RHOD (Ras Homolog Family Member D)

These studies reveal that BMPR2 signaling regulates TAK1-d splice variant to mediate mitochondrial Ca2+ transport, which is dependent on the MCU. Our studies suggest that BMPR2 signaling utilizes mtCa2+ transport to regulate both mitochondrial bioenergetics and/or cell survival. Our studies provide novel insight into how aberrant BMPR2 signaling is pathogenic and suggests that the response could vary depending on the cell type.

This study demonstrates that β-Asarone induces apoptosis in B16F10 melanoma cells by triggering Ca²⁺ overload and mitochondrial dysfunction.

The differential immune phenotypes associated with ER expression suggest distinct immune evasion strategies requiring tailored therapeutic approaches. This comprehensive characterization provides critical insights for developing personalized immunotherapeutic strategies incorporating metabolic modulation and hormone receptor status stratification.

Key recommendations encompass the following aspects: Supplementing statistical power justification through explicit definition of parameters including ≥80% desired power, minimal effect size, and intra-group variability; Report exact P values with confidence intervals to improve statistical transparency; Clarification of p38 MAPK versus cPLA2 pathway contributions via co-inhibition experiments; Exclusion of TRP channel confounding effects when using 2-APB through targeted TRPV6 inhibition; Distinction between direct Cd²⁺ effects and toxicity-induced compensatory responses; Provision of explicit rationale for selecting Mag-Fluo-4/AM and Rhod-2/AM fluorescent probes; Experimental verification of PMCA inhibition synergism with cadmium-induced cytosolic Ca²⁺ overload. These recommendations would enhance the robustness of the original study's conclusions.

In conclusion, through a specific bioinformatics workflow, in addition to in vitro and further clinical validations, we found three novel markers to precisely identify CTCs. These markers, when used together, enable a significantly more efficient identification of CTCs compared to conventional epithelial markers.

Our findings suggest that eccDNAs, particularly ecDNA amplifications like HIF1A, contribute significantly to cisplatin resistance mechanisms in HGSOC. These insights highlight eccDNA as a potential target for overcoming therapeutic resistance and improving treatment outcomes in ovarian cancer.

(2) Under green light (λ ~ 550 nm), the CO bond in Rhod ben is broken, thus releasing the anticancer drug (bendamostatin) targeted in breast cancer cells. Therefore, Rhod-ben is expected to become a new "diagnosis and imaging" fluorescent probe for breast cancer cells or cancer cells with ROS overexpression.

The experiment was set up with solvent control group (0.1% ethanol), VES dose groups, 100 nmol/L rapamycin (RAPA) as autophagy positive control group (RAPA group), 15 μg/ml tunicamycin (TM) was used as the endoplasmic reticulum stress (ERS) positive control group (TM group), 10 μmol/ml 2-aminoethyl diphenylborinate (2-APB group) was used to inhibit IP(3)R (2-APB group) and VES+2-APB group...Compared with VES group, LC3 and Beclin1 protein expressions in two kinds of gastric cancer cells in VES+2-APB groups were significantly decreased (P<0.05) . VES may activate intracellular calcium redistribution through IP(3)R-Grp75-VDAC1 calcium channel and induce autophagy in gastric cancer cells.

Furthermore, RHOD plays a distinct suppressor role in tumor development, partly associated with its regulatory effect on autophagy. These findings reveal the important roles of RHOD in autophagy and tumor development.

In vivo experiments demonstrated significant tumor volume reduction and increased survival rates in tumor-bearing mice treated with Cu/Ca-CDs, without any observed toxicity to normal tissues or changes in body weight, underscoring the efficacy and biosafety of Cu/Ca-CDs. These findings highlight Cu/Ca-CDs as a promising strategy for precision oncology, offering effective tumor targeting, dual-mode imaging, and synergistic anti-tumor efficacy with reduced side effects.

The targeting effect of Ir-rhod reduces its systemic toxicity in vivo, enhancing its biosafety profile. To our knowledge, Ir-rhod is an effective mitochondria-targeted Ir complex capable of inducing tumor cell death by disrupting mitochondrial function, offering a potent strategy to suppress cisplatin resistance in non-small cell lung cancer.

These results demonstrate the potential of liposome formulations for therapeutic siRNA delivery. The encapsulation enhances cellular uptake and gene silencing efficiency, making the liposome formula a promising candidate for targeted gene therapy in hepatic carcinoma. Further research should explore it's in vivo biodistribution and potential combination therapies.