LINC02163 targeting miR-338-3p affects proliferation, invasion and migration of breast cancer cells

Jingchen ZHANG; Xin LI; Jiangtao LI; Haiping LI; Yanli CHEN; Bing NIU; Chuanchuan QI; Beibei YE

doi:10.19401/j.cnki.1007-3639.2022.09.009

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LINC02163 targeting miR-338-3p affects proliferation, invasion and migration of breast cancer cells

Article | 更新时间：2025-12-31

- LINC02163 targeting miR-338-3p affects proliferation, invasion and migration of breast cancer cells
- China Oncology Vol. 32, Issue 9, Pages: 818-826(2022)
- 作者机构：
  
  郑州人民医院乳腺科,河南郑州 450053
- 作者简介：
  
  ZHANG Jingchen
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2022.09.009
  CLC： R737.9
- Received：06 January 2022，
  
  Revised：2022-03-25，
  
  Published：30 September 2022
- 稿件说明：
移动端阅览
Jingchen ZHANG, Xin LI, Jiangtao LI, et al. LINC02163 targeting miR-338-3p affects proliferation, invasion and migration of breast cancer cells[J]. China Oncology, 2022, 32(9): 818-826.
DOI：

Jingchen ZHANG, Xin LI, Jiangtao LI, et al. LINC02163 targeting miR-338-3p affects proliferation, invasion and migration of breast cancer cells[J]. China Oncology, 2022, 32(9): 818-826. DOI： 10.19401/j.cnki.1007-3639.2022.09.009.

摘要

背景与目的：

长链非编码RNA（long non-coding RNA

lncRNA）已被发现在乳腺癌中失调

与肿瘤恶性行为密切相关。本研究旨在探究LINC02163靶向miR-338-3p对乳腺癌细胞增殖、侵袭及迁移的影响。

方法：

收集郑州人民医院2020年1月

#x02014;2021年9月收治的9例乳腺癌患者的乳腺癌组织及距其2 cm外的癌旁组织样本

通过实时荧光定量聚合酶链反应（real-time fluorescence quantitative polymerase chain reaction

RTFQ-PCR）检测组织样本、人正常乳腺上皮细胞系（MCF-10A）和乳腺癌细胞系（MCF-7、BT-20、MDA-MB-231、T47D）中LINC02163的表达。将MDA-MB-231分为control组、sh-NC组、sh-LINC02163组、sh-LINC02163+inhibitor-NC组和sh-LINC02163+miR-338-3p inhibitor组。采用MTT法、transwell实验及划痕实验分别检测MDA-MB-231细胞活力、侵袭及迁移能力。采用蛋白质印迹法（Western blot）检测MDA-MB-231细胞c-Myc、基质金属蛋白酶（matrix metalloproteinase

MMP）2、MMP9、E-钙粘素（E-cadherin）及N-钙粘素（N-cadherin）蛋白的表达。通过双荧光素酶报告基因实验分析LINC02163与miR-338-3p的靶向关系。采用体内成瘤实验检测BALB/c裸鼠肿瘤体积及重量。采用免疫组织化学法检测裸小鼠移植瘤组织的Ki-67增殖指数。

结果：

与癌旁组织相比

LINC02163在乳腺癌组织中的表达显著升高（

0.05）。与MCF-10A细胞相比

LINC02163在MCF-7、BT-20、MDA-MB-231及T47D细胞中的表达均显著升高

并且其在MDA-MB-231细胞中升高最为显著（

0.05）。与control组比

sh-LINC02163组LINC02163表达、细胞存活率、侵袭细胞数及迁移率、c-Myc、MMP2、MMP9、N-cadherin表达、肿瘤体积及重量、Ki-67增殖指数显著降低

miR-338-3p、E-cadherin表达显著升高（

0.05）。与sh-LINC02163组相比

sh-LINC02163+miR-338-3p inhibitor组LINC02163表达无显著变化（

0.05）

细胞存活率、侵袭细胞数及迁移率、c-Myc、MMP2、MMP9、N-cadherin表达、肿瘤体积及重量、Ki-67增殖指数显著增加

miR-338-3p、E-cadherin表达显著降低（

0.05）。在乳腺癌中LINC02163与miR-338-3p存在潜在的靶向关系。

结论：

沉默LINC02163表达通过促进miR-338-3p表达来抑制乳腺癌细胞增殖、侵袭及迁移。

Abstract

Background and purpose:

Long non-coding RNA (lncRNA) has been found to be dysregulated in breast cancer and is closely related to the malignant behavior of tumors. This study aimed to explore the effects of LINC02163 targeting miR-338-3p on the proliferation

invasion and migration of breast cancer cells.

Methods:

Breast cancer tissue samples and the adjacent tissue samples (2 cm to cancer tissue) were collected from 9 female breast cancer patients admitted to People

#x02019;s Hospital of Zhengzhou

from January 2020 to September 2021. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the expression of LINC02163 in tissue samples

human normal breast epithelial cell line (MCF-10A) and breast cancer cell lines (MCF-7

BT-20

MDA-MB-231

T47D). MDA-MB-231 was divided into control group

sh-NC group

sh-LINC02163 group

sh-LINC02163+inhibitor-NC group and sh-LINC02163+miR-338-3p inhibitor group. MTT method

transwell test and scratch test were used to detect the MDA-MB-231 cell viability

invasion and migration ability. Western blot was used to detect the protein expression of c-Myc

matrix metalloproteinase (MMP) 2

MMP9

E-cadherin and N-cadherin in MDA-MB-231 cells. Dual luciferase reporter gene was used to detect the targeting relationship between LINC02163 and miR-338-3p. In vivo tumor formation experiment was used to detect tumor volume and weight in nude mice. Immunohistochemical method was used to detect the Ki-67 proliferation index in tumor tissues of BALB/c nude mice.

Results:

Compared with adjacent tissues

the expression of LINC02163 in breast cancer tissues was significantly higher (

0.05). Compared with MCF-10A cells

the expression of LINC02163 in MCF-7

BT-20

MDA-MB-231 and T47D cells was significantly higher

and it increased most significantly in MDA-MB-231 cells (

0.05). Compared with the control group

the LINC02163 expression

cell survival rate

number of invasive cells

migration rate

expressions of c-Myc

MMP2

MMP9 and N-cadherin

tumor volume and weight

and Ki-67 proliferation index were significantly reduced in the sh-LINC02163 group

while the expressions of miR-338-3p and E-cadherin were significantly increased (

0.05). Compared with the sh-LINC02163 group

the expression of LINC02163 in the sh-LINC02163+miR-338-3p inhibitor group did not change significantly (

0.05)

the cell survival rate

number of invasive cells

migration rate

expressio

ns of c-Myc

MMP2

MMP9 and N-cadherin

tumor volume and weight

and Ki-67 proliferation index were significantly increased

while the expressions of miR-338-3p and E-cadherin were significantly reduced (

0.05). LINC02163 had a potential targeting relationship with miR-338-3p in breast cancer.

Conclusion:

Silencing the expression of LINC02163 can inhibit the proliferation

invasion and migration of breast cancer cells by promoting the expression of miR-338-3p.

关键词

Keywords

references

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