-3p的表达水平低于癌旁组织(P<0.05)。抑制Lnc DRAIC表达或过表达miR-223-3p可提高HepG2细胞的增殖抑制率和凋亡率(P<0.05)。照射后细胞存活率降低，细胞增殖抑制率和凋亡率升高(P<0.05)。Lnc DRAIC靶向调控miR-223-3p，干扰miR-223-3p表达，逆转了抑制LncRNA DRAIC表达对HepG2细胞增殖、凋亡和放射敏感性的影响。结论抑制LncRNA DRAIC表达可通过上调miR-223-3p抑制HepG2细胞增殖，促进细胞凋亡，增强细胞放射敏感性。 |
| 英文摘要: |
| 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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