Our results suggest that overexpression of E2F1, induced both by LOH at the RB locus and anomalous phosphorylation of the RB protein, is involved in the development of non-small cell lung carcinoma.

data identify E2F1 as a critical determinant of the cellular response to death-receptor-mediated apoptosis, and suggest that its downregulation contributes to the immune escape of lung adenocarcinoma tumor cells

Overexpression of E2F-1 is associated with neuroendocrine lung tumors

There is over-expression of E2F-1 gene and deletion of p14(ARF) gene in the tumorigenesis of the lung cancer in Gejiu and Xuanwei regions in Yunnan Province.

GCN5 has a role in potentiating growth of non-small cell lung cancer by promoting E2F1, cyclin D1, and cyclin E1 expression

Genomic deregulation of the E2F/Rb pathway leads to activation of the oncogene EZH2 in small cell lung cancer.

A differentially regulated gene module, which is enriched for cell cycle-related and E2F1 targeted genes, plays a role in the molecular differences between smoker and non-smoker lung cancer.

Studied a new therapeutic alternative in the treatment of multiresistant lung adenocarcinoma via siRNA-specific transfection of six crucial molecules involved in lung carcinogenesis: SFR, E2F1, Survivin, HIF1, HIF2 and STAT3.

ATO has potent in vitro and in vivo activity in lung adenocarcinoma, partially mediated through E2F1 downregulation and apoptosis

High E2F1 expression is associated with metastasis in non-small cell lung cancers.

Stimulation of multiplenon-small cell lung cancer cell lines with nicotine led to enhanced recruitment of beta-arrestin-1 and E2F1 on vimentin

COMMD9 participates in TFDP1/E2F1 activation and plays a critical role in non-small cell lung cancer.

Cell proliferation and apoptosis were almost completely abolished in the PAa cells cotreated with TRIM28 siRNA and etoposide following knockdown of E2F1. The results of our study demonstrated that the combination of TRIM28 siRNA and etoposide may be effective against nonsmall cell lung cancer (NSCLC)and has the potential of being a new therapeutic tool for future treatment.

Reports showed that high expression of the transcription factor E2F1 was involved in the invasion and metastasis of small cell lung cancer (SCLC). Further results provided evidence that E2F1 promoted EMT by regulating ZEB2 gene expression in SCLC.

Our findings reveal that the rs3213173 (C/T) and rs3213176 (G/A) polymorphisms of the E2F1 gene are genetic risk factors for susceptibility to lung cancer and Head and Neck cancer in the North Indian Population.

HAGLR could physically interact with DNMT1, and recruit DNMT1 on E2F1 promoter to increase local DNA methylation. HAGLR promoted lung adenocarcinoma progression by recruiting DNMT1 to modulate the promoter methylation and expression of E2F1.

LncRNA SNHG3 is activated by E2F1 and promotes proliferation and migration of non-small-cell lung cancer cells through activating TGF-beta pathway and IL-6/JAK2/STAT3 pathway.

LINC00461/miR-4478/E2F1 feedback loop promotes non-small cell lung cancer cell proliferation and migration.

Silencing of KIF3A suppressed TNBC cell proliferation by repressing the Rb-E2F signaling pathway and inhibited migration and invasion by repressing epithelial-mesenchymal transition. The tumor size was smaller and the number of lung metastatic nodules was lower in KIF3A depletion MDA-MB-231 cell xenograft mice than in the negative control group. In addition, KIF3A overexpression correlated with chemoresistance.

Identification of nsSNPs of transcription factor E2F1 predisposing individuals to lung cancer and head and neck cancer.

E2F1-mediated repression of WNT5A expression promotes brain metastasis dependent on the ERK1/2 pathway in EGFR-mutant non-small cell lung cancer.