Cat.No. : CSC-SC011784 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC011784 |
| 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 | PIK3CB |
| 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 | Pik3cb phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit beta [ Rattus norvegicus ] |
| Gene Symbol | Pik3cb |
| Gene Description | phosphatidylinositol 3-kinase, catalytic, beta polypeptide |
| Gene ID | 85243 |
| UniProt ID | Q9Z1L0 |
| mRNA Refseq | NM_053481.1 |
| Protein Refseq | NP_445933.1 |
| Chromosome Location | 8q31 |
| Function | 1-phosphatidylinositol-3-kinase activity; 1-phosphatidylinositol-3-kinase activity; ATP binding; insulin receptor substrate binding; insulin receptor substrate binding; kinase activity; phosphatidylinositol 3-kinase activity; phosphatidylinositol-4,5-bisphosphate 3-kinase activity; phosphotransferase activity, alcohol group as acceptor; |
| Pathway | Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; Adaptive Immune System, organism-specific biosystem; Aldosterone-regulated sodium reabsorption, organism-specific biosystem; Aldosterone-regulated sodium reabsorption, conserved biosystem; Alpha6-Beta4 Integrin Signaling Pathway, organism-specific biosystem; Amoebiasis, organism-specific biosystem; |
| 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 |
Tumor cell senescence reduces sensitivity to chemotherapeutic drugs; therefore, eliminating senescent cells is an ideal strategy to improve chemotherapy sensitivity. The interaction between the PI3K/Akt and Hippo/YAP1 pathways is receiving increasing attention, but the roles of PIK3CB and YAP1 and their effects on head and neck tumor cell senescence and chemotherapy sensitivity remain unclear. Here, the study shows that in head and neck squamous cell carcinoma (HNSCC) tumors, elevated PIK3CB expression is associated with advanced disease stage, older age, and reduced survival rate. The expression of PIK3CB and YAP1 is closely related and affects senescence pathways and cell proliferation. Regulating PIK3CB expression affects tumor cell proliferation, senescence, and DNA damage. The combination of navitoclax and paclitaxel can reduce tumor cell proliferation and autonomous migration ability, and this effect is influenced by PIK3CB levels.
An overexpression model was constructed to explore the effects of PIK3CB overexpression on senescence in head and neck cancer cells. Western blotting was used to detect the efficiency of PIK3CB overexpression (Figure 1A, B). Subsequently, the effect of PIK3CB overexpression on HNSCC cell growth over 96 hours was detected using the CCK8 assay. The results showed that the growth rate of PIK3CB-overexpressing SCC15 and HN30 cell lines was significantly faster than that of the control group (Figure 1C, D). Colony formation assays showed that the number and size of colonies in PIK3CB-overexpressing SCC15 and HN30 cells were significantly increased (Figure 1E, F), indicating that enhanced PIK3CB expression significantly promotes tumor cell proliferation and growth. Cell cycle analysis showed that compared with the control group, PIK3CB-overexpressing SCC15 and HN30 cell lines had an increased proportion of cells in the S phase and a decreased proportion of cells in the G0/G1 phase (Figure 1G, H), indicating that PIK3CB overexpression accelerates the cell cycle progression of HNSCC cells. Finally, β-galactosidase staining results showed that compared with the control group, the proportion of β-galactosidase-positive cells in PIK3CB-overexpressing HNSCC cells was significantly reduced (Figure 1I, J), suggesting that PIK3CB overexpression may inhibit HNSCC cell senescence.
Figure 1. Overexpression of PIK3CB inhibits senescence in HNSCC cells. (Liu J, et al., 2025)
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