MiRNA-34a overexpression inhibits multiple myeloma cancer stem cell growth in mice by suppressing TGIF2
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- 英文论文题名：MiRNA-34a overexpression inhibits multiple myeloma cancer stem cell growth in mice by suppressing TGIF2
- 论文作者：Songyan Wu ; Miao Li ; Fangfang Shi ; Di Wu ; Meng Pan ; Ning Gu ; Jun Dou
- 英文论文作者：Songyan Wu ; Miao Li ; Fangfang Shi ; Di Wu ; Meng Pan ; Ning Gu ; Jun Dou ; School of Medicine ; Southeast University ; Center of Blood-bank ; School of Biological Science & Medical Engineering ; Southeast University
- 年：2016
- 作者机构：School of Medicine,Southeast University;Center of Blood-bank;School of Biological Science & Medical Engineering,Southeast University;
- 英文论文关键词：Multiple myeloma ; miR-34a ; cancer stem cells ; transforming growth interaction factor 2
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R733.3
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：2
- 文件大小：386k
- 原文格式：D
- 会议级别：全国
摘要
Background: Hematological malignancy originated from B-cell line, multiple myeloma(MM), is a kind of plasma cellsin bone marrow hyperplasia and cause of osteoclast-mediated skeletal destruction disease. MiR-34 a plays an important epigenetic regulating role in malignant tumors and presents a therapeutic potential. Objective: In this study, we investigated the effects of overexpression of miR-34 a in MM cancer stem cells(CSCs) on tumor growth and bone lesions. Methods: miR-34 a expression in RPMI8226 cells and recombinant containing miR-34 a detected and constructed. Effects of miR-34 a on the abilities of proliferation, apoptotic resistance, and clonal formation were separately detected in the different cells by CCK8, soft agar, and flow cytometry assays CD138~-CD34~-MM CSCs were isolated fromRPMI 8226 cell line using magnetic activated cell sorting system according to surface CD molecules of human MM CSCs. Effects of upregulating the miR-34 a expression on the oncogenicity, bone mineral density and tumor formation times, tumor sizes, and tumor bearing mouse survival were respectively observed by subcutaneous injection of CD138~-CD34~-CSCs and different control cells in NOD/SCID mice. The expression of transforming growth interaction factor 2(TGIF2) was also analyzed in different cells and tissues by qPCR and Western blot assays. Results: miR-34 a overexpression inhibited proliferation, colony formation, and increased cell apoptosis in vitro. The apparent epigenetic modulation induced by miR-34 a overexpression was found no only in MM cells but also in CSC xenograft MM. Both bioinformatics prediction and dual-luciferase reporter assay showed that the TGIF2 is sufficient to confer miR-34 a regulation. The results of qRT-PCR and Western blot assays demonstrated that the expression of TGIF2 was significant decreased in tumor tissues from mice injected with miR-34a-MM CSCs. Conclusion: miR-34 a overexpression in MMCSCs significantly suppressed the tumorigenicity and lytic bone lesions in mouse model by inducing apoptosis and inhibiting TGIF2 expression.
Background: Hematological malignancy originated from B-cell line, multiple myeloma(MM), is a kind of plasma cellsin bone marrow hyperplasia and cause of osteoclast-mediated skeletal destruction disease. MiR-34 a plays an important epigenetic regulating role in malignant tumors and presents a therapeutic potential. Objective: In this study, we investigated the effects of overexpression of miR-34 a in MM cancer stem cells(CSCs) on tumor growth and bone lesions. Methods: miR-34 a expression in RPMI8226 cells and recombinant containing miR-34 a detected and constructed. Effects of miR-34 a on the abilities of proliferation, apoptotic resistance, and clonal formation were separately detected in the different cells by CCK8, soft agar, and flow cytometry assays CD138~-CD34~-MM CSCs were isolated from RPMI 8226 cell line using magnetic activated cell sorting system according to surface CD molecules of human MM CSCs. Effects of upregulating the miR-34 a expression on the oncogenicity, bone mineral density and tumor formation times, tumor sizes, and tumor bearing mouse survival were respectively observed by subcutaneous injection of CD138~-CD34~-CSCs and different control cells in NOD/SCID mice. The expression of transforming growth interaction factor 2(TGIF2) was also analyzed in different cells and tissues by q PCR and Western blot assays. Results: miR-34 a overexpression inhibited proliferation, colony formation, and increased cell apoptosis in vitro. The apparent epigenetic modulation induced by miR-34 a overexpression was found no only in MM cells but also in CSC xenograft MM. Both bioinformatics prediction and dual-luciferase reporter assay showed that the TGIF2 is sufficient to confer miR-34 a regulation. The results of qRT-PCR and Western blot assays demonstrated that the expression of TGIF2 was significant decreased in tumor tissues from mice injected with miR-34a-MM CSCs. Conclusion: miR-34 a overexpression in MMCSCs significantly suppressed the tumorigenicity and lytic bone lesions in mouse model by inducing apoptosis and inhibiting TGIF2 expression.
Background: Hematological malignancy originated from B-cell line, multiple myeloma(MM), is a kind of plasma cellsin bone marrow hyperplasia and cause of osteoclast-mediated skeletal destruction disease. MiR-34 a plays an important epigenetic regulating role in malignant tumors and presents a therapeutic potential. Objective: In this study, we investigated the effects of overexpression of miR-34 a in MM cancer stem cells(CSCs) on tumor growth and bone lesions. Methods: miR-34 a expression in RPMI8226 cells and recombinant containing miR-34 a detected and constructed. Effects of miR-34 a on the abilities of proliferation, apoptotic resistance, and clonal formation were separately detected in the different cells by CCK8, soft agar, and flow cytometry assays CD138~-CD34~-MM CSCs were isolated from RPMI 8226 cell line using magnetic activated cell sorting system according to surface CD molecules of human MM CSCs. Effects of upregulating the miR-34 a expression on the oncogenicity, bone mineral density and tumor formation times, tumor sizes, and tumor bearing mouse survival were respectively observed by subcutaneous injection of CD138~-CD34~-CSCs and different control cells in NOD/SCID mice. The expression of transforming growth interaction factor 2(TGIF2) was also analyzed in different cells and tissues by q PCR and Western blot assays. Results: miR-34 a overexpression inhibited proliferation, colony formation, and increased cell apoptosis in vitro. The apparent epigenetic modulation induced by miR-34 a overexpression was found no only in MM cells but also in CSC xenograft MM. Both bioinformatics prediction and dual-luciferase reporter assay showed that the TGIF2 is sufficient to confer miR-34 a regulation. The results of qRT-PCR and Western blot assays demonstrated that the expression of TGIF2 was significant decreased in tumor tissues from mice injected with miR-34a-MM CSCs. Conclusion: miR-34 a overexpression in MMCSCs significantly suppressed the tumorigenicity and lytic bone lesions in mouse model by inducing apoptosis and inhibiting TGIF2 expression.
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