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首页> 外文期刊>RSC Advances >Linc00472 suppresses breast cancer progression and enhances doxorubicin sensitivity through regulation of miR-141 and programmed cell death4
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Linc00472 suppresses breast cancer progression and enhances doxorubicin sensitivity through regulation of miR-141 and programmed cell death4

机译：LINC00472抑制乳腺癌进展，通过MIR-141的调节提高多柔比星敏感性，并编程细胞死亡4

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摘要

The existence of drug resistance strikingly hampers the therapy of many malignancies, including breast cancer. Long non-coding RNAs (LncRNAs) have been reported to participate in the regulation of various biological processes associated with cancer progression. Whereas, the role of linc00472 in breast cancer pathogenesis and doxorubicin (ADR) resistance have not been well elucidated. In the present study, it is found that linc00472 expression was decreased in breast cancer tissues and cells. Moreover, higher linc00472 expression was positively associated with favorable disease status and prognosis for breast cancer patients. Functional analyses revealed that linc00472 overexpression suppressed proliferation and invasion, facilitated apoptosis and enhanced ADR sensitivity in breast cancer cells. Mechanistic studies discovered that linc00472 acted as a competing endogenous RNA (ceRNA) of miR-141 to sequester miR-141 from its target mRNA PDCD4 (programmed cell death 4). Furthermore, the inhibition effect of linc00472 on breast cancer cell progression and ADR resistance could be partly abrogated by miR-141 up-regulation or PDCD4 knockdown. In vivo assays also demonstrated that linc00472 hindered tumor growth by suppressing miR-141 expression and enhancing PDCD4 expression. In conclusion, linc00472 blocked breast cancer progression and induced ADR sensitivity through regulation of miR-141 and PDCD4, highlighting a potential therapeutic strategy for breast cancer patients.
机译：耐药性引人注目地妨碍了许多恶性肿瘤的治疗，包括乳腺癌。据报道，长期非编码RNA（LNCRNA）参与与癌症进展相关的各种生物过程的调节。鉴于LINC00472在乳腺癌发病机制和多柔比星（ADR）抗性的作用并不良好阐明。在本研究中，发现乳腺癌组织和细胞中的LINC00472表达降低。此外，较高的LINC00472表达与乳腺癌患者的有利疾病状态和预后正相关。功能分析表明，LINC00472过表达抑制了抑制增殖和侵袭，促进凋亡和增强的乳腺癌细胞敏感性。机械研究发现，LINC00472用作MIR-141的竞争内源性RNA（Cerna），以从其靶mRNA PDCD4（编程的细胞死亡4）中解除miR-141。此外，MiR-141上调或PDCD4敲低可以部分消除LINC00472对乳腺癌细胞进展和ADR抗性的抑制作用。体内测定还证明，通过抑制miR-141表达和增强PDCD4表达，LINC00472阻碍了肿瘤生长。总之，LINC00472通过调节MIR-141和PDCD4阻断乳腺癌进展和诱导ADR敏感性，突出了乳腺癌患者的潜在治疗策略。

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  • 来源
    《RSC Advances》 |2018年第16期|共14页
  • 作者

    Lu Pengwei; Yang Xue; Yang Yunqing; Wang Fang; Li Lin; Gu Yuanting;

  • 作者单位

    Zhengzhou Univ Dept Breast Surg Affiliated Hosp 1 1 Jianshe East Rd Zhengzhou 450000 Henan Peoples R China;

    Zhengzhou Univ Dept Breast Surg Affiliated Hosp 1 1 Jianshe East Rd Zhengzhou 450000 Henan Peoples R China;

    Zhengzhou Univ Dept Breast Surg Affiliated Hosp 1 1 Jianshe East Rd Zhengzhou 450000 Henan Peoples R China;

    Zhengzhou Univ Dept Breast Surg Affiliated Hosp 1 1 Jianshe East Rd Zhengzhou 450000 Henan Peoples R China;

    Zhengzhou Univ Dept Breast Surg Affiliated Hosp 1 1 Jianshe East Rd Zhengzhou 450000 Henan Peoples R China;

    Zhengzhou Univ Dept Breast Surg Affiliated Hosp 1 1 Jianshe East Rd Zhengzhou 450000 Henan Peoples R China;

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  • 中图分类 化学;
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