HIF1A (Hypoxia inducible factor 1, alpha subunit)

Mechanistically, MBRT downregulated HIF-1α/VEGFR signaling, alleviating hypoxia and angiogenesis, and enhanced vascular normalization via increased pericyte coverage. These findings suggest MBRT reprograms the TNBC microenvironment, supporting its potential as a radiosensitizing strategy for clinical translation.

This study suggests XPD exerts therapeutic effects on HMG by modulating hormone levels. Through AMPK activation, XPD inhibits fatty acid synthesis and energy metabolism, which reduces intracellular lipid accumulation and suppresses excessive cell proliferation. Additionally, it improves cellular energy status, thereby alleviating abnormal cell proliferation caused by energy metabolic disorders. XPD also promotes autophagy by inhibiting the downstream mTOR pathway, further suppressing cell proliferation. Moreover, it inhibits VEGF expression to exert anti-angiogenic effects, reducing blood supply to hyperplastic breast tissue and restricting its growth-thus contributing to HMG treatment.

This research explored the effectiveness of RGD peptide-functionalized gold nanoparticles (AuNPs) loaded with the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) to enhance the radiosensitivity of non-small cell lung cancer (NSCLC) by suppressing hypoxia signaling, thereby mitigating oxidative stress and inflammatory responses...RGD-AuNPs-SAHA effectively remodeled the hypoxic tumor microenvironment, attenuated oxidative stress, and suppressed pro-tumorigenic signaling, leading to significant apoptosis and DNA damage. These findings highlight its potential as a radiosensitizer for NSCLC, offering a promising strategy to improve radiation therapy outcomes.

Hence, we designed a degradable embolic microsphere (RegFe@MS) capable of simultaneously loading hydrophobic regorafenib and magnetic iron oxide nanoparticles...This strategy can not only inhibit the post-embolization angiogenic response but also maximally suppress the proliferation and invasion of residual tumors. Furthermore, RegFe@MS has demonstrated remarkable therapeutic effects in the rabbit orthotopic liver cancer model.

Translational and clinical studies suggest exercise can enhance chemotherapy and immunotherapy efficacy, while precision exercise prescriptions based on FITT principles, biomarkers, and patient-specific tolerance may maximize therapeutic benefits. This review summarizes the molecular and systemic mechanisms of exercise-induced metabolic-immune reprogramming and outlines strategies for clinical translation in oncology.

Consequently, the expression of glycolysis-related enzymes increased. In conclusion, the present study identified a close association between F-53B and the onset and progression of TNBC, providing important evidence for investigating the toxicological mechanism of F-53B.

Co-inhibition of mTOR or the SLC3A2/SLC7A5 complex using dactolisib or JPH203 restores sensitivity to KRAS inhibitors in vitro and in vivo. These findings support combinatorial targeting of mTOR signaling or amino acid transport to overcome intrinsic resistance in KRAS-mutant lung cancer.

GO and KEGG analyses indicated that the main pathways included the hypoxia-inducible factor 1 (HIF-1) signaling pathway, phosphatidylinositol 3-kinase-protein kinase B (PI3K-AKT) signaling pathway, and advanced glycation end products-receptor for advanced glycation end products (AGE-RAGE) signaling pathway, involving processes such as signal transduction, receptor complex formation, and cytokine activity. The core acupoint prescription for PCOS might exert therapeutic effects through multiple targets and pathways, providing a theoretical basis for mechanistic research on acupoint prescriptions.

Secondly, exosome USP35 derived from GC cells has been shown to promote the mesothelial-mesenchymal transformation (MMT) of PMCs, preparing the "soil" for cancer cell adhesion and growth and contributing to the establishment of a pre-peritoneal-metastasis adaptive microenvironment. In summary, USP35 synergistically promotes the establishment of this environment through the dual mechanisms of regulating energy metabolic reprogramming of tumor cells and inducing the MMT of PMCs via the exosome pathway, providing a new theoretical basis for searching for therapeutic targets of gastric cancer with peritoneal dissemination.

Our study indicates that hypoxia mediates the increase of CD25 in OSA patients. In turn, our data revealed sCD25 were related to tumour aggressiveness in OSA patients with melanoma or lung cancer, and suggest sCD25 as a potential novel biomarker to stratify OSA patients with lung cancer by mortality risk.

Western blot analysis revealed that Akt, ERK1/2, integrin β1, HIF-1α, MMP-9, MMP-7, CDK2, cyclin A2, pro-caspase-9, pro-caspase-8, pro-caspase-3, and lamin A/C were decreased in a dose-dependent manner, whereas Smac/DIABLO, cleaved caspase-9, cleaved caspase-8, and cleaved caspase-3 were increased in a concentration-dependent manner, indicating downregulation of proliferation, activation of upstream signal transduction influencing cell cycle arrest and apoptosis, deactivation of metastasis, induction of cell cycle arrest at the S and G2/M phases, and activation of intrinsic and extrinsic apoptotic pathways. These findings suggest that the ethyl acetate fraction of O. humifusa induces apoptosis, cell cycle arrest, and anti-metastasis as well as contributing to upstream signal transduction of anti-proliferation, apoptosis, and cell cycle arrest in human triple-negative breast cancer cells.

CRM1 inhibition by Selinexor re-establishes nuclear PHD2 residency, increases the degradation of HIF-1α in hypoxia, abrogates P-gp-mediated lysosomal anthracycline trapping, and confers potent in-vitro and in-vivo chemosensitization. These data provide mechanistic rationale for integrating Selinexor into salvage regimens for R/R-AML.