Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat. No. : CSC-SC007320
Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x106 frozen cells/vial
| Cat. No. | CSC-SC007320 |
| 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 | HSPB2 |
| 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 | HSPB2 heat shock 27kDa protein 2 [ Homo sapiens ] |
| Gene Symbol | HSPB2 |
| Synonyms | HSPB2; heat shock 27kDa protein 2; heat shock 27kD protein 2; heat shock protein beta-2; Hs.78846; MKBP; DMPK-binding protein; heat-shock protein beta-2; HSP27; LOH11CR1K; MGC133245; |
| Gene ID | 3316 |
| Uni Prot ID | Q16082 |
| m RNA Refseq | BC109393 |
| Chromosome Location | 11q22-q23 |
| Function | enzyme activator activity; protein binding; |
| Pathway | MAPK signaling pathway, organism-specific biosystem; |
| MIM | 602179 |
Through miRNA microarray analysis, it was found that the expression of miR-17-5p was significantly upregulated in colorectal cancer (CRC) tissues. The mRNA expression level of miR-17-5p in CRC tissues was significantly higher than that in adjacent normal tissues. In the CRC group, the expression of miR-17-5p was higher in cancer tissues with lymph node metastasis than in those without lymph node metastasis. Here, researchers found that overexpression of miR-17-5p inhibited CRC cell apoptosis and promoted cell proliferation, migration, and invasion. Transcriptome sequencing and miRNA target gene prediction software suggested that HSPB2 might be a target gene of miR-17-5p, and luciferase reporter gene assays confirmed for the first time that miR-17-5p directly binds to the 3'-UTR region of HSPB2. In rescue experiments, the tumor-suppressive effect of HSPB2 was detected, and miR-17-5p was found to promote cell proliferation, migration, and invasion by targeting HSPB2. These studies indicate that miR-17-5p promotes CRC invasion and metastasis by inhibiting HSPB2, suggesting its potential as a novel diagnostic biomarker and therapeutic target for CRC.
Here, researchers constructed HSPB2-overexpressing HCT116 and LOVO cells (Figure 1A-B). CCK8 and colony formation assays showed that the viability and colony-forming ability of HSPB2-overexpressing colorectal cancer cells were inhibited compared to the control group (Figure 1C-D). Transwell assays demonstrated that HSPB2 overexpression significantly reduced cell migration and invasion. Furthermore, the researchers found that overexpression of miR-17-5p inhibited both mRNA and protein levels of HSPB2 (Figure 1A-B), while silencing endogenous miR-17-5p increased HSPB2 mRNA and protein levels. When miR-17-5p and HSPB2 expression were increased simultaneously, the reintroducing HSPB2 caused by co-overexpression attenuated the tumor-promoting effect of overexpressed miR-17-5p, as shown by reduced proliferation (Figure 1C-D), migration and invasion.
Figure 1. Reintroduction of HSPB2 could reverse the promotion of miR-17-5p in cell proliferation. (Yu W, et al., 2022)
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