E2F8 (E2F Transcription Factor 8)

These results indicated that E2F8 promotes proliferation, migration, and invasion of EC cells by transcriptionally activating EGFL6.

In conclusion, E2F8 promotes EC progression by transcriptionally activating DTL and activating the MAPK pathway. These findings provide novel mechanistic insights into EC progression and suggest that the E2F8/DTL/PDCD4/MAPK axis may serve as a potential therapeutic target for EC.

Furthermore, our ML model achieved an accuracy of 89.58% to predict patient survival. The clinical and biological features proposed here in conjunction with ML can improve the interpretation of CRC mechanisms and predict patient survival.

In vivo experiments confirmed that ginsenoside CK suppressed tumor formation by downregulating EZH2, activating the dendritic cell-NK cell axis, and remodeling the tumor immune microenvironment. Ginsenoside CK inhibits EZH2, activating the dendritic cell-NK cell axis and remodeling the tumor immune microenvironment, thereby suppressing HCC cell activity and tumorigenicity.

Notably, the 3' untranslated region (3'UTR) of ESPL1 showed strong binding sites for hsa-let-7b-5p. We also identified Hesperidin as a high affinity ESPL1 binders, suggesting novel therapeutic candidates targeting this oncogenic network.

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.

Our findings suggest that this four-gene panel holds significant promise as a robust prognostic tool for breast cancer survival. This research paves the way for further investigations into targeted therapies and personalized medicine approaches in the management of breast cancer.

In vivo studies further validated its efficacy, showing significant tumor suppression in a lung cancer model without observable systemic toxicity. Collectively, these findings highlight pyrrolidinium fullerenes as promising candidates for targeted cancer therapy, paving the way for further development of YTHDF1 inhibitors as novel anticancer agents.

Our work illustrated the oncogenic role of GRPEL2 in CRC development and determined the molecular mechanism of E2F8/GRPEL2/TIGAR pathway. These findings will provide novel insights and promising therapeutic targets for CRC treatment in the future.