Title:MALAT1 Promotes Tumorigenesis and Increases Cellular Sensitivity to Herceptin in HER2-positive Breast Cancer
Volume: 21
Issue: 10
Author(s): Chuansheng Yang, Hongbo Zhu, Yeru Tan, Renjie Zhu, Xiaoping Wu, Yuehua Li*Cunchuan Wang*
Affiliation:
- The First Affiliated Hospital, University of South China, Hengyang 421001, Hunan Province,China
- The First Affiliated Hospital, Jinan University, Guangzhou 510632,China
Keywords:
HER2-positive breast cancer, long non-coding RNA, MALAT1, DNMTs, tumorigenesis, herceptin resistance.
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.