Nci h1792

Manufactured by American Type Culture Collection

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The NCI-H1792 is a cell line derived from a human lung cancer. It is a widely used tool in cancer research and drug development. The cell line maintains the characteristics of the original tumor and can be used for various in vitro studies.

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H1792 (39 citations)

16 protocols using nci h1792

Characterization of Isogenic KRAS-Mutant Colon and Lung Cancer Cell Lines

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The paired isogenic HCT116 KRAS^WT/− and HCT116 KRAS^WT/G13D colon cancer cell lines were kind gifts from Dr. Bert Vogelstein (Johns Hopkins, Baltimore, MD). A549, NCI-358, NCI-H460, NCI-H522, NCI-H1568, NCI-H1792, NCI-H23, NCI-H1975, and NCI-H1437 were obtained from the ATCC (Manassas, VA). HCT116 cells were cultured in DMEM (Invitrogen) with 10% FBS (Invitrogen) and 1% Pen/Strep (Invitrogen). All lung cancer cell lines were cultured in RPMI 1640 (Gibco) with 10% FBS and 1% Pen/Strep. HCT116 Cell lines were validated by PCR amplification and Sanger Sequencing to confirm the mutation at the genomic level. Strict bio-banking procedures were followed and cells were tested for contamination, including mycoplasma. All other cell lines were obtained from ATCC and used within 2–4 months.

Zhou Y., Dang J., Chang K.Y., Yau E., Aza-Blanc P., Moscat J, & Rana T.M. (2016). miR-1298 inhibits mutant KRAS-driven tumor growth by repressing FAK and LAMB3. Cancer research, 76(19), 5777-5787.

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KRAS Mutation Cell Line Characterization

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Authenticated NCI-H358, NCI-H1792, and NCI-H1793 cell lines were purchased from ATCC. NCI-H1793 harbor homozygous wild-type KRAS, both NCI-H358 and NCI-H1792 are heterozygous for KRAS^G12C; KRAS is not amplified in any of the cell lines [51 (link)]. Cells were grown in RPMI 1640 Medium supplemented with 10% fetal bovine serum (FBS). Cells were cultured at 37°C in a humidified incubator at 95% O₂ and 5% CO₂ and were routinely passaged at 80% confluency. All cell lines were confirmed negative for mycoplasma.

Warren H.R., Ross S.J., Smith P.D., Coulson J.M, & Prior I.A. (2022). Combinatorial approaches for mitigating resistance to KRAS-targeted therapies. Biochemical Journal, 479(18), 1985-1997.

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NSCLC Cell Lines Authentication

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The human NSCLC cell lines, A549, NCI-H23, NCI-H358, NCI-H460, NCI-H647, NCI-H1355, and NCI-H1792 were purchased from ATCC and authenticated with short tandem repeat (STR) profiling by Genesky Biotechnologies Inc (Shanghai, China). A549 cells were maintained in Ham’s F-12 Medium (Corning, NY, USA), and the remaining cell lines were maintained in RPMI 1640 medium (Corning), supplemented with sodium pyruvate (1 mM) and glucose (2500 mg/L). All culture media were supplemented with 10% heat-inactivated fetal bovine serum (FBS).

Wang Y., Li X., Liu X., Chen Y., Yang C., Tan C., Wang B., Sun Y., Zhang X., Gao Y., Ding J, & Meng L. (2019). Simultaneous inhibition of PI3Kα and CDK4/6 synergistically suppresses KRAS-mutated non-small cell lung cancer. Cancer Biology & Medicine, 16(1), 66-83.

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Cell Lines Acquisition for Cancer Research

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NCI-H358, Calu1, NCI-H1373, NCI-H1792, NCI-H23 and NCI-H2122 were purchased from the American Type Culture Collection (ATCC). HCC-44 and HOP-62 were acquired from MD Anderson Cancer Center (MDACC) and National Cancer Institute, respectively. LU-99 was generous gift from Dr. Sheri Moores (The Janssen Pharmaceutical Companies of Johnson & Johnson).

