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[Inhibitory effect of lentiviral vector-mediated SHIP gene transfection on proliferation of leukemia K562 cells and PI3K/Akt pathway regulation].
Ai Zheng. 2009 Apr; 28(4):366-72.AZ

Abstract

BACKGROUND AND OBJECTIVE

The hemopoietic-restricted Src homology 2-containing inositol 5'-phosphatase (SHIP) acts as a negative regulator for the proliferation and survival of hematopoietic cells by hydrolysing the phosphoinositide 3-kinase (PI3K)-generated second messenger, PtdIns(3,4,5)-P3 (PI-3,4,5-P3) to PtdIns(3,4)-P2 (PI-3,4-P2). This study was to investigate the biological function of SHIP gene in pathogenesis of leukemia cells by lentiviral vector-mediated SHIP transfection.

METHODS

Ectopic SHIP gene was transfected into leukemia K562 cells by the mediation of lentiviral vector. The mRNA level of SHIP was detected by fluorescent quantitative reverse transcription-polymerase chain reaction (FQ-PCR). The expression of SHIP, Akt, and phosphorylated Akt (p-Akt) was detected by Western blot. The proliferation and morphology of K562 cells before and after SHIP gene transfection were compared.

RESULTS

The proliferation of K562 cells was inhibited after transfection: the proliferation inhibition rate was increased from (9.9+/-1.5)% on Day 3 to (40.6+/-2.3)% on Day 5. K562 cells were SHIP-negative but expressed high level of p-Akt which was down-regulated from 0.533 to 0.245 (P<0.01) after SHIP transfection. Apoptotic characteristics were showed in K562 cells after SHIP transfection. The early apoptosis rate was significantly higher in K562-wtSHIP-FIV-G cells than in K562-FIV-G cells and untransfected K562 cells [(38.3+/-4.3)% vs. (8.2+/-0.9)% and (7.7+/-0.8)%, P<0.05].

CONCLUSIONS

SHIP gene can inhibit cell proliferation and promote cell apoptosis via inactivating PI3K/Akt pathway. Loss of SHIP might activate PI3K/Akt pathway and promote the proliferation of K562 cells.

Authors+Show Affiliations

Department of Hematology, The Second Affiliated Hospital, Hebei Midical University, Shijiazhuang, Hebei, 050000, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

19622295

Citation

Yang, Lin, et al. "[Inhibitory Effect of Lentiviral Vector-mediated SHIP Gene Transfection On Proliferation of Leukemia K562 Cells and PI3K/Akt Pathway Regulation]." Ai Zheng = Aizheng = Chinese Journal of Cancer, vol. 28, no. 4, 2009, pp. 366-72.
Yang L, Luo JM, Liu XJ, et al. [Inhibitory effect of lentiviral vector-mediated SHIP gene transfection on proliferation of leukemia K562 cells and PI3K/Akt pathway regulation]. Ai Zheng. 2009;28(4):366-72.
Yang, L., Luo, J. M., Liu, X. J., Wen, S. P., Du, X. Y., & Yao, L. (2009). [Inhibitory effect of lentiviral vector-mediated SHIP gene transfection on proliferation of leukemia K562 cells and PI3K/Akt pathway regulation]. Ai Zheng = Aizheng = Chinese Journal of Cancer, 28(4), 366-72.
Yang L, et al. [Inhibitory Effect of Lentiviral Vector-mediated SHIP Gene Transfection On Proliferation of Leukemia K562 Cells and PI3K/Akt Pathway Regulation]. Ai Zheng. 2009;28(4):366-72. PubMed PMID: 19622295.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Inhibitory effect of lentiviral vector-mediated SHIP gene transfection on proliferation of leukemia K562 cells and PI3K/Akt pathway regulation]. AU - Yang,Lin, AU - Luo,Jian-Min, AU - Liu,Xiao-Jun, AU - Wen,Shu-Peng, AU - Du,Xing-Yan, AU - Yao,Li, PY - 2009/7/23/entrez PY - 2009/7/23/pubmed PY - 2011/6/24/medline SP - 366 EP - 72 JF - Ai zheng = Aizheng = Chinese journal of cancer JO - Ai Zheng VL - 28 IS - 4 N2 - BACKGROUND AND OBJECTIVE: The hemopoietic-restricted Src homology 2-containing inositol 5'-phosphatase (SHIP) acts as a negative regulator for the proliferation and survival of hematopoietic cells by hydrolysing the phosphoinositide 3-kinase (PI3K)-generated second messenger, PtdIns(3,4,5)-P3 (PI-3,4,5-P3) to PtdIns(3,4)-P2 (PI-3,4-P2). This study was to investigate the biological function of SHIP gene in pathogenesis of leukemia cells by lentiviral vector-mediated SHIP transfection. METHODS: Ectopic SHIP gene was transfected into leukemia K562 cells by the mediation of lentiviral vector. The mRNA level of SHIP was detected by fluorescent quantitative reverse transcription-polymerase chain reaction (FQ-PCR). The expression of SHIP, Akt, and phosphorylated Akt (p-Akt) was detected by Western blot. The proliferation and morphology of K562 cells before and after SHIP gene transfection were compared. RESULTS: The proliferation of K562 cells was inhibited after transfection: the proliferation inhibition rate was increased from (9.9+/-1.5)% on Day 3 to (40.6+/-2.3)% on Day 5. K562 cells were SHIP-negative but expressed high level of p-Akt which was down-regulated from 0.533 to 0.245 (P<0.01) after SHIP transfection. Apoptotic characteristics were showed in K562 cells after SHIP transfection. The early apoptosis rate was significantly higher in K562-wtSHIP-FIV-G cells than in K562-FIV-G cells and untransfected K562 cells [(38.3+/-4.3)% vs. (8.2+/-0.9)% and (7.7+/-0.8)%, P<0.05]. CONCLUSIONS: SHIP gene can inhibit cell proliferation and promote cell apoptosis via inactivating PI3K/Akt pathway. Loss of SHIP might activate PI3K/Akt pathway and promote the proliferation of K562 cells. UR - https://www.unboundmedicine.com/medline/citation/19622295/[Inhibitory_effect_of_lentiviral_vector_mediated_SHIP_gene_transfection_on_proliferation_of_leukemia_K562_cells_and_PI3K/Akt_pathway_regulation]_ L2 - http://www.cancercommun.com/fulltextnew.asp?y=2009&amp;m=4&amp;ym=366 DB - PRIME DP - Unbound Medicine ER -