Biomedical journal · 2020
LncRNA MALAT1 promotes breast cancer progression and doxorubicin resistance via regulating miR-570-3p.
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Yue Xin, Wu Wen-Ying, Dong Ma, Guo Meng
Аннотация
BACKGROUND: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA (lncRNA) that regulates disease progression in various types of cancers. The aim of this study was to explore the role of MALAT1 in breast cancer (BC) progression and doxorubicin resistance.
METHODS: Real-time polymerase chain reaction (RT-PCR) was used to determine the expression of MALAT1 in BC tissues and cells; MTT and Transwell assay were used to detect the proliferation, migration and invasion of BC cells, respectively; drug resistance test was performed to assess the sensitivity of BC cells to doxorubicin; dual-luciferase reporter gene assay was conducted to verify the interaction between MALAT1 and miR-570-3p.
RESULTS: MALAT1 was highly expressed in BC tissues compared with normal tissues adjacent to cancer as well as in BC cells. In addition, inhibition the expression of MALAT1 could significantly suppress the proliferation, migration and invasion of BC cells. Meanwhile, down-regulation of MALAT1 sensitized BC cells to doxorubicin. Moreover, bioinformatics analysis suggested that miR-570-3p was the potential downstream target of MALAT1. Dual-luciferase reporter gene assay confirmed that MALAT1 could directly target miR-570-3p. Additionally, miR-570-3p was lowly expressed in BC tissues and cells. Up-regulation of miR-570-3p not only significantly inhibited the proliferation, metastasis, and invasion of BC cells, but also increased the sensitivity of BC cells to doxorubicin.
CONCLUSION: MALAT1 functions as a novel oncogenic lncRNA in regulating the progression and doxorubicin resistance of BC by targeting miR-570-3p.
METHODS: Real-time polymerase chain reaction (RT-PCR) was used to determine the expression of MALAT1 in BC tissues and cells; MTT and Transwell assay were used to detect the proliferation, migration and invasion of BC cells, respectively; drug resistance test was performed to assess the sensitivity of BC cells to doxorubicin; dual-luciferase reporter gene assay was conducted to verify the interaction between MALAT1 and miR-570-3p.
RESULTS: MALAT1 was highly expressed in BC tissues compared with normal tissues adjacent to cancer as well as in BC cells. In addition, inhibition the expression of MALAT1 could significantly suppress the proliferation, migration and invasion of BC cells. Meanwhile, down-regulation of MALAT1 sensitized BC cells to doxorubicin. Moreover, bioinformatics analysis suggested that miR-570-3p was the potential downstream target of MALAT1. Dual-luciferase reporter gene assay confirmed that MALAT1 could directly target miR-570-3p. Additionally, miR-570-3p was lowly expressed in BC tissues and cells. Up-regulation of miR-570-3p not only significantly inhibited the proliferation, metastasis, and invasion of BC cells, but also increased the sensitivity of BC cells to doxorubicin.
CONCLUSION: MALAT1 functions as a novel oncogenic lncRNA in regulating the progression and doxorubicin resistance of BC by targeting miR-570-3p.