XCL1 mediated by activation of mTOR pathway can promote the proliferation of drug-resistant breast cancer cell

白玉盘; 杨小利; 欧周罗

doi:10.3969/j.issn.1007-3969.2014.10.010

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XCL1 mediated by activation of mTOR pathway can promote the proliferation of drug-resistant breast cancer cell

更新时间：2025-12-31

- XCL1 mediated by activation of mTOR pathway can promote the proliferation of drug-resistant breast cancer cell
- China Oncology Vol. 24, Issue 10, Pages: 770-776(2014)
- 作者机构：
  
  复旦大学附属肿瘤医院肿瘤研究所，复旦大学乳腺研究所，复旦大学上海医学院肿瘤学系,上海
- 作者简介：
- 基金信息：
- DOI：10.3969/j.issn.1007-3969.2014.10.010
  CLC：
- Published Online：12 November 2014，
  
  Published：12 November 2014
- 稿件说明：
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白玉盘,杨小利,欧周罗. mTOR信号通路介导产生XCL1可促进乳腺癌耐药细胞株的增殖[J]. 中国癌症杂志, 2014, 24(10): 770-776.

白玉盘, 杨小利, 欧周罗. XCL1 mediated by activation of mTOR pathway can promote the proliferation of drug-resistant breast cancer cell[J]. China Oncology, 2014, 24(10): 770-776.
白玉盘,杨小利,欧周罗. mTOR信号通路介导产生XCL1可促进乳腺癌耐药细胞株的增殖[J]. 中国癌症杂志, 2014, 24(10): 770-776. DOI： 10.3969/j.issn.1007-3969.2014.10.010.

白玉盘, 杨小利, 欧周罗. XCL1 mediated by activation of mTOR pathway can promote the proliferation of drug-resistant breast cancer cell[J]. China Oncology, 2014, 24(10): 770-776. DOI： 10.3969/j.issn.1007-3969.2014.10.010.

摘要

背景与目的：统计表明90%以上肿瘤患者的死亡与肿瘤耐药相关，而在乳腺癌中常见PI3K/Akt/mTOR信号通路的异常激活，以此通路为靶点的药物已成为乳腺癌治疗的研究热点。本研究主要分析C族趋化因子配基1(C chemokine ligand 1，XCL1)对乳腺癌耐药细胞增殖的影响及其产生机制。方法：建立吉西他滨耐药性人乳腺癌细胞系MDA-MB-231/Gem。采用CCK8检测MDA-MB-231和MDA-MB-231/Gem的增殖能力，RT-PCR、ELISA检测2株细胞株XCL1表达差异，Western blot检测mTOR的表达。结果：与MDA-MB-231相比，MDA-MB-231/Gem的增殖能力增强，XCL1在耐药细胞株表达增强。mTOR在耐药细胞株表达水平及磷酸化水平增强。在MDAMB-231中加入外源性XCL1 24 h后，细胞增殖能力增强。而在MDA-MB-231/Gem中加入抗XCL1抗体后，细胞增殖能力降低。mTOR抑制剂处理MDA-MB-231/Gem后，细胞增殖能力降低，XCL1产生减少。结论：趋化因子XCL1的分泌可促进乳腺癌耐药细胞的增殖并由mTOR信号通路介导产生。

Abstract

Background and purpose: More than 90% of cancer patients are incurable because of drug resistance. Activation of PI3K/Akt/mTOR signaling pathway in breast cancer

as a target for chemotherapy drugs has become a hot topic of breast cancer treatment. This study aimed to investigate the effect and mechanism of XCL1 on the proliferation of drug-resistant breast cancer cell

whether is related with the mTOR signaling pathway. Methods: Established gemcitabine-resistant breast cancer cell lines (MDA-MB-231/Gem). CCK8 to detect the proliferation of MDA-MB-231 and MDA-MB-231/Gem

RT-PCR and ELISA to determine the XCL1 expression level of the two cell lines

Western blot to detect the expression of mTOR. Results: Compared with MDA-MB-231

MDA-MB-231/Gem showed an enhanced proliferative capacity. The expression of XCL1 was increased in the resistant cell lines. Both of protein level and phosphorylation level of mTOR increased in drug-resistant cell lines. The MDA-MB-231 added exogenous XCL1 for 24 h

showed an enhanced cell proliferation. Adding anti-XCL1 antibodies in MDA-MB-231/Gem could reduce cell proliferation and treating MDA-MB-231/Gem with the mTOR inhibitor could also reduce cell proliferation

as well as the XCL1 expression level. Conclusion: XCL1 promotes the proliferation of drug-resistant breast cancer cells mediated by activation of the mTOR pathway.

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