Cat.No. : CSC-SC007318 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC007318 |
| 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. |
| Gene | HSPB1 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | HEK293 (CHO and other cell types are also available) |
| Stability | Validated for at least 10 passages |
| Application | 1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Size Form | 2 × 10^6 cells / vial |
| Shipping | Dry Ice |
| Storage | Liquid nitrogen |
| 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. |
| Gene Name | HSPB1 heat shock 27kDa protein 1 [ Homo sapiens ] |
| Gene Symbol | HSPB1 |
| Synonyms | HSPB1; heat shock 27kDa protein 1; heat shock 27kD protein 1; heat shock protein beta-1; Hs.76067; Hsp25; HSP27; HSP28; HSP 27; 28 kDa heat shock protein; heat shock 27 kDa protein; stress-responsive protein 27; estrogen-regulated 24 kDa protein; CMT2F; HMN2B; SRP27; HS.76067; DKFZp586P1322; |
| Gene ID | 3315 |
| UniProt ID | P04792 |
| mRNA Refseq | BC012292 |
| Chromosome Location | 7q11.23 |
| Function | protein binding; protein kinase C binding; protein kinase C delta binding; protein kinase C inhibitor activity; protein kinase binding; ubiquitin binding; |
| Pathway | Amoebiasis, organism-specific biosystem; Amoebiasis, conserved biosystem; Destabilization of mRNA by AUF1 (hnRNP D0), organism-specific biosystem; FAS pathway and Stress induction of HSP regulation, organism-specific biosystem; Gene Expression, organism-specific biosystem; IL-3 Signaling Pathway, organism-specific biosystem; IL-6 Signaling Pathway, organism-specific biosystem; |
| MIM | 602195 |
| 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 |
Chemotherapy resistance is one of the main reasons for treatment failure and poor prognosis in breast cancer patients, especially in those with triple-negative breast cancer. Here, researchers discovered a novel function of heat shock protein β-1 (HSPB1) in regulating chemotherapy resistance and ferroptosis in breast cancer. Based on TCGA and GEO databases, they found that HSPB1 is upregulated in breast cancer tissues and is associated with poor prognosis in breast cancer patients, being considered an independent prognostic factor for breast cancer. Functional experiments showed that HSPB1 can promote the growth and metastasis of cancer cells in vitro and in vivo. Mechanistic studies revealed that HSPB1 can bind to IκB-α, promoting its ubiquitination-mediated degradation, thereby leading to enhanced nuclear translocation and activation of the NF-κB signaling pathway. Furthermore, HSPB1 overexpression resulted in increased IL6 secretion, further promoting breast cancer progression. These findings suggest that the upregulation of HSPB1 may be a key factor driving breast cancer progression and chemotherapy resistance by regulating ferroptosis, and targeting HSPB1 may be an effective anti-breast cancer strategy.
To investigate whether HSPB1 can alter the tumor biological characteristics of breast cancer cells, researchers constructed HSPB1-overexpressing MDA-MB-231 and MDA-MB-468 cell lines (Figure 1A). MTT and colony formation assays showed that HSPB1 overexpression promoted the proliferation of breast cancer cells (Figure 1B, C). Correspondingly, EdU assays showed that HSPB1 overexpression led to increased DNA synthesis activity (Figure 1D). Wound healing and Transwell assays demonstrated that the migration and invasion abilities of HSPB1-overexpressing MDA-MB-231 and MDA-MB-468 cells were increased (Figure 1E, F). Epithelial-mesenchymal transition (EMT) is a major mechanism of cancer cell migration and invasion. Therefore, the researchers further evaluated the effect of HSPB1 on the expression of EMT markers. Western blot results showed that in HSPB1-overexpressing cells, the expression of the epithelial marker (E-cadherin) decreased, while the expression of mesenchymal markers (Fibronectin, N-cadherin, Vimentin) increased (Figure 1G), indicating that HSPB1 has a significant regulatory effect on the EMT process in breast cancer cells. Furthermore, HSPB1 overexpression led to a significant change in cell morphology, from a cobblestone-like morphology to a fibroblast-like morphology. In summary, these results indicate that HSPB1 plays a pro-cancer role in breast cancer cells.
Figure 1. HSPB1 overexpression promoted breast cancer growth, migration, and invasion in vitro. (Liang Y, et al., 2023)
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