Back to Search
Start Over
MALAT1 Promotes Tumorigenesis and Increases Cellular Sensitivity to Herceptin in HER2-positive Breast Cancer
- Source :
- Current Cancer Drug Targets. 21:860-869
- Publication Year :
- 2021
- Publisher :
- Bentham Science Publishers Ltd., 2021.
-
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 & 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.
- Subjects :
- Cancer Research
Carcinogenesis
Breast Neoplasms
medicine.disease_cause
Small hairpin RNA
Mice
Breast cancer
Cell Line, Tumor
Drug Discovery
medicine
Animals
Humans
PTEN
skin and connective tissue diseases
Cell Proliferation
Pharmacology
MALAT1
biology
Cell growth
business.industry
Trastuzumab
medicine.disease
Long non-coding RNA
Gene Expression Regulation, Neoplastic
MicroRNAs
Oncology
SKBR3
biology.protein
Cancer research
Female
RNA, Long Noncoding
business
Subjects
Details
- ISSN :
- 15680096
- Volume :
- 21
- Database :
- OpenAIRE
- Journal :
- Current Cancer Drug Targets
- Accession number :
- edsair.doi.dedup.....b24e797476df96018d3f0171da871279