SHI-1

Specification
Background
Scientific Data
Q & A
Customer Review

Cat.No.

CSC-C0630

Description

Established in 2002 from the bone marrow of a 37-year-old male with relapsed acute monocytic leukemia (AML-M5b); described to carry t(6;11)(q27;q23) with MLL-MLLT4 (MLL-AF6) rearrangement and a TP53 point mutation

Species

Homo sapiens (Human)

Source

Bone Marrow

Recommended Medium

80% SuperCult® IMDM + 20% h.i. FBS.

Culture Properties

suspension

Morphology

round cells growing singly in suspension

Karyotype

Human pseudodiploid karyotype with 12% polyploidy; 46(44-46)<2n>XY, -18, +mar, t(6;11)(q27;q23), add(8)(p23), del(10)(p11), del(17)(p12); carries t(6;11) effecting rearrangement of MLL with MLLT4 (AF6); matches published karyotype

Disease

Acute Monocytic Leukemia

Quality Control

Mycoplasma: negative in microbiological culture, PCR assays
Immunology: CD3 -, CD13 +, CD15 +, CD19 -, CD33 +, CD34 -, CD41 +, CD235a -
Viruses: PCR: EBV -, HBV -, HCV -, HIV -, HTLV-I/II -, SMRV -

Storage and Shipping

Frozen with 70% medium, 20% FBS, 10% DMSO at about 20 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen

Synonyms

shi-1; SHI1

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.

SHI-1 is a human acute monocytic leukemia (AML-M5b) cell line, created from the peripheral blood mononuclear cells of a male patient. The line harbors the classic t(6;11)(q27;q23) translocation that results in the oncogenic MLL- AF6 fusion transcript as well as a p53 mutation and a FLT3-ITD allele. These genetic alterations result in constitutive activation of STAT5, PI3K/AKT and MAPK pathways. Morphologically, SHI-1 cells are in suspension, round to slightly irregular in shape, 12-15 µm in diameter, with finely dispersed chromatin and prominent nucleoli and often contain Auer rods; by immunophenotyping, they show strong expression of myeloid/monocytic markers CD13, CD33, CD14, CD15 and moderate expression of CD11b, but are negative for CD34 and CD117. They can be grown autonomously in RPMI-1640 (or IMDM) medium containing 10-15 % fetal bovine serum, doubling every 30-36 hours with a stable karyotype even after many years in culture.

The line is functionally characterized by high tumorigenicity in nude mice, high levels of MMP-2/-9 secretion and multidrug-resistant phenotypes (high levels of LRP and GST-π and low P-gp). This makes it a useful model for research into leukemogenesis, particularly the roles of MLL-AF6 and FLT3-ITD, as well as pre-clinical testing of FLT3 inhibitors (midostaurin, gilteritinib), epigenetic drugs (azacitidine, decitabine) and new MDR-reversing agents (artesunate, curcumin). The line is also amenable to differentiation studies. PMA or 1,25-(OH)₂-vitamin D₃ treatment induces macrophage-like adhesion and up-regulation of CD14, CD86 and HLA-DR.

Suchilactone Inhibited Proliferation and Promoted Apoptosis of AML Cells In Vitro

Suchilactone, a lignan compound from Monsonia angustifolia, has limited research on its pharmacological activity, particularly regarding its potential inhibitory effect on acute myeloid leukemia (AML). Wu's team aims to investigate suchilactone's antitumor effects and its underlying mechanism in AML.

To assess antitumor activity, they screened suchilactone against multiple cancer lines. It most potently blocked proliferation of the AML line SHI-1 (IC₅₀ = 17 µM), outperforming Jurkat, THP-1, and solid-tumor lines (Fig. 1B-H). From these results, they found that suchilactone has a better inhibitory effect on the proliferation of AML cell line SHI-1, then they will continue to explore its mechanism. They treated SHI-1 cell with suchilactone for 24 h, flow cytometry showed that suchilactone induced apoptosis of SHI-1 cell, and that 20 µM suchilactone induced apoptosis in nearly 50% of the SHI-1 cells (Fig. 2A, B). These results showed that suchilactone inhibited growth of AML cells by suppressing cell proliferation and inducing apoptosis.

Effects of suchilactone on proliferation of various tumour cells. — Fig. 1. Effects of suchilactone on proliferation of various tumour cells (Wu J J, Deng Y, *et al.*, 2021).

Suchilactone promoted apoptosis of SHI-1 cell in vitro . — Fig. 2. Suchilactone promoted apoptosis of SHI-1 cell *in vitro* (Wu J J, Deng Y, *et al.*, 2021).

Drug Tolerance of Ara-C-resistant AML Cells

Acute myeloid leukemia (AML) is highly aggressive; FLT3-wild-type relapsed/refractory (R/R) patients lack effective therapies. Using FLT3-wild-type AML line SHI-1 and its Ara-C-resistant derivative RHI-1, Chae et al. explored mechanisms of resistance to cytarabine (Ara-C) and daunorubicin (DNR).

Cell viability assay was conducted to elucidate the responses of SHI-1 and RHI-1 cells to Ara-C (0-0.64 μM) and DNR (0-2 μM) either alone or as a combination after 24 and 48 h of treatment. Ara-C and DNR treatments significantly decreased the viability of SHI-1 cells in a concentration-dependent manner within 48 h (Fig. 3A, B). The cell viability results for the combination treatments followed a similar pattern to that of the single treatments with DNR. Although the combination treatment decreased cell viability to the same extent as DNR monotherapy, combination added no synergy. RHI-1 cells exhibited resistance to Ara-C and DNR treatments (Fig. 3A, B). Although DNR treatment was cytotoxic to RHI-1 cells, its effect was 1.3-4 times lower than that in SHI-1 cells. Despite the different mechanisms of action of DNR and Ara-C, RHI-1 cells exhibited significant tolerance to DNR, regardless of the presence or absence of Ara-C. Collectively, RHI-1 cells were resistant to both Ara-C and DNR and the combined treatments.

Impact of Ara-C and DNR combinations on cell viability and intracellular drug accumulation in SHI-1 and RHI-1 cell lines. — Fig. 3. Impact of Ara-C and DNR combinations on cell viability and intracellular drug accumulation in SHI-1 and RHI-1 cell lines (Chae S Y, Jang S-Y, *et al.*, 2025).

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