| 陈朝琴,薛治乾,李文霞.长链非编码 SNHG15靶向 miR-141对甲状腺癌细胞侵袭及凋亡的影响研究[J].安徽医药,2021,25(10):2075-2079. |
| 长链非编码 SNHG15靶向 miR-141对甲状腺癌细胞侵袭及凋亡的影响研究 |
| Effects of long-chain non-coding SNHG15 targeting miR-141 on invasion and apoptosis of thyroid cancer cells |
| |
| DOI：10.3969/j.issn.1009-6469.2021.10.039 |
| 中文关键词: 甲状腺肿瘤 RNA，长链非编码 RNA，小核仁 长链非编码核仁小 RNA宿主基因 15 微小 RNA-141 侵袭 凋亡 |
| 英文关键词: Thyroid neoplasms RNA,long noncoding RNA,small nucleolar LncRNA SNHG15 MicroRNA-141 Invasion Apoptosis |
| 基金项目: |
|
| 摘要点击次数: 1219 |
| 全文下载次数: 402 |
| 中文摘要: |
| 目的探讨长链非编码( lncRNA)核仁小 RNA宿主基因 15(SNHG15)靶向调节微小 RNA-141(miR-141)对甲状腺癌细胞侵袭、凋亡影响及机制。方法本研究起止时间为 2018年 10月至 2019年 5月，参照 Lipofectamine 2000说明将 SNHG15小干扰 RNA(siRNA)、 siRNA阴性对照( siRNA control)、 miR-141抑制剂( miR-141 inhibitor)或抑制剂阴性对照( inhibitor control)转染至甲状腺癌 FRO细胞，细胞随机分组空白对照(si-control)组、转染阴性对照( si-NC)组、转染 SNHG15 siRNA(si-SNHG15)组、染 SNHG15 siRNA和 inhibitor control(si-SNHG15+anti-control)组和转染 SNHG15 siRNA和 miR-141 inhibitor(si-SNHG15+anti转miR-141)组，转染 48 h，qRT-PCR检测 SNHG15和 miR-141 mRNA表达； Transwell小室及流式细胞术分别检测细胞侵袭能力及凋亡率；双荧光，素酶报告系统检测 SNHG15和 miR-141的靶向关系。 Western blotting检测上皮钙黏素( E-cadherin)、 B细胞淋巴瘤/白血病 -2(Bcl-2)和 Bcl-2相关 X蛋白( Bax)蛋白表达。结果与 si-control组比较， si-SNHG15组中 SNHG15 mRNA表达［( 1.000)比( 0.263±0.032)］明显降低，细胞侵袭能力［( 168.6±7.1)个比( 78.2±3.3)个］明显降低，凋亡率［( 4.31±0.42)%比(33.11±1.69)%］明显升高， E-cadherin［(0.105±0.011)比( 0.602±0.058)］和 Bax表达［(0.049±0.008)比( 0.263±0.028)］明显升高， Bcl-2表达［(0.587±0.063)比( 0.131±0.015)］明显降低(P<0.05)。 SNHG15与 miR-141存在靶向关系。与 si-SNHG15+anti-control组比较， si-SNHG15+anti-miR-141组细胞侵袭能力［(79.9±4.2)个比( 130.3±5.2)个］明显升高，凋亡率［(34.08±1.63)%比( 15.66± 0.87)%］降低， E-cadherin［( 0.641±0.062)比( 0.309±0.032)］和 Bax表达［( 0.282±0.030)比( 0.144±0.015)］明显降低， Bcl-2表达［( 0.138±0.017)比( 0.478±0.052)］明显升高( P<0.05)。结论 lncRNA SNHG15可靶向调节 miR-141影响甲状腺癌细胞侵袭和凋亡，机制与调节 E-cadherin、Bcl-2和 Bax表达有关。 |
| 英文摘要: |
| Objective To explore the effect of long-chain non-coding RNA (lncRNA) small nucleolar RNA host gene 15 (SNHG15) targeting miR-141 on invasion and apoptosis of thyroid cancer and its mechanism.Methods This research started from October 2018 and ended in May 2019. According to Lipofectamine 2000, SNHG15 small interfering RNA (siRNA), siRNA negative control (siRNAcontrol), miR-141 inhibitor (miR-141 inhibitor) or Inhibitor negative control (inhibitor control) was transfected into thyroid cancer FROcells. The cells were randomly assigned into blank control (si-control) group, transfection negative control (si-NC) group, transfection of SNHG15 siRNA (si-SNHG15) group, transfection of SNHG15 siRNA and inhibitor control (si-SNHG15+anti-control) group and transfection of SNHG15 siRNA and miR-141 inhibitor (si-SNHG15+anti-miR-141) group. Cells were transfected for 48 hours, and the expressions of SNHG15 and miR-141 were detected by qRT-PCR. The invasive ability and apoptotic rate of cells were detected by Transwell chamber and flow cytometry. The targeting relationship between SNHG15 and miR-141 was detected by double luciferase reporting system. Western blotting was used to detect the expressions of E-cadherin, B-cell lymphoma/leukemia-2 (Bcl-2) and Bcl-2 related X protein (Bax) proteins.Results In the si-SNHG15 group, by comparison with the si-control group, the expressions of SNHG15 mRNA [(1.000) vs (0.263±0.032)] and Bcl-2 [(0.587±0.063) vs (0.131±0.015)] and the cell invasion ability [(168.6±7.1) vs (78.2±3.3)] were significantly lower, , while the apoptotic rate [(4.31±0.42) % vs (33.11±1.69)%], and the expressions of E-cadherin [(0.105±0.011) vs (0.602±0.058)] and Bax [(0.049±0.008) vs ( 0.263±0.028)] were significantly higher (P<0.05). SNHG15 had a targeting relationship with miR-141. In the si-SNHG15+anti-miR-141 group, by comparison with the si-SNHG15+anti-control group, the cell invasion ability [(79.9±4.2) vs (130.3±5.2)] and Bcl-2 expression [(0.138±0.017) vs (0.478±0.052)] were significantly higher, while the apoptosis rate [(34.08± 1.63)% vs (15.66±0.87)%], and the expressions of E-cadherin [(0.641±0.062) vs (0.309±0.032)] and Bax [(0.282±0.030) vs (0.144±0.015)] were significantly lower (P<0.05).Conclusion lncRNA SNHG15 can target miR-141 to affect the invasion and apoptosis of thyroid cancer cells, and its mechanism is related to regulating the expressions of E-cadherin, Bcl-2 and Bax. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
