E2F7 (E2F Transcription Factor 7)

[This retracts the article DOI: 10.1155/2021/5338934.].

S100A2 is transcriptionally activated by E2F7. Targeting E2F7/S100A2 axis may diminish LUAD immune evasion.

Tissue mRNA expression levels of E2F7 correlated with patient prognosis in PC. In the low E2F7 mRNA expression group, patients who received S-1 as adjuvant chemotherapy had a better prognosis than those who received gemcitabine (GEM).

There existed a positive correlation between E2F2 expression level and Dasatinib sensitivity, negatively related to drug sensitivity of Nelarabine, XK-469, Cyclophosphamide, etc. Pazopanib, Doxorubicin, and Paclitaxel sensitivity was all positively associated with E2F5 expression. According to these analysis and validation results, E2F genes are relevant to the occurrence and progression of various cancers, which may be biomarkers for tumor diagnostics and prognosis. The discovery of new therapeutic targets can lead to reshaping TME to promote tumor-suppressive metastasis rather than tumor-friendly metastasis.

E2F7 promotes ESCC progression and cisplatin resistance by transcriptionally activating DVL3 and activating the Wnt signaling pathway. Targeting the E2F7-DVL3 axis may provide a promising therapeutic strategy for ESCC treatment.

In renal cancer tissues, a robust inverse correlation was detected between the expression of E2F7 and that of Beclin-1, LC3, and E-cadherin. E2F7 expression showed a substantial beneficial association. Notably, elevated E2F7 expression was associated with advanced clinical and pathologic stages of the tumor. A dual-luciferase assay confirmed the interaction between E2F7 and Beclin-1.

We analyzed 103,171 single-cell transcriptomes from 18 MM samples (10 optimal responders [OR] and 8 suboptimal responders [SOR] to bortezomib-melphalan-prednisone) to investigate cell-type composition, malignant plasma cell subclusters, and tumor-microenvironment crosstalk. In contrast to the known role as a tumor suppressor in solid and hematologic cancers, our integrative analyses identified PTPRG among seven stemness-related genes upregulated in MalPlasma3 and poor-survival cells, which was echoed in the observed reduced cell viability and increased apoptosis in MM cell lines following siRNA-mediated PTPRG knockdown. This single-cell multi-omic dissection implicates a proliferative, stem-like MalPlasma3 subcluster and identified PTPRG as a key mediator of drug resistance and poor outcome in MM, offering novel prognostic biomarkers and therapeutic targets.

Critically, inhibition of miR-1183 rescued the suppressive effects of DDX11-AS1 knockdown on glioma tumorigenic phenotypes and restored E2F7 expression levels. This study demonstrates that lncRNA DDX11-AS1 promotes glioma progression by regulating the miR-1183/E2F7 axis, indicating a potential therapeutic target for glioma.

To assess the level of glycolysis in BC cells, we detected the expression of key proteins LDHA, HK2, and GLUT1 through WB, and measured the extracellular acidification rate and oxygen consumption rate with kits. Cell experiments combining bioinformatics analysis demonstrated that both E2F7 and SPC24 were greatly upregulated in BC, with SPC24 primarily enriched in the glycolysis metabolic pathway. Further experiments manifested that SPC24 reinforced cell stemness through aerobic glycolysis reprogramming, and SPC24 was modulated by transcription factor E2F7. E2F7 transcriptionally activates the upregulation of SPC24 in BC, which boosts stemness through aerobic glycolysis reprogramming.

Grx2 plays an oncogenic role in colon cancer cells and also affects the relapse-free survival of patients with colon cancer. Grx2 may be a novel prognostic biomarker and therapeutic target for colon cancer.