Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress 2023 EHA Congress 2023 ASCO Annual Meeting
Clinical Collections
Advances in Alzheimer’s

At a glance: The ONWARDS insulin icodec trials

A round-up of the ONWARDS phase 3 clinical trials evaluating the novel weekly insulin icodec in people with diabetes.
ADVANCED SEARCH
Log in
Top
Indian Journal of Hematology and Blood Transfusion
Published in: Indian Journal of Hematology and Blood Transfusion 3/2017

01-09-2017 | Original Article

The miR-125a-3p Inhibits TIM-3 Expression in AML Cell Line HL-60 In Vitro

Authors: Fatemeh Emamdoost, Hossein Khanahmad, Mazdak Ganjalikhani-hakemi, Abbas Doosti

Published in: Indian Journal of Hematology and Blood Transfusion | Issue 3/2017

Login to get access

Abstract

Acute Myeloid Leukemia is a cancer of leukemic stem cells (LSCs) with a rapid progression. It is characterized by overproduction of immature myeloid cells in bone marrow which crowds out normal hematopoietic stem cells (HSC). TIM-3, an immune regulatory molecule, is an LSC specific surface marker in AML with high expression on these cells compared to HSCs. Studies have indicated that micro RNAs (miRNAs) may play an important role in either cancer progression or suppression. Based on bioinformatics assessments, we have predicted that miR-125a-3p could be a miRNA with high suppressive activity on TIM-3 expression. The purpose of this study was to investigate the inhibitory effect of miR-125a-3p on TIM-3 gene expression in an AML cell line, HL-60, in vitro. HL-60 cells were cultured in RPMI 1640 supplied with 10 % FBS. TIM-3 expression was induced on the cells using phorbol miristate acetate. The cells were transfected with miR-125-3p for 24 h and the gene and protein expression of TIM-3 were measured using q-RT-PCR and flow-cytometery methods, respectively. The results of this study showed that miR-125a-3p has a strong silencing effect on TIM-3 gene and protein expression on HL-60 cell line. Based to our results, miR125a-3p can strongly silence TIM-3 expression in AML cell line. Thus, our results have confirmed the bioinformatics prediction of suppressive effect of miR-125a-3p on TIM-3with Mirwalk and Target Scan softwares.
Literature
1.
Becton D, Dahl GV, Ravindranath Y, Chang MN, Behm FG, Raimondi SC et al (2006) Randomized use of cyclosporin A (CsA) to modulate P-glycoprotein in children with AML in remission: pediatric Oncology Group Study 9421. Blood 107(4):1315–1324CrossRefPubMedPubMedCentral
2.
Sperr W, Wimazal F, Kundi M, Fonatsch C, Thalhammer-Scherrer R, Schernthaner G et al (2001) Survival analysis and AML development in patients with de novo myelodysplastic syndromes: comparison of six different prognostic scoring systems. Ann Hematol 80(5):272–277CrossRefPubMed
3.
Creutzig U, Ritter J, Schellong G (1990) Identification of two risk groups in childhood acute myelogenous. Blood 75(10):1932–1940PubMed
4.
Sayehmiri K, Eshraghian MR, Mohammad K, Alimoghaddam K, Foroushani AR, Zeraati H et al (2008) Prognostic factors of survival time after hematopoietic stem cell transplant in acute lymphoblastic leukemia patients: cox proportional hazard versus accelerated failure time models. J Exp Clin Cancer Res 27(1):1–9CrossRef
5.
Arnaout M, Radomski K, Srivastava D, Tong X, Belt J, Raimondi S et al (2000) Treatment of childhood acute myelogenous leukemia with an intensive regimen(AML-87) that individualizes etoposide and cytarabine dosages: short- and long-term effects. Leukemia 14(10):1736–1742CrossRefPubMed
6.
Gleason MK, Lenvik TR, McCullar V, Felices M, O’Brien MS, Cooley SA et al (2012) Tim-3 is an inducible human natural killer cell receptor that enhances interferon gamma production in response to galectin-9. Blood 119(13):3064–3072CrossRefPubMedPubMedCentral
7.
Jan M, Chao MP, Cha AC, Alizadeh AA, Gentles AJ, Weissman IL et al (2011) Prospective separation of normal and leukemic stem cells based on differential expression of TIM3, a human acute myeloid leukemia stem cell marker. Proc Natl Acad Sci 108(12):5009–5014CrossRefPubMedPubMedCentral