Solanki H.S., Welsh E.A., Fang B., Izumi V., Darville L., Stone B., Franzese R., Chavan S., Kinose F., Imbody D., Koomen J.M., Rix U, & Haura E.B. (2021). Cell-type Specific Adaptive Signaling Responses to KRASG12C inhibition. Clinical cancer research : an official journal of the American Association for Cancer Research, 27(9), 2533-2548.

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Cell Line Culture and Maintenance

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RKO, WiDr, MCF7, T47D, MDA-MB-468, SW1417, NCI-H358, MIAPaCa-2, NCI-H1573, NCI-H1792, SKMEL2, Calu-1, Calu-6, HCT15, SW620, HCT116, HCC1937, BT20, MDA-MB-231, MDA-MB-157, Hs 578T, HT-29, SK-BR-3, BT-474, T84, and LoVo cells were purchased from the American Type Culture Collection (ATCC). HeLa, MDA-MB-436, BT-549, and SUM159 were provided by Ramon Parsons, and SNU387 cells were provided by Amaia Lujambio (both at Icahn School of Medicine at Mount Sinai). SW1736, Hth104, and 8505C cells were provided by James Fagin (Memorial Sloan Kettering Cancer Center). Cell lines were maintained in a humidified incubator at 37° C with 5% CO₂, cultured in RPMI 1640, DMEM, DMEM/F12, or F12 supplemented with 10% FBS, 2 mM glutamine and 100 IU/ml penicillin and streptomycin.

Ahmed T.A., Adamopoulos C., Karoulia Z., Wu X., Sachidanandam R., Aaronson S.A, & Poulikakos P.I. (2019). SHP2 Drives Adaptive Resistance to ERK Signaling Inhibition in Molecularly Defined Subsets of ERK-Dependent Tumors. Cell reports, 26(1), 65-78.e5.

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Cell Line Culture and Maintenance

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Cell Line Sources and Materials

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NCI‐H1792, NCI‐H2122, NCI‐H23, NCI‐H358, HCC827, A549, SW1573, SW837, Mia PaCa‐2, TOV‐21G, MDA‐MB‐231, and CALU‐6 cell lines were purchased from American Type Culture Collection (ATCC). KYSE‐410 cells were from the European Collection of Cell Cultures (ECACC). SNU668 and HCC‐44 cells were from the Korean Cell Line Bank (KCLB). CO‐04‐0070 PDC cells were provided by WuXi AppTec. Mouse KPL cell line was a gift of Ji et al.^[⁵¹ (link)
^] Cells were maintained in RPMI1640 or DMEM (Basalmedia) supplemented with 10% fetal bovine serum (FBS) (Gibco) and 1% penicillin–streptomycin (Gibco). AMG510, MRTX849, Defactinib, and GSK2256098 were purchased from DC chemicals. IN10018 was provided by InxMed. All the siRNAs used in the study were synthesized by Genepharma. Primers used in this study were synthesized by Biosune and listed together with siRNA sequences in Table S1, Supporting Information. The antibodies tested in the study were summarized in Table S2, Supporting Information.

Zhang B., Zhang Y., Zhang J., Liu P., Jiao B., Wang Z, & Ren R. (2021). Focal Adhesion Kinase (FAK) Inhibition Synergizes with KRAS G12C Inhibitors in Treating Cancer through the Regulation of the FAK–YAP Signaling. Advanced Science, 8(16), 2100250.

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Lung Cancer Cell Line Culture and Maintenance

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Human lung cancer cell lines, A549, NCI-H1734, NCI-H1792, NCI-H441, NCI-H23, NCI-H1975 and NCI-H520 cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA). Normal human tracheobronchial epithelial (NHTBE) cells were obtained from the Lonza (Walkersville, MD, USA). Cell lines were passaged for less than 6 months following resuscitation and were not authenticated. All cancer cell lines were maintained under 5% CO₂ at 37°C in RPMI-1640 medium (Life Technologies, Carlsbad, CA, USA) supplemented with 10% heat-inactivated fetal bovine serum (FBS, Sigma-Aldrich, St. Louis, MO, USA) and 1% Antibotic-Antimycotic (Anti-Anti, Life Technologies). NHTBE cells were cultured in BEBM supplemented with growth factors and hormones provided by manufactory (Lonza), and three-demensional organotypic air-liquid interface (ALI) cell culture method was utilized for NHTBE cell culture, as described previously [5 (link), 17 (link)–19 (link)]. HEK293T cells were maintained in DMEM medium supplemented with 10% FBS and 1% Anti-Anti.

