DDIT4 (DNA Damage Inducible Transcript 4)

Our results nominate DDIT4 as a promising therapeutic target for HCC intervention. Further preclinical and clinical investigations are warranted to validate DDIT4's translational potential and explore targeted strategies to stabilize its tumor-suppressive functions.

Erastin (ER), a small-molecule compound, induces ferroptosis through ROS accumulation...Our findings highlight ASNS, CHAC1, PCK2, DDIT4, and ATF3/4 as potential biomarkers for ferroptosis in CRC. Monitoring the expression of these genes may help identify patients who are responsive to ferroptosis inducers and facilitate the development of personalized treatment strategies.

In addition, multi-center datasets and immunohistochemistry revealed a significant up-regulation of DDIT4, FURIN, PTTG1 and RIPK2 at transcriptional and protein expression levels in LUAD tissues compared to normal tissues. PTDGs are potential biological markers for prognostic risk stratification of patients with LUAD.

Importantly, multiomics analyses reveal a unique mechanism of action: APT NPs induce the upregulation of the stress-responsive gene DNA damage-inducible transcript 4 (DDIT4), which inhibits the mammalian target of the rapamycin complex 1 (mTORC1) signaling pathway...In vivo, the MCF-7 tumor-bearing mouse model confirms potent antitumor efficacy without significant side effects. This work not only introduces a hypoxia-insensitive PDT agent but also provides novel insights into the mechanistic interaction between transcriptional and metabolic regulation in PDT, highlighting the potential of AIE-active materials for cancer therapy.

This integrative molecular and phenotypic profiling of blood-derived components identified potentially distinct molecular signatures, such as overexpression of IL12, ANGPT1 downregulation and HIF1A downregulation, in the literature described as linked to the patient's beneficial prognosis. These findings suggest that advanced liquid biopsy techniques may provide complementary insights into prognostic biomarkers and therapeutic targets in HGSOC.

DDIT4 promotes CRC progression and is regulated by miR-200b-3p. Targeting the miR-200b-3p/DDIT4 axis may represent a novel therapeutic approach for CRC treatment.

These findings suggest that baicalein may represent a promising, non-toxic therapeutic option for endometrial cancer, particularly when used in combination with metformin. Further investigation is warranted to assess the clinical relevance of this strategy.

To mimic ChaC1 overexpression by inducing endogenous ChaC1 high expression, a complementary ChaC1-induction-based screening was performed and revealed proteasome inhibitors (e.g., bortezomib, ixazomib, delanzomib) as potent inducers of endogenous ChaC1 via ATF4-dependent transcriptional activation. This functional convergence demonstrates that ChaC1 activation, either achieved through genetic manipulation or pharmacological induction, creates a synthetic lethal context for AUR in HCC cells. Together, our study establishes a ChaC1-based pharmacological discovery platform that identifies proteasome inhibitor and auranofin combination as a mechanistically rational anti-HCC strategy, providing both methodological innovation in drug repurposing screening and immediate translational potential for HCC treatment.

Our study reveals a distinct lipid signature in gastric metaplasia characterized by TG and LD accumulation, providing novel therapeutic insights into targeting lipid metabolism to prevent GIM malignant transformation and reduce cancer risk.

This finding suggests that PhenDC3 may induce DNA replication stress in this cell line. Collectively, these results support the feasibility of employing canine cancer cells as a model system to investigate the role of G-quadruplex structures in cancer.

This resulted in altered expression of its interacting hub gene Steroidogenic acute regulatory protein (Star), thus modulating the pathogenesis of ovarian disorders. This study elucidated that O3 exposure synergistically increases the risk of uterine and ovarian disorders through multiple mechanisms, including disrupting hormonal balance, compromising immune homeostasis, and dysregulating gene expression and RNA splicing, thus providing new experimental evidence for assessing the hazards of O3 exposure to female reproductive health.

In the present study, Imatinib-sensitive K-562S cells were subjected to CBD treatment (IC50: 17.69 μM) for 4 and 12 h, followed by RNA sequencing to identify differentially expressed genes (DEGs)...The results presented in this study validate the considerable potential of CBD to induce broad transcriptional and signalling alterations, related to immune modulation, apoptosis, and metabolic processes in K-562S cells. These findings provide novel insights into the therapeutic potential of CBD and lay the groundwork for further investigation into its precision applications in haematological malignancies.