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MONO-MAC-1

MONO-MAC-1

Cat.No.: CSC-C0353

Species: Human

Source: acute monocytic leukemia

Morphology: single, round/multiformed cells in suspension

Culture Properties: suspension

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Cat.No.
CSC-C0353
Description
Established from the peripheral blood of a 64-year-old man with acute monocytic leukemia (AML FAB M5) at relapse in 1985 following myeloid metaplasia; simultaneous sister cell line of MONO-MAC-6 (DSM ACC 124); cells are described to be less differentiated than MONO-MAC-6 and to support productive infection with HIV-1
Species
Human
Source
acute monocytic leukemia
Recommended Medium
90% RPMI1640 + 10% h.i. FBS + 1x non-essential amino acids + 1 mM sodium pyruvate
Culture Properties
suspension
Morphology
single, round/multiformed cells in suspension
Karyotype
Human near-diploid karyotype with 10% polyploidy - 49(43-52)<2n>XY, +8, +12, +13, +18, -20, inv dup(3)(q21q27), add(8)(q24), t(9;11)(p22;q23), t(10;12;17)(q24;q13;q11), r(12)(??), del(13)(q1?2q21), t(16;21)(q13;q22.2) - diploid version of its sister MONO-
Applications
Frozen with 70% medium, 20% FBS, 10% DMSO;
Ship in dry ice; Store in liquid nitrogen
Disease
A new in vitro model system to study HIV-1 infection in human cells of the mononuclear phagocyte series.
Quality Control
Mycoplasma: negative in DAPI, microbiological culture, RNA hybridization, PCR assays
Immunology: CD3 -, CD13 +, CD14 -, CD15 +, CD19 -, CD34 -, cyCD68 +, HLA-DR +
Viruses: ELISA: reverse transcriptase negative; PCR: EBV -, HBV -, HCV -, HHV-8 -, HIV -, HTLV-I/II -, MLV -, SMRV -
Storage and Shipping
Maintain at 0.3-1.0 x 106 cells/ml; split ratio 1:2 to 1:3 every 2-3 days; seed out at ca. 1 x 106 cells/ml
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

MONO-MAC-1 cells are a cell line that was established from the peripheral blood of a 64-year-old man diagnosed with acute monocytic leukemia (AML FAB M5) at relapse in 1985. These cells were obtained following myeloid metaplasia, which refers to the abnormal transformation of bone marrow cells into cells of the myeloid lineage.

The MONO-MAC-1 cell line is a sister cell line of MONO-MAC-6 (DSM ACC 124), meaning they share a common origin or are derived from the same parental cell population. However, MONO-MAC-1 cells are described as being less differentiated than MONO-MAC-6 cells.

Establishing MONO-MAC-1 cells has provided researchers with a useful tool for investigating the molecular mechanisms underlying ALL and HIV-1 infection. These cells have been utilized in numerous studies aiming to uncover the factors involved in the differentiation of monocytes, the pathogenesis of HIV-1, and the development of novel therapeutic interventions for leukemia and HIV/AIDS.

Modulation of CCR7 Receptor Expression in Mono-MAC-1 Cells by LXRα Activation and PGE2

Cell migration via chemokine receptor CCR7 expression is an essential function of the immune system. Prostaglandin E2 (PGE2), an important immunomodulatory molecule, increases CCR7 expression and function in monocytes. MONO-MAC-1 (MM-1) is a human cell line with the properties of blood monocytes that can be used as a model system to study monocytic functions in vitro.

MM-1 cells were treated with 1 μM PGE2 and 1 μM T0901317, a synthetic liver X receptor α (LXRα) agonist, for 8 or 24 h. As previously observed, PGE2 induces CCR7 mRNA expression with a maximal effect after stimulation for 8 h. Treatment of MM-1 cells with T0901317 alone does not modify the expression of CCR7 mRNA (Fig. 1a). An increase in LXRα levels following treatment with PGE2 or T0901317 alone. mRNA production plateaued after 8 h of stimulation with PGE2 or T0901317 alone (Fig. 1b). ABCG1 mRNA levels were augmented when cells were treated with T0901317 alone. PGE2 did not affect ABCG1 transcription (Fig. 1c).

MM-1 cells were treated with the stimulants for 24 or 48 hours before migration through polycarbonate filters (5 μm pore size) for 4 h. The chemotaxis assay results showed that PGE2 increases MM-1 cell migration to both CCR7 natural ligands CCL19 (Fig. 2a) and CCL21 (Fig. 2b) after treatment for 24 h. The LXR agonist alone did not affect the migratory capacity of MM-1 cells in response to CCL19 whereas 24 h treatment with T0901317 significantly increased migration in response to CCL21. To further investigate the effects of PGE2 and T0901317 on CCR7 expression, migration assays were repeated with freshly isolated human blood monocytes. Results showed that monocyte migration toward CCL19 and CCL21 is increased following the treatment of blood monocytes with PGE2 and T0901317 (Fig. 3).