Lee J.W., Park H.S., Park S.A., Ryu S.H., Meng W., Jürgensmeier J.M., Kurie J.M., Hong W.K., Boyer J.L., Herbst R.S, & Koo J.S. (2015). A Novel Small-Molecule Inhibitor Targeting CREB-CBP Complex Possesses Anti-Cancer Effects along with Cell Cycle Regulation, Autophagy Suppression and Endoplasmic Reticulum Stress. PLoS ONE, 10(4), e0122628.

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Lung Cancer Cell Lines Characterization

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The lung cancer cell lines A549, NCI-H358, NCI-H1792, NCI-H23, SW900 and SW1573 were purchased from the American Type Culture Collection. SK-LU-1, Calu-1, Calu-6 and NCI-H460 were provided by Takashi Takahashi (Nagoya University, Japan). RERF-LC-AD2, LU-65 and LU-99 cells were obtained from the Japanese Cell Research Bank (Osaka, Japan). HCC2108 cells were obtained from Korean Cell Line Bank (Seoul, South Korea). The NCI-H1573 and NCI-H2030 cells were provided from Massachusetts General Hospital Cancer Center. Cells were cultured in RPMI1640 (Invitrogen) with 10% FBS. Characteristic of cell lines used in this study were summarized in Supplementary Table S4. Cells were obtained between 2012 and 2016. Experiments using A549, SW900, LU-65 and HCC2108 cells were done within 6 months from the acquisition of these cells from cell banks. All other cell lines were tested and authenticated by short tandem repeat (STR) analysis with GenePrint 10 System (Promega) by the Japanese Cell Research Bank at the time of submission. Cells were regularly screened for Mycoplasma using a MycoAlert Mycoplasma Detection Kit (Lonza). NVP-BGJ398, GDC-0941, ABT-263, selumetinib, afatinib, and trametinib were obtained from Active Biochem. Compounds were dissolved in DMSO to a final concentration of 10 mmol/l and stored at −20°C when not in use.

Kitai H., Ebi H., Tomida S., Floros K.V., Kotani H., Adachi Y., Oizumi S., Nishimura M., Faber A.C, & Yano S. (2016). Epithelial-to-mesenchymal transition defines feedback activation of receptor tyrosine kinase signaling induced by MEK inhibition in KRAS mutant lung cancer. Cancer discovery, 6(7), 754-769.

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Immunohistochemical Analysis of NSCLC

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Clinical samples were obtained from 214 patients with NSCLC who were surgically treated at Harbin Medical University Cancer Hospital from January 2007 to December 2010. Thirty matched metastatic lymph nodes from 30 patients whose primary tumor expressed high levels of EHD1 were selected for immunohistochemical (IHC) examination. Fresh tissues (paired NSCLC tumor samples and matched adjacent normal tissue samples) were resected from 20 NSCLC patients between June 2013 and June 2014. This study was approved by the Institute Research Medical Ethics Committee of Harbin Medical University. All of the patients gave their informed consent.
The human lung adenocarcinoma cell lines A549, NCI-H1299, NCI-H1975, NCI-H1792, NCI-H1650 and HCC827, the lung squamous cell carcinoma cell lines NCI-H520, NCI-H2170 and SK-MES, and the large cell carcinoma cell line NCI-H460 were purchased from American Type Culture Collection (ATCC, Manassas, VA), which employed short tandem repeat (STR) profiling to ensure cell line authenticity 3 months before the initiation of this study. No other forms of authentication were implemented by the author during the course of the study.

Meng Q., Xing Y., Ren T., Lu H., Xi Y., Jiang Z., Hu J., Li C., Sun L., Sun D, & Cai L. (2016). Mammalian Eps15 homology domain 1 promotes metastasis in non-small cell lung cancer by inducing epithelial-mesenchymal transition. Oncotarget, 8(14), 22433-22442.

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