PTEN Knockout BEAS-2B Cell Line

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PTEN Knockout BEAS-2B Cell Line
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Cat.No.:

EDC90163

Species:

Human

Cell Name:

BEAS-2B

Gene:

PTEN

Gene ID:

5728

Size:

1×10⁶cells

PTEN Knockout BEAS-2B Cell Line is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performotion Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDC90163
Product Name PTEN Knockout BEAS-2B Cell Line
Species Human
Cell Line BEAS-2B
Gene ID
Gene PTEN
Summary
This gene was identified as a tumor suppressor that is mutated in a large number of cancers at high frequency. The protein encoded by this gene is a phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase. It contains a tensin like domain as well as a catalytic domain similar to that of the dual specificity protein tyrosine phosphatases. Unlike most of the protein tyrosine phosphatases, this protein preferentially dephosphorylates phosphoinositide substrates. It negatively regulates intracellular levels of phosphatidylinositol-3,4,5-trisphosphate in cells and functions as a tumor suppressor by negatively regulating AKT/PKB signaling pathway. The use of a non-canonical (CUG) upstream initiation site produces a longer isoform that initiates translation with a leucine, and is thought to be preferentially associated with the mitochondrial inner membrane. This longer isoform may help regulate energy metabolism in the mitochondria. A pseudogene of this gene is found on chromosome 9. Alternative splicing and the use of multiple translation start codons results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Feb 2015]
Digestion Time 2 min
Morphology Adherent
Passage Ratio 1:3-1:2
Complete Culture Medium BEGM kit (Lonza/Clonetics，CC-3170)
Freezing Medium 92.5% Complete medium + 7.5% DMSO
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
LociSTR Info (Sample Cell)
Sample Cell Line: BEAS-2B		STR Info (Cell bank)
Cell Line: BEAS-2B
Allele1Allele2Allele1Allele2
Amelogenin X Y X Y
D5S818 12 13 12 13
D13S317 13 13
D7S820 10 13 10 13
D16S539 12 12
vWA 17 18 17 18
TH01 7 9.3 7 9.3
TPOX 6 11 6 11
CSF1PO 9 12 9 12
D19S433 13.2 15.2 13.2 15.2
D21S11 28 30 28 30
D18S51 18 19 18 19
D6S1043 12 18
D3S1358 15 17 15 17
Penta D 2.2 13 2.2 13
D2S441 11 11.3 11 11.3
D8S1179 13 15 13 15
Penta E 5 8 5 8
D12S391 17 18 17 18
D2S1338 22 23 22 23
FGA 20 24 20 24
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.

FAQ

The choice depends on whether you are studying PTEN's role in bronchial epithelial biology or lung cancer initiation in a non-transformed background. The Knockout line is appropriate for asking whether PTEN loss is sufficient to drive transformation phenotypes in a non-tumorigenic lung epithelial context — BEAS-2B is SV40-immortalized but non-tumorigenic, providing a tractable model for studying early oncogenic events. Overexpression is useful for studying PTEN restoration effects in PI3K-active contexts. For lung cancer initiation research, the EDITGENE PTEN Knockout in BEAS-2B is highly relevant — PTEN loss in the bronchial epithelium is implicated in lung adenocarcinoma initiation, and the non-tumorigenic background enables study of transformation phenotypes induced by PTEN loss alone or in combination with other oncogenic alterations. This product complements the parallel PTEN Knockout in HAP1; BEAS-2B is preferred for lung-relevant tumor initiation and bronchial epithelial signaling studies. Rescue with wild-type or structure-function variant PTEN enables comprehensive mechanism studies.
Primary applications: • Lung cancer initiation: anchorage-independent growth, transformation phenotypes, and proliferation in BEAS-2B following PTEN loss in a non-tumorigenic background. • Cooperating oncogene studies: combined PTEN loss with KRAS, EGFR, or MYC overexpression to model lung cancer initiation cooperativity. • Bronchial epithelial signaling: PI3K-AKT pathway analysis in respiratory epithelial context. • Premalignant biology: study of early transformation events in lung epithelium with defined PTEN status. EDITGENE recommends this BEAS-2B-based model for lung cancer initiation research; the parallel PTEN Knockout in HAP1 is preferred for biochemistry and PI3K pathway mechanism studies.
Yes. PTEN rescue experiments in BEAS-2B are well-suited for lung cancer initiation research: • Construct design: use a codon-modified PTEN sequence with a small C-terminal tag (FLAG, HA). • Lung cancer initiation rescue: assessment of PTEN rescue-mediated reversal of transformation phenotypes (anchorage-independent growth, proliferation). • Cooperating mutation analyses: rescue with PTEN combined with oncogenic KRAS or EGFR expression for cooperativity studies. • Functional readout: rescue should suppress PI3K pathway hyperactivation and restore non-transformed bronchial epithelial growth characteristics. BEAS-2B transduces efficiently with lentivirus and supports stable rescue line generation in a non-tumorigenic lung epithelial background.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

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