HDGF (Heparin Binding Growth Factor)

Moreover, HDGF re-expression counteracted the suppressive effects of MAZ knockdown on HGSOC cell malignant behaviors, HUVEC tube formation, M2 macrophage polarization, and the growth of xenograft tumors. In conclusion, our study unveils the MAZ/HDGF axis as a novel SE-mediated oncogenic pathway in HGSOC, providing previously unrecognized insights into SE-driven oncogenesis and highlighting potential targets for HGSOC treatment.

Collectively, these analyses provide an insight into the interplay between the m5C modification and rG4 to fine-tune the post-transcriptional regulation during development. It also suggests the possible involvement of m5C colocalized sites with PQS in modulating the expression of oncogene Hdgf, as well as the oncogenic and therapeutic targets like Med24 and Emc3.

RBPs display single-cell-level heterogeneity and are associated with pathways relevant to HCC progression. HDGF is identified as a candidate oncogenic RBP based on in vitro phenotypes and correlative splicing analyses. These findings highlight the potential of RBPs, including HDGF, as candidates for further mechanistic and therapeutic exploration in HCC.

Our findings establish HDGF as a key promoter of HSCC progression through dual regulation of EMT and AKT/mTOR/VEGF pathways, suggesting its potential as a therapeutic target. These results provide mechanistic insights for developing HDGF-targeted strategies against this lethal malignancy, warranting further clinical exploration.

Knocking down CircRAD18 can reduce HDGF expression by up-regulating miR-185-5p, thereby weakening DNR resistance in AML cells, inhibiting KG1a cell proliferation under DNR treatment, and promoting apoptosis.

Furthermore, the HDGF receptor nucleolin (NCL) was overexpressed in microglia under high glucose stimulation. Therefore, blocking HDGF from Müller cells in DR reduced the excessive inflammatory response of microglia, highlighting HDGF as a potential therapeutic target.

HDGF may serve as a clinically relevant biomarker for disease progression, while LINC00839 and miR-345-5p represent promising therapeutic targets. These findings provide a foundation for future investigations into ceRNA-based diagnostics and treatments in OC.

Our results reveal that HDGF is an oncogene frequently amplified and upregulated, leading to suppression of PTEN expression and activity, thereby contributing to malignant progression in liver cancer. HDGF upregulation in resected paired-HCC specimens may constitute a valuable prognostic biomarker for HCC patients.

Mechanistically, we found that HDGF modulates DNA damage response and, by recruiting C-terminal binding protein-interacting protein (CtIP), it facilitates homologous recombination repair to influence CRC drug sensitivity. Furthermore, we propose that HDGF may serve as a recognition protein for H3K36me3, participating in the repair of damaged transcriptionally active genes, thus maintaining genomic stability in CRC.

These findings indicate that the novel IGF2BP2-HDGF axis is pivotal for ESCC cancer progression and can serve as a target for developing therapeutics.

In vivo experimental results have demonstrated that TMSN@siHDGF-Gint4.T significantly inhibits tumor growth and extends the survival time of GBM-bearing mice. Thus, the as-developed TMSN@siHDGF-Gint4.T affords a potential approach for the combination treatment of GBM.

Moreover, antioxidants of N-acetyl cysteine and MitoQ treatment significantly inhibited HDGF-mediated cell proliferation and invasive capacity...Finally, genetic knockdown nucleolin (NCL) and antibody neutralization of surface NCL, the HDGF receptor, abolished the HDGF-induced increase in ROS and mitochondrial energetics. In conclusion, this study has demonstrated for the first time that the HDGF/NCL signaling axis induces ROS generation by elevating ROS generation in mitochondria, thereby stimulating liver carcinogenesis.