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Human H1299 lung carcinoma cells treated with AVJ16 or DMSO (vehicle)

ABSTRACT: H1299 cells were treated with 1.5uM AVJ16 or DMSO for 96 hours and then analyzed by MS

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Lung Adenocarcinoma

SUBMITTER: Joel Yisraeli

LAB HEAD: Joel Yisraeli

PROVIDER: PXD054641 | Pride | 2025-09-01

REPOSITORIES: Pride

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			Action	DRS
	20210531-02-N1.raw	Raw
	20210531-04-N2.raw	Raw
	20210531-06-N3.raw	Raw
	20210531-08-N4.raw	Raw
	20210531-10-N5.raw	Raw

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Publications

AVJ16 inhibits lung carcinoma by targeting IGF2BP1.

Wallis Nadav N Gershon Tehila T Shaaby Sojod S Oberman Froma F Grunewald Myriam M Duran Deborah D Singh Amandeep A Vainer Gilad G Spiegelman Vladimir S VS Sharma Arun K AK Yisraeli Joel K JK

Oncogene 20250708 35

IGF2BP1 is an oncofoetal RNA binding protein (RBP) expressed in many tumors. Interest has focused of late on the role of RBPs in cancer, although their mechanism of action is not always well understood. Using a newly described small molecule inhibitor of IGF2BP1, termed AVJ16, we have analyzed the effects of this inhibition on RNA binding, RNA expression, and protein expression. AVJ16 treatment downregulates RNAs encoding members of several pro-oncogenic signaling pathways, including Hedgehog, W ...[more]

PMID: 40629079

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2018-12-04 | PXD011241 | Pride

H1299 cells: p53 transcriptional response in hypoxia

Project description:Transcriptional profiling of H1299 non-small cell lung carcinoma cells transfected with either wt p53 or mut(175) p53 driven by the 5xHRE promoter (5 repeats of hypoxia-inducible factor response elements) and treated for 16 h with normoxia (21% O2) or hypoxia(<0.1% O2). 5xHRE promoter ensures that p53 expression is induced in hypoxic conditions only. Goal was to determine the transcriptional response of p53 in hypoxia and the 175 p53 mutant was used as a control as it is DNA-binding defective and transcription-incompetent mutant. Four-condition experiment: wt p53-transfected H1299 cells treated with normoxia, mut p53-transfected H1299 cells treated with normoxia, wt p53-transfected H1299 cells treated with hypoxia, mut p53-transfected H1299 cells treated with hypoxia. Biological replicates: 1 normoxic sample with wt p53, 1 normoxic sample with mut p53, 3 hypoxic samples with wt p53, 3 hypoxic samples with mut p53.

2014-01-08 | E-GEOD-53893 | biostudies-arrayexpress

NCI-H1299 cell line transfected with human DENND2D and vector

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2010-05-27 | E-GEOD-16890 | biostudies-arrayexpress

Identification of AGR2 interacting proteins in H1299 cells using SILAC quantification

Project description:LC-MS/MS analysis with SILAC quantification to identify proteins interacting with AGR2 protein in H1299 lung cancer cells

2022-01-03 | PXD012687 | Pride

Expression data for cultured NCI-H1299 parental and spheroid cells as well as their derived xenograft models

Project description:Current approaches to the preclinical investigation for novel cancer therapies rely heavily on the use of traditional cancer cell lines maintained in serum-containing conditions. The discrepancy between promising preclinical efficacy and clinical outcome of most novel anticancer agents emphasizes a need for developing predictive preclinical models that preserve the integrity of original patient tumors, including cancer stem cell (CSC) compartment. In this study, we isolate and characterize CSCs from a non-small cell lung cancer cell line, NCI-H1299, by selectively propagating the cells in a stem-cell culture condition. Isolated CSCs proliferated as nonadherent spheroids, displayed capacity to differentiate and self-renew and exhibited higher tumorigenic potential compared to the parental cells. The gene expression profiles of NCI-H1299 parental cells (serum-containing medium), CSCs (stem-cell medium), and xenograft tumor derived from both cell types were studied by Affymetrix array analysis

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RNA-seq of H1299 cells stably transfected with empty vector or the p53 mutant R273H.

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MicroRNA expression data from H1299 cells

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Transcription profiling by array of human p73 over-expressing H1299 cells

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Gene profile in H1299 cells treated with PTD-DRBD GAPDH siRNA or treated with Lipofection GAPDH siRNA

Project description:Whole genome microarrays were probed with total mRNA from PTD-DRBD GAPDH siRNA treated H1299 cells at 12 h and 24 h. Using a 1.6x fold increase/decrease filter of cellular mRNAs, we detected a dramatic reduction in the target GAPDH mRNA along with a limited number of both up and down regulated genes. The up regulated genes were reduced in numbers and to nearly background 1.6x levels at 24 h, while the down regulated genes increased slightly in numbers and maintained a similar magnitude at 24 h. In contrast, lipofection treated cells showed both a dramatic increase in both the total number of genes altered and the magnitude of the increase. In addition, the numbers of genes affected increased between 12 h and 24 h, suggesting that lipofection of siRNAs into cells results in a substantial alteration to the transcriptome and may thereby confound interpretation of experimental outcomes. Moreover, the GAPDH specific knockdown was significantly smaller than PTD-DRBD mediated knockdown. Total RNA obtained from H1299 cells treated with PTD-DRBD GAPDH siRNA, Lipofection GAPDH siRNA or PBS (Control) after 12 or 24 hours post-treatment

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