8.
Zhu C, Anderson AC, Schubart A, Xiong H, Imitola J, Khoury SJ et al (2005) The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunity. Nat Immunol 6(12):1245–1252CrossRefPubMed
9.
Kikushige Y, Shima T, S-i Takayanagi, Urata S, Miyamoto T, Iwasaki H et al (2010) TIM-3 is a promising target to selectively kill acute myeloid leukemia stem cells. Cell Stem Cell 7(6):708–717CrossRefPubMed
10.
Zhong X, Coukos G, Zhang L (2012) miRNAs in human cancer. Next-generation MicroRNA expression profiling technology. Springer, Berlin, pp 295–306CrossRef
11.
12.
13.
Giovannetti E, Erozenci A, Smit J, Danesi R, Peters GJ (2012) Molecular mechanisms underlying the role of microRNAs (miRNAs) in anticancer drug resistance and implications for clinical practice. Crit Rev Oncol Hematol 81(2):103–122CrossRefPubMed
14.
Cho WC (2010) MicroRNAs: potential biomarkers for cancer diagnosis, prognosis and targets for therapy. Int J Biochem Cell Biol 42(8):1273–1281CrossRefPubMed
15.
Nakayama M, Akiba H, Takeda K, Kojima Y, Hashiguchi M, Azuma M et al (2009) Tim-3 mediates phagocytosis of apoptotic cells and cross-presentation. Blood 113(16):3821–3830CrossRefPubMed
16.
17.
Kikushige Y, Shima T, Yuda J, Miyamoto T, Akashi K, editors. Leukemogenic function of TIM-3, a leukemia stem cell marker, in acute myelogenous leukemia and myelodysplastic syndromes. ASH Annual Meeting Abstracts; 2012
18.
Jiang L, Huang Q, Zhang S, Zhang Q, Chang J, Qiu X et al (2010) Hsa-miR-125a-3p and hsa-miR-125a-5p are downregulated in non-small cell lung cancer and have inverse effects on invasion and migration of lung cancer cells. BMC Cancer 10(1):318CrossRefPubMedPubMedCentral
19.
Hashiguchi Y, Nishida N, Mimori K, Sudo T, Tanaka F, Shibata K et al (2012) Down-regulation of miR-125a-3p in human gastric cancer and its clinicopathological significance. Int J Oncol 40(5):1477–1482PubMed
20.
Ninio-Many L, Grossman H, Levi M, Zilber S, Tsarfaty I, Shomron N et al (2014) MicroRNA miR-125a-3p modulates molecular pathway of motility and migration in prostate cancer cells. Oncoscience 1(4):250CrossRefPubMedPubMedCentral
21.
Tang H, Li RP, Liang P, Zhou YL, Wang GW miR-125a inhibits the migration and invasion of liver cancer cells via suppression of the PI3K/AKT/mTOR signaling pathway. Oncol Lett
22.
Ufkin ML, Peterson S, Yang X, Driscoll H, Duarte C, Sathyanarayana P (2014) miR-125a regulates cell cycle, proliferation, and apoptosis by targeting the ErbB pathway in acute myeloid leukemia. Leuk Res 38(3):402–410CrossRefPubMedPubMedCentral
Metadata
Title
The miR-125a-3p Inhibits TIM-3 Expression in AML Cell Line HL-60 In Vitro
Authors
Fatemeh Emamdoost
Hossein Khanahmad
Mazdak Ganjalikhani-hakemi
Abbas Doosti
Publication date
01-09-2017
Publisher
Springer India
Published in
Indian Journal of Hematology and Blood Transfusion / Issue 3/2017
Print ISSN: 0971-4502
Electronic ISSN: 0974-0449
DOI
https://doi.org/10.1007/s12288-016-0733-4

Other articles of this Issue 3/2017

Indian Journal of Hematology and Blood Transfusion 3/2017 Go to the issue

Correspondence

Skin GVHD Mimicking Betadine Rash in a Post Allogeneic Transplant Patient

Short Communication

Congenital Hypotransferrinemia, an Unusual Cause of Iron Deficiency Anemia: Report of Two Cases

Correspondence

Transfusion Related Acute Lung Injury in a Platelet Refractory Neutropenic Patient

Original Article

Primary Thrombophilia in México XI: Activated Protein C Resistance Phenotypes are Multifactorial

Original Article

Incidence and Residual Risk of HIV, HBV and HCV Infections Among Blood Donors in Tehran

Correspondence

Transfusion Dependent Beta-Thalassemia Developing Avascular Necrosis of Femoral Head: A Rare Case
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Watch now

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine
Image Credits