Genome-edited Cells
Blood (peripheral blood)
The PTEN Knockout MOLM-13 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from an FLT3-ITD and MLL-AF9 positive acute myeloid leukemia model. PTEN is a tumor suppressor lipid phosphatase that inhibits AKT signaling by dephosphorylating PIP3, thereby regulating cell survival and proliferation. This knockout model enables study of PTEN-dependent PI3K/AKT pathway regulation in AML and is suitable for inhibitor screening, functional genomics, and in vivo xenograft studies. It provides a powerful tool for dissecting tumor suppressor mechanisms and drug resistance in high-risk leukemia.
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The PTEN Knockout MOLM-13 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the MOLM-13 acute myeloid leukemia (AML) cell line. This model features targeted disruption of the PTEN tumor suppressor gene, providing a defined loss-of-function system for studying PTEN-dependent pathways in AML. The parental MOLM-13 line harbors FLT3-ITD and MLL-AF9 oncogenic lesions, making it a relevant model for AML driven by these mutations. The CRISPR/Cas9-mediated gene disruption enables robust functional studies of PTEN??s role in leukemia biology and targeted therapy development.
MOLM-13 was established from the peripheral blood of a 20-year-old male with relapsed AML M5a and carries both FLT3 internal tandem duplication (FLT3-ITD) and MLL-AF9 fusion. FLT3-ITD constitutively activates downstream signaling including PI3K/AKT, while MLL-AF9 aberrantly regulates gene expression programs that maintain leukemic stemness. This co-occurrence creates a dependency on PI3K/AKT survival signaling, rendering the cells sensitive to PTEN status. MOLM-13 is therefore a widely used model for studying high-risk AML and evaluating targeted inhibitors.
PTEN is a lipid phosphatase that dephosphorylates PIP3 to PIP2, directly antagonizing class I PI3K. This prevents AKT1 membrane recruitment and activation by PDK1, inhibiting downstream mTORC1, S6K, and 4E-BP1. PTEN is regulated by p53, EGR1, and PPAR??, and interacts with MAGI scaffold proteins. Loss of PTEN causes PIP3 accumulation, constitutive AKT activation, and phosphorylation-mediated inhibition of TSC1/TSC2, relieving Rheb-dependent mTORC1 suppression. Active AKT also inactivates FOXO3 and BAD, promoting survival and proliferation. PTEN ubiquitination by NEDD4-1 modulates its stability. PTEN thus restrains the PI3K/AKT/mTOR axis, impacting cell cycle, apoptosis, and genomic stability.
In MOLM-13 cells, PTEN knockout removes a key brake on PI3K/AKT signaling that is already hyperactivated by FLT3-ITD and MLL-AF9. This model enables investigation of PTEN loss on leukemogenesis and drug resistance, particularly in FLT3-ITD-driven AML. It provides a platform to assess whether PTEN deficiency alters sensitivity to FLT3 inhibitors, PI3K/AKT inhibitors, or standard chemotherapeutics. Comparing PTEN-proficient and deficient MOLM-13 cells allows identification of PTEN-specific vulnerabilities and synthetic lethal interactions relevant to AML therapy.
This knockout cell line is suitable for functional assays including Western blotting for PTEN and phospho-AKT, MTS proliferation assays, Annexin V/PI apoptosis assays, and colony formation assays. It can be used in drug sensitivity screens targeting the PI3K pathway and in murine xenograft models to study in vivo leukemic progression. RT-qPCR can monitor FOXO target gene expression. The model also facilitates genetic interaction studies through rescue experiments. For additional information or to inquire about this product, please contact Ascent Research.
