CellEDIT - CRISPR-Engineered LNCap Cell Line
The LNCap cell line: cancer cell model for androgen-dependent prostate cancer
We’ll handle the CRISPR editing of your LNCap cells, so you can focus on your next discoveries
LNCap is a prostate cancer cell line that expresses (mutated) androgen receptors and prostate specific antigens (PSA). LNCap was derived from a lymph node metastasis of a 50-year-old Caucasian male in 1977.
LNCap Cell Line Information
Organism
Homo Sapiens, Human
Tissue Type
Prostate
Cell Type
Epithelial
Disease
Carcinoma
Donor Information
Age
50
Gender
Male
Ethnicity
Caucasian
Research field description
Most prostate cancers are adenocarcinomas that express androgen receptors (AR) and prostate specific antigens (PSA). First line treatment for prostate adenocarcinomas therefore consists of hormonal treatment aiming to inhibit androgen receptor signaling, as most prostate cancer cells are androgen dependent. The LNCap cell line is crucial for modeling prostate cancer progression as they are unique in their ability to model key stages of prostate cancer progression.
LNCap cells expresses a mutated AR gene with wider steroid-binding specificity, making it important for studying the interaction between AR activity and prostate cancer in different stages of the disease. As such, studies of these cells have clarified aspects of tumorigenesis, metastasis, and drug response, especially regarding androgen receptor signaling.
LNCap is often used to study downstream targets of AR such as PSA and NKx3.1, which are essential for prostatic epithelial cell function.
Other Prostate Cancer Cell Lines:
Other prostate cancer cell lines include PC3, 22RV1 and DU1145 and are commonly used model cell lines for in vitro prostate cancer research and drug discovery and differ in their aggressiveness and tumorigenic properties. A combination of these cell lines is sometimes used to study a panel prostate cancer cell model of increasingly aggressive forms of prostate cancer.
Advance your research with CellEDIT’s expertise
Efficient on
Hard-to-transfect cells
Vector-free
direct intra-nuclear delivery
Minimized Off-Target
Immortalized Cells
Learn how the CellEDIT workflow was used to generate 5 monoclonal HPRT knockouts in C2C12 cell line through direct intra-nuclear injection of only 51 cells.
Hard-to-Transfect Cells
Discover how
the CellEDIT workflow was used to produce 3 monoclonal HPRT1 knockouts in SK-MES-1 cell, a notoriously hard-to-transfect cell line.
Available Edits using CellEDIT Engineered Cells
Knockout
Save time in the lab by empowering your research with CellEDIT. Confidently streamline your drug discovery workflow and investigate gene function with effective CRISPR knockouts.
Multiplex Editing
At CellEDIT, we provide you with multiplexed cell lines in 10 weeks. The efficiency and gentleness of our vector-free editing through intra-nuclear delivery, makes it an ideal system to perform multiplex gene editing in one go.
Related Resources
Educational
Technical
Introduction to CRISPR Knockout Gene Editing with CellEDIT
An Overview of CellEDIT' CRISPR Cell Line Development Services
CellEDIT' CRISPR Cell Line Development Workflow
CellEDIT's Engineered Cell Lines
CRISPR-Engineered U2OS Cell Line
CRISPR-Engineered MDA MB 231 Cell Line
CRISPR-Engineered A549 Cell Line
CRISPR-Edited Hek293 Cell Line
CRISPR-Engineered C2C12 Cell Line
Media & Downloads
On-Demand CellEDIT's CRISPR Cell Line Engineering Webinar
CellEDIT's Application Note n*1 - Introducing the CellEDIT Workflow
CellEDIT's Application Note n*2 - Overcoming the hard-to-transfect cell line hurdle
Open Access Publication featuring CellEDIT: Antony, Justin S., Anabel Migenda Herranz, Tahereh Mohammadian Gol, Susanne Mailand, Paul Monnier, Jennifer Rottenberger, Alicia Roig‐Merino et al. " Accelerated generation of gene-engineered monoclonal CHO cell lines using FluidFM nanoinjection and CRISPR/Cas9" Biotechnology Journal 19, no. 4 (2024): 2300505.
Case Study - Streamlined U2OS Cell Line Modification with the CellEDIT Service Workflow, featuring our CellEDIT Customer: Dr. Kanstantsin Siniuk.