Fig. 1 Effects of PGE2 and T0901317 on CCR7, ABCG1, and LXRα transcription in MM-1 cells. (Tanné B, et al., 2015)Fig. 1 Effects of PGE2 and T0901317 on CCR7, ABCG1, and LXRα transcription in MM-1 cells. (Tanné B, et al., 2015)

Fig. 2 PGE2 alone and in combination with T0901317 induces functional CCR7-specific migration of MM-1 cells. (Tanné B, et al., Fig. 2 PGE2 alone and in combination with T0901317 induces functional CCR7-specific migration of MM-1 cells. (Tanné B, et al., 2015)

Fig. 3 Freshly isolated monocytes migrate toward the CCR7-specific ligands CCL19 and CCL21. (Tanné B, et al., 2015)Fig. 3 Freshly isolated monocytes migrate toward the CCR7-specific ligands CCL19 and CCL21. (Tanné B, et al., 2015)

CSF-1R Upregulation with Tyrosine Kinase in Mono-Mac-1 Cell Lines

The oncogenic potential of colony-stimulating factor 1 receptor (CSF-1R) has been well described, while its relevance for human AML is still undetermined. To assess the relevance of CSF-1R in AML, three myeloid cell lines, Mono-Mac 1, THP-1, and U937, were treated with compounds that affect the CSF-1R and other pathways. After allowing the cells to grow for three days, only Mono-Mac 1 cells demonstrated reduced proliferation with CSF-1R inhibitor (cFMS-I) treatment. In Mono-Mac 1 cells, cFMS-I increased the G1 population from 57.92% to 64.04% (Fig. 4B), Sunitinib increased G1 cells from 57.92% to 63.4% (Fig. 4C), and U0126 increased the G1 population from 57.92% to 62.6% (Fig. 4D).

The effects of cFMS-I (1 μM), sunitinib (0.1 μM), and U0126 (10 μM) on ERK activity were compared in Mono-Mac 1 cells with and without CSF-1 treatment (Fig. 5B). As shown in Fig. 5A, the Mono-Mac 1cells had high ERK activity, and CSF-1 induced slight ERK activation. cFMS-I, sunitinib, and U0126 all inhibited ERK activity. sunitinib caused the greatest inhibition of ERK, followed by cFMS-I, and U0126 had the smallest effect on ERK. CSF-1R was detected in Mono-Mac 1 cells (Fig. 5C). The CSF-1R was down-regulated after 5 minutes of treatment with CSF-1 (Fig. 5D). Mono-Mac 1 cells were treated with cFMS-I (0.01-1 μM) and sunitinib (0.01-1μM) (Fig. 5E). By western blot, both treatments did indeed show a profound and dose-dependent increase in the amount of total CSF-1R receptor in Mono-Mac 1 cells (Fig. 5F).

Fig. 4 The effect of colony-stimulating factor 1 receptor inhibitor, sunitinib, and U0126 on Mono-Mac 1 cell cycle distribution. (Kogan M, et al., 2012)Fig. 4 The effect of colony-stimulating factor 1 receptor inhibitor, sunitinib, and U0126 on Mono-Mac 1 cell cycle distribution. (Kogan M, et al., 2012)

Fig. 5 Cell signaling and colony-stimulating factor 1 receptor (CSF-1R) receptor function with drug treatment in acute myelogenous leukemia cell lines. (Kogan M, et al., 2012)Fig. 5 Cell signaling and colony-stimulating factor 1 receptor (CSF-1R) receptor function with drug treatment in acute myelogenous leukemia cell lines. (Kogan M, et al., 2012)

Is DAPI toxic to cells?

DAPI is toxic to cells unless extremely diluted, and so is typically used for fixed-cell staining.

How do MONO-MAC-1 cells differ from MONO-MAC-6 cells?

MONO-MAC-1 cells are described as less differentiated than MONO-MAC-6, providing researchers with a spectrum of differentiation states to explore in monocytic leukemia research.

What unique characteristic makes MONO-MAC-1 cells valuable for research?

MONO-MAC-1 cells are known to support productive infection with HIV-1, making them a valuable tool for investigating viral-host interactions, HIV pathogenesis, and potential therapeutic strategies.

Why are MONO-MAC-1 cells significant for studying AML FAB M5?

By providing insights into the less-differentiated state of AML FAB M5 cells, MONO-MAC-1 cells play a crucial role in expanding our knowledge of leukemia progression, paving the way for novel research discoveries and therapeutic developments.

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Average Rating: 5.0    |    3 Scientist has reviewed this product

Reliable results

Creative Bioarray provides products with high cell viability, to ensure reliable results.

30 Jan 2022


Ease of use

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Exceptional quality

I recently procured MONO-MAC-1 cell products from Creative Bioarray, and I must commend the exceptional quality of the cells. They were vital for my research on monocytic leukemia, showing robust characteristics and responsiveness.

11 Oct 2023


Ease of use

After sales services

Value for money


Reliable products

The cells I received were of high quality, greatly aiding my research endeavors.

11 Dec 2023


Ease of use

After sales services

Value for money


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