Panoply™ Human PIM1 Over-expressing Stable Cell Line

Name: Panoply™ Human PIM1 Over-expressing Stable Cell Line
SKU: CSC-SC011797
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CSC-SC011797

Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x10⁶ frozen cells/vial

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Cell Line Information

Cell Culture Information

Safety and Packaging

Gene Information

Cat. No.	CSC-SC011797
Description	Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level.
Target Gene	PIM1
Gene Species	Homo sapiens (Human)
Host Cell	HEK293 (CHO and other cell types are also available)
Host Cell Species	Species varies
Applications	1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research
Size	2 × 10^6 cells / vial
Stability	Validated for at least 10 passages
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid nitrogen
Shipping	Dry Ice

Revival

Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media.

Mycoplasma	Negative
Format	One frozen vial containing millions of cells
Storage	Liquid nitrogen
Safety Considerations	The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach.
Ship	Dry ice

Gene Name	PIM1 pim-1 oncogene [ Homo sapiens ]
Gene Symbol	PIM1
Synonyms	PIM1; pim-1 oncogene; PIM; serine/threonine-protein kinase pim-1; Oncogene PIM1; pim-1 kinase 44 kDa isoform; pim-1 oncogene (proviral integration site 1); proto-oncogene serine/threonine-protein kinase pim-1;
Gene ID	5292
Uni Prot ID	P11309
m RNA Refseq	BC020224
Chromosome Location	6p21
Function	ATP binding; manganese ion binding; metal ion binding; nucleotide binding; protein binding; protein serine/threonine kinase activity; transcription factor binding;
Pathway	Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; C-MYB transcription factor network, organism-specific biosystem; IL-5 Signaling Pathway, organism-specific biosystem; Jak-STAT signaling pathway, organism-specific biosystem; Jak-STAT signaling pathway, conserved biosystem; Role of Calcineurin-dependent NFAT signaling in lymphocytes, organism-specific biosystem;
MIM	164960

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Identifying the key driver genes that maintain breast cancer stem cells (BrCSCs) is crucial for designing new strategies to eradicate these cells and improve patient prognosis. Here, researchers found that PIM1, an oncogenic serine/threonine kinase previously implicated in breast cancer development, is involved in the regulation of BrCSCs and holds promise as a new target for eradicating BrCSCs. Specifically, PIM1 enhances the stem cell-like properties of breast cancer cells by promoting the phosphorylation and cytoplasmic localization of RUNX3. The nuclear export of RUNX3 inactivates its tumor suppressor function, leading to breast cancer cells acquiring stem cell-like characteristics. Inhibiting PIM1 significantly promotes the retention of RUNX3 in the nucleus, restoring its transcriptional function and attenuating the stem cell-like properties of breast cancer cells. These findings deepen our understanding of the oncogenic role of PIM1 and highlight its importance in designing new strategies targeting BrCSCs.

Cell invasion and epithelial-mesenchymal transition (EMT) are often closely associated with the stem cell-like properties of cancer cells. Here, researchers investigated the roles of PIM1 and RUNX3 in the EMT process of breast cancer cells. In PIM1-overexpressing cells, the expression of the epithelial marker E-cadherin was significantly downregulated, while the expression of mesenchymal markers N-cadherin, vimentin, and the stem cell-associated transcription factor SOX2 was upregulated (Figure 1A). These changes could be reversed by overexpressing RUNX3(4A)-FLAG, while overexpression of RUNX3-FLAG only slightly attenuated these changes. Consistent with this, Transwell assays showed that PIM1 overexpression enhanced cell invasion, and this effect was reversed by overexpressing RUNX3(4A)-FLAG, but not by overexpressing RUNX3-FLAG (Figure 1B, C). All these results indicate that PIM1 promotes the EMT process in breast cancer cells, while RUNX3 attenuates this effect, and RUNX3(4A) reverses this effect. Furthermore, RUNX3(4A), which cannot be phosphorylated by PIM1, more significantly reversed the pro-EMT effect of PIM1. These studies suggest that PIM1 may exert its pro-breast cancer stem cell properties and pro-EMT effects by phosphorylating RUNX3, as breast cancer cells can acquire stem cell-like properties through the EMT process.

Figure 1. RUNX3(4A) attenuated the EMT induced by PIM1. (Liu H, et al., 2020)

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