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Current Cancer Drug Targets

Editor-in-Chief

ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

Research Article

MALAT1 Promotes Tumorigenesis and Increases Cellular Sensitivity to Herceptin in HER2-positive Breast Cancer

Author(s): Chuansheng Yang, Hongbo Zhu, Yeru Tan, Renjie Zhu, Xiaoping Wu, Yuehua Li* and Cunchuan Wang*

Volume 21, Issue 10, 2021

Published on: 18 June, 2021

Page: [860 - 869] Pages: 10

DOI: 10.2174/1568009621666210618164300

Price: $65

Abstract

Background: The function of MALAT1, a long non-coding RNAs (lncRNA), in HER2- positive breast cancer remains largely unexplored.

Objectives: This study aimed to investigate the effect of MALAT1 on tumor development in HER2-positive breast cancer.

Methods: We detected MALAT1 expression in HER2-positive breast cancer cells and tissues, and analyzed the effects of MALAT1 on cell proliferation in HER2-positive breast cancer cells lines (BT-474 and SKBR3). A mouse xenograft model was established for detecting the function of MALAT1 in HER2-positive breast cancer.

Results and Discussion: As a result, MALAT1 was remarkably up-regulated in HER2-positive breast cancer both in cells and tissues. In addition, the silencing of MALAT1 inhibited the proliferation of HER2-positive breast cancer cells both in vitro and in vivo. Furthermore, knockdown of MALAT1 by shRNA down-regulated DNMT1, DNMT3a, and DNMT3b, while up-regulated BRCA1 and PTEN in HER2-positive breast cancer both in cell lines and mouse xenograft models.

Conclusion: In short, MALAT1 might be a potential biomarker and therapeutic target for HER2- positive breast cancer therapy.

Keywords: HER2-positive breast cancer, long non-coding RNA, MALAT1, DNMTs, tumorigenesis, herceptin resistance.

Graphical Abstract

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