NCI-H1299 KO cell line| High Efficiency | 100% guarantee | Ubigene
NCI-H1299 cell line, also known as H1299 or CRL-5803, is a human non-small cell lung carcinoma (NSCLC) cell line derived from the lymph node. Similar to other immortalized cell lines, H1299 cells can divide infinitely. Also, H1299 cells have a homozygous partial deletion of the TP53 gene, therefore they do not express the tumor suppressor p53 protein that will lead to their proliferative propensity. Moreover, it is reported that these cells can secrete the peptide hormone neuromedin B (NMB), but not gastrin-releasing peptide (GRP). With these interesting characteristics, NCI-H1299 cells become a popular cell line in biological fields that involves gene knockout, gene knock-in, and point mutation.
Lung cancer is the second most prevalent and the most lethal malignancy in both men and women throughout the world. On the other hand, NSCLC accounts for about 85% of lung cancer, which is the leading cause of cancer death in the world. As H1299 cell line was derived from the lymph node, so these cells have been widely used in lung cancer research. Characterizing the accumulated genetic alterations in cancer cells is of importance in both understanding tumor biology and guiding drug design. Besides, it might benefit the patients with a given targeted cancer therapy via gene-customized cancer-related cells, such as gene knockout H1299 cells, etc. As studies showed, NCI-H1299 cell line is a stable cell line with a homozygous knockout of some human genes using CRISPR/Cas9. So NCI-H1299 ko cell line is commonly-used in the treatment of lung cancer.
Paclitaxel reduced the ability of migration and proliferation of Rsf-1-knockout NCI-H1299
Paclitaxel is a classic drug for the treatment of lung cancer, but it readily induces resistance. Therefore, new ways to overcome drug resistance are urgently needed. Rsf-1 expression is high in lung cancer and increases paclitaxel tolerance through the NF-κB pathway. Many other genes are also involved in drug resistance, such as genes that affect apoptosis and the cell cycle. Chen and colleagues knocked out Rsf-1 in lung cancer cells and xenograft mice using CRISPR-Cas9 technology and tested whether Rsf-1 affects the sensitivity of lung cancer to paclitaxel by regulating the activation of the NF-κB pathway and the expression of its downstream genes. The result indicated that paclitaxel reduced the ability of Rsf-1-knockout NCI-H1299 and NCI-H460 cells to migrate and proliferate, and increased apoptosis. In mice with xenograft tumors derived from Rsf-1-knockout cells, the anti-tumor effect of paclitaxel was enhanced. Therefore, targeting Rsf-1 by CRISPR-Cas9 technology has also become one of the approaches for treating lung cancer.
Knockdown PON2 gene to investigate NCI-H1299 cell line proliferation
Previous research demonstrated that the expression of paraoxonase 2 (PON2), a lactonase/arylesterase with anti-oxidant properties, are markedly enhanced in cancer tissues of NSCLC patients compared with corresponding adjacent non-tumorous tissues. Moreover, increased PON2 expression might contribute to the resistance of NSCLC cells to classical anti-NSCLC therapeutic drugs. However, researchers found that stably reduced PON2 expression by siRNA can reduce the proliferation of NSCLC cells such as NCI-H1299 cells.
To further elucidate the role of PON2 in NSCLC cell proliferation, two gene-editing systems, TALEN and CRISPR/Cas, were applied in the NSCLC cell line NCI-H1299. The result indicated that Cas9 expression was induced by exogenous doxycycline in NSCLC cells in a reversible fashion, providing a platform to investigate how changes in gene expression modulate NSCLC cell proliferation.
CRISPR/Cas9 knockout NCI-H1299 cell line strategies
Work flow of knockout NCI-H1299 cell line
1.X. Chen, X. Sun and J. Guan, et al, Rsf-1 Influences the Sensitivity of Non-Small Cell Lung Cancer to Paclitaxel by Regulating NF-κB Pathway and Its Downstream Proteins, Cell. Physiol. Biochem, 2017, 44(6), 2322.
2.Antitumor effects of Tubeimoside-1 in NCI-H1299 cells are mediated by microRNA-126-5p-induced inactivation of VEGF-A/VEGFR-2/ERK signaling pathway. Hanbing Shi, Hongxia Bi, Xingyuan Sun, Haiying Dong, Yunfei Jiang, Haijun Mu, Guohua Liu, Weili Kong, Ruizhi Gao, Jiang Su. Mol Med Rep. 2018 Mar; 17(3): 4327–4336.