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MALAT-1 is Associated with the Doxorubicin Resistance in U-2OS Osteosarcoma Cells
Chang Liu1,2, Xuesong Han1, Bo Li2
1Department of Orthopedics, The 900th Hospital of Joint Logistic Support Force, Fuzhou, Fujian Province, 350025, People's Republic of China.
Purpose:
Our study aimed to investigate the relationship between MALAT-1 (metastasis-associated lung adenocarcinoma transcript 1) expression and the chemotherapy drug resistance in osteosarcoma.
Methods:
The U-2OS osteosarcoma cell line was selected for the experiment. The cells were treated with methotrexate, doxorubicin, cisplatin, and ifosfamide, respectively. RT-PCR was applied to detect the MALAT-1 expression in cells. The doxorubicin-resistant cell line was constructed. The cells were divided into doxorubicin-sensitivity group (DS/shCtrl), doxorubicin-resistance group (DR/shCtrl) and shMALAT1-doxorubicin-resistance group (DR/shMALAT1). The colony formation assay and 5-ethynyl-2'-deoxyuridine (EdU) assay were used to detect cell proliferation. PI staining was used to detect the cell cycle. Transwell assay and wound healing assay were used to observe the migration and invasion ability. Annexin V-FITC assay was used to detect cell apoptosis. Western blot was used to detect the protein expression and potential mechanism. The impacts of MALAT-1 expression were verified in vivo.
Results:
The MALAT-1 was upregulated in the doxorubicin-resistant U-2OS osteosarcoma cells. Downregulating MALAT-1 in the doxorubicin-resistant cells inhibited the proliferation, migration, and invasiveness, increased the ratio of cells in the G0/G1 phase, promoted apoptosis. In the doxorubicin-resistant U-2OS cells, the extracellular regulated protein kinases (ERK) phosphorylation was declined, which could be reversed by downregulating MALAT-1. In vivo assay indicated that the growth of doxorubicin-resistant solid osteosarcoma could be suppressed by downregulating MALAT-1.
Conclusion:
Our study provides evidence that doxorubicin may upregulate MALAT-1 in osteosarcoma. Downregulating MALAT-1 in the doxorubicin resistance U-2OS cells could reverse the resistance and may improve chemotherapeutic efficiency. Some conclusions in previous literature may be one-sided.
Insights
Downregulating metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) in osteosarcoma cells reversed chemotherapy resistance. This finding suggests MALAT-1 as a potential therapeutic target to enhance drug efficacy in osteosarcoma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Osteosarcoma is a primary bone malignancy with limited treatment options.
- Chemotherapy resistance remains a significant challenge in improving patient outcomes for osteosarcoma.
Purpose of the Study:
- To investigate the role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) in chemotherapy drug resistance in osteosarcoma.
- To determine if targeting MALAT-1 can overcome resistance to common chemotherapeutic agents.
Main Methods:
- Utilized the U-2OS osteosarcoma cell line and treated with various chemotherapy drugs.
- Assessed MALAT-1 expression using RT-PCR and constructed doxorubicin-resistant cell lines.
- Evaluated cell proliferation, cell cycle, migration, invasion, and apoptosis after MALAT-1 downregulation.
- Confirmed findings in vivo to assess the therapeutic potential of targeting MALAT-1.
Main Results:
- Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) was found to be upregulated in doxorubicin-resistant osteosarcoma cells.
- Downregulating MALAT-1 inhibited proliferation, migration, and invasion while promoting apoptosis and G0/G1 phase arrest.
- Extracellular regulated protein kinases (ERK) phosphorylation was affected by MALAT-1 levels, with downregulation reversing resistance-associated declines.
- In vivo studies demonstrated that reducing MALAT-1 suppressed the growth of doxorubicin-resistant osteosarcoma.
Conclusions:
- Doxorubicin treatment may lead to the upregulation of MALAT-1 in osteosarcoma.
- Downregulating MALAT-1 can reverse doxorubicin resistance in osteosarcoma cells, potentially improving chemotherapeutic efficiency.
- Targeting MALAT-1 presents a promising strategy to overcome drug resistance and enhance treatment outcomes in osteosarcoma.
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