1.Inhibition of K562 cell growth and tumor angiogenesis in nude mice by antisense VEGF(121) cDNA transfection.
Guorui RUAN ; Yanrong LIU ; Shanshan CHEN ; Yazheng QIN ; Jinlan LI ; Jiayu FU ; Hong YU ; Yan CHANG
Chinese Journal of Hematology 2002;23(4):179-182
OBJECTIVETo investigate the effect of antisense vascular endothelial growth factor (VEGF)(121) cDNA transfection on the growth of K562 cells in nude mice.
METHODSK562 cells transfected with the antisense (AS) or sense (S) VEGF(121) cDNA, and the vector (V, pcDNA3) alone were transplanted subcutaneously into nude mice and the growth of the transfected cells in vivo was investigated. The effects of transfected K562 cells on human bone marrow endothelial cells (BMEC) were analyzed by MTT assay, the microvessel density (MVD) in tumor mass by vWF immunohistochemistry stain.
RESULTSK562/V tumor grew more slowly [(207.5 +/- 192.9) mm(3) vs (445.0 +/- 150.9) mm(3), P < 0.05] and K562/S tumor more rapidly than K562/V tumor did [(1 174.6 +/- 508.7)/mm(3) vs (445.0 +/- 150.9) mm(3), P < 0.01]. K562/S cell culture supernatant was more strongly in promoting the proliferation of BMEC than K562/V supernatant did, but K562/AS supernatant resulted in a marked decrease of the promoting effect as compared with K562/V's. The MVDs in K562/AS, K562/S, and K562/V tumors were [(11.0 +/- 7.6)/0.72 mm(2) vs (50.8 +/- 11.7)/0.72 mm(2) vs (18.9 +/- 7.0)/0.72 mm(2)], respectively.
CONCLUSIONSAntisense VEGF(121) cDNA transfected K562 cells show growth retardation in transplanted nude mice, decrease of tumor MVD, and decrease of promoting BMEC proliferation capacity.
Animals ; Bone Marrow Cells ; cytology ; drug effects ; Cell Division ; genetics ; physiology ; Culture Media, Conditioned ; pharmacology ; DNA, Antisense ; genetics ; DNA, Complementary ; genetics ; Endothelial Growth Factors ; genetics ; physiology ; Endothelium, Vascular ; cytology ; drug effects ; Female ; Humans ; K562 Cells ; Lymphokines ; genetics ; physiology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms, Experimental ; blood supply ; genetics ; pathology ; Neovascularization, Pathologic ; genetics ; physiopathology ; Transfection ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
2. Prognostic significance of early assessment of minimal residual disease in acute myeloid leukemia with mutated NPM1 patients
Ting ZHAO ; Honghu ZHU ; Jing WANG ; Jinsong JIA ; Shenmiao YANG ; Hao JIANG ; Jin LU ; Huan CHEN ; Lanping XU ; Xiaohui ZHANG ; Bin JIANG ; Guorui RUAN ; Debing WANG ; Xiaojun HUANG ; Qian JIANG
Chinese Journal of Hematology 2017;38(1):10-16
Objective:
To explore prognostic significance of early assessment of minimal residual leukemia (MRD) in adult patients with
3.LRRC25 plays a key role in all-trans retinoic acid-induced granulocytic differentiation as a novel potential leukocyte differentiation antigen.
Weili LIU ; Ting LI ; Pingzhang WANG ; Wanchang LIU ; Fujun LIU ; Xiaoning MO ; Zhengyang LIU ; Quansheng SONG ; Ping LV ; Guorui RUAN ; Wenling HAN
Protein & Cell 2018;9(9):785-798
Leukocyte differentiation antigens (LDAs) play important roles in the immune system, by serving as surface markers and participating in multiple biological activities, such as recognizing pathogens, mediating membrane signals, interacting with other cells or systems, and regulating cell differentiation and activation. Data mining is a powerful tool used to identify novel LDAs from whole genome. LRRC25 (leucine rich repeat-containing 25) was predicted to have a role in the function of myeloid cells by a large-scale "omics" data analysis. Further experimental validation showed that LRRC25 is highly expressed in primary myeloid cells, such as granulocytes and monocytes, and lowly/intermediately expressed in B cells, but not in T cells and almost all NK cells. It was down-regulated in multiple acute myeloid leukemia (AML) cell lines and bone marrow cells of AML patients and up-regulated after all-trans retinoic acid (ATRA)-mediated granulocytic differentiation in AML cell lines and acute promyelocytic leukemia (APL; AML-M3, FAB classification) cells. Localization analysis showed that LRRC25 is a type I transmembrane molecule. Although ectopic LRRC25 did not promote spontaneous differentiation of NB4 cells, knockdown of LRRC25 by siRNA or shRNA and knockout of LRRC25 by the CRISPR-Cas9 system attenuated ATRA-induced terminal granulocytic differentiation, and restoration of LRRC25 in knockout cells could rescue ATRA-induced granulocytic differentiation. Therefore, LRRC25, a potential leukocyte differentiation antigen, is a key regulator of ATRA-induced granulocytic differentiation.
Antigens, Differentiation
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immunology
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metabolism
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Cell Differentiation
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drug effects
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Cell Line, Tumor
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Granulocytes
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cytology
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drug effects
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immunology
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metabolism
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Humans
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Leukocytes
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cytology
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drug effects
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immunology
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metabolism
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Membrane Proteins
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antagonists & inhibitors
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immunology
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metabolism
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RNA, Small Interfering
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pharmacology
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Tretinoin
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pharmacology