ANXA5 (Annexin A5)

The tumor-driven proliferation of aggressive LSC clones, caused by dysregulated self-renewal, leads to highly proliferative tumor masses. The current findings showed that the cells couldn't recover from chronic, persistent B[a]P-induced damage, even at the lowest tested concentrations, leading to irreversible and invasive lesions.

The pathways affected are: Ephrin Receptor Signaling, TGF-β Signaling, STAT3 Pathway, EGF Signaling, Tumor Microenvironment Pathway, BAG2 Signaling Pathway, H-17A Signaling Pathway, EIF2 Signaling. Annexin-V and Tubulin tracker kits identified the apoptotic capabilities of the PR series compounds.

The ability of TUBB4A to counteract STAT1 inhibition effects suggested that targeting this regulatory axis represents a potential therapeutic strategy. The findings of the present study contributed novel mechanistic insights that may facilitate the development of innovative melanoma treatment modalities.

All compounds reduced ethanol-induced loss of viability and apoptosis, and PQM-242 additionally prevented ethanol-mediated Bax upregulation. Overall, PQM-242 and PQM-249 demonstrated enhanced cellular safety and maintained protective activity, supporting their further investigation as candidate molecules for AUD.

CuHL1 exhibits potent cytotoxicity in the low micromolar range (IC50 ≈ 2 µM), surpassing cisplatin by up to 81-fold...Functional assays confirm reduced migratory capacity in MDA-MB-231 cells. These findings position CuHL1 as a promising candidate for TNBC therapy, meriting further in vivo evaluation.

The cytotoxic effects of these compounds were linked to apoptosis, as confirmed by positive annexin V and PI staining observed under a fluorescence microscope, as well as molecular docking studies. Additionally, compounds 1 and 2 elicited significant antiviral activity against DENV-2 with EC50 values of 17.89 and 12.59 μg/mL, respectively.

Cell counting kit-8 (CCK-8) assay, 5-Ethynyl-2'-deoxyuridine (EdU) assay, colony formation assay and Annexin V-FITC/PI assay were performed to detect the anti-cancer effects of HQD and EGFR-TKIs (1st generation EGFR-TKI gefitinib or 3rd generation EGFR-TKI Osimertinib) in different NSCLC cell lines. Moreover, the drug safety, anti-cancer effect and potential mechanism of the therapy of HQD and EGFR-TKIs were confirmed in vivo. HQD enhances the anti-cancer effect of EGFR-TKIs in NSCLC through ROS-mediated CSC makers inhibition by suppressing stat3/GPX4 axis to induce redox ratio, providing a novel strategy for the treatment of NSCLC patients.

Gene expression analysis showed upregulation of FAS (1.67-fold; P<0.001), FASL (1.28 fold; P=0.005), BAX (2.34 fold; P<0.001), BAK (1.29 fold; P=0.004), and BIM (1.4 fold; P<0.001) and downregulation of BCL-2 (0.44 fold; P<0.001), BCL-XL (0.47 fold; P<0.001), PI3K (P<0.001), AKT (P<0.001), and MTOR (P<0.001). Vipera raddei kurdistanica venom may exert selective cytotoxic effects against gastric cancer cells and may induce apoptosis through both intrinsic and extrinsic pathways, potentially via inhibition of the PI3K/AKT/mTOR signalling axis.

MiR-200c restoration inhibits FOXP3 and suppresses metastatic progression in breast cancer. Targeting the miR-200c/FOXP3 axis presents a novel and promising therapeutic approach for advanced breast cancer.

SY might induce apoptosis in tumour cells with counter mechanisms on angiogenesis, proliferation and metastasis in Drosophila model. Gene amplification, protein specificity, etc are the future prospects of present work.

In vivo, perivascular delivery of PDK4-IN-1 in the mouse carotid artery injury model significantly ameliorated neointimal hyperplasia. Inhibition of PDK4 perturbs pathological VSMC phenotypic switching, suppresses proliferation, promotes apoptosis and autophagy, and mitigates neointimal formation, highlighting PDK4 as a promising therapeutic target for vascular proliferative diseases.

Etoposide was used as a reference in characterization, release, and loading studies...Plain liposomes exhibited minimal cytotoxicity, confirming their biocompatibility. Liposomal bromophenol, which we have introduced to the literature for the first time, is expected to be a promising nanocarrier system that could be effective in cancer treatment by improving the therapeutic index of new drug candidates such as marine bromophenols.