PROM1 (Prominin 1)

By targeting hypoxia-driven metabolic reprogramming, EGCG offers a dietary-based approach to modulate the CSC niche and potentially delay or prevent GBM progression. Moreover, the use of 3D spheroid models highlights their relevance in preclinical chemoprevention research, bridging the gap between simplistic 2D cultures and the complex biology of solid tumors.

Our findings suggest that GBM-derived 3D neurosphere cultures exhibit HIF-1α-regulated molecular features consistent with CSC and a potential mimicry of chemoresistance-associated traits rather than a direct demonstration of chemoresistance. These correlative observations support a potential link between metabolic reprogramming and the emergence of such phenotypes in response to hypoxic stress. Further investigation is needed to establish causal relationships and to better understand the underlying mechanisms.

TRIM28 knockout was associated with broad transcriptomic changes involving more than 500 differentially expressed genes, decreased proliferative activity monitored by time-lapse imaging, and reduced sensitivity to paclitaxel, cisplatin, and curcumin. Altogether, our results demonstrate that TRIM28, rather than CD133, functions as a central regulator of CSC-associated phenotypes in colorectal cancer. These findings highlight the importance of epigenetic context in CSC biology and may inform the development of more effective therapeutic strategies.

This led us to establish that SOX2 is a key player in controlling the PROM1 gene, which in turn influences how cells react to stress factors, including those induced by chemoradiation treatment. The discoveries in this study shed light on the complex web of mechanisms that control the survival and resistance of GSCs, offering promising new avenues for targeting and potentially overcoming therapy resistance.

The study highlights distinct gene expression and gut microbiome differences between BM and BNM patients. HPV infection may play a crucial role in BM development, offering new potential biomarkers and therapeutic targets for early diagnosis and treatment of BM in breast cancer.

Thus, by engaging with two different types of leukemia-associated antigens i.e., CAR antigens and NKG2D ligands, CAR-iNKT provide a powerful platform for the treatment of KMT2Ar-ALL. This approach can be readily adapted for other high-risk malignancies, including those with otherwise difficult to target leptomeningeal involvement.

These findings underscore the complex interplay of the EGFR/SORT1 axis in regulating VM and in driving to the transcriptional regulation of chemoresistance and CSC molecular signatures of GBM associated with VM. These insights could inspire novel therapeutic strategies targeting the EGFR/SORT1 complex in GBM.

Chronically exposed cells also exhibited an induction of the pAKT/AKT pathway and SOX9 transcription factor. The targeting of MFAP5 and CEACAM 5/6 could, therefore, provide a potential therapeutic approach to CKD.

This study provides a rapid, selective, and sensitive platform for determining the CD133 biomarker, which can be used for the early detection of lung cancer and monitoring of its development. Moreover, in a next step, it could be integrated into the design of an interesting single-use device with point-of-care (POC) application feasibility for measurement of CD133 levels.

Similarly, the downregulation of PROM1 and its potential effects on cell surface interactions warrant further exploration. Future studies should focus on elucidating the mechanisms underlying these observations, exploring their potential as therapeutic targets, and investigating the specific pathways affected by their dysregulation.

The key genes are mainly concentrated within signaling pathways such as metabolic pathways, fatty acid metabolism, and cancer pathways. Twelve differentially expressed mRNAs in the co-expression network can be used as biomarkers and intervention targets for the diagnosis and treatment of alcoholic hepatitis.

Cox regression analysis identified high CD133 and CD166 expression as independent factors associated with reduced survival (HR = 3.237, p = 0.014 and HR = 2.866, p = 0.020). Our results support the hypothesis that CD133 and CD166 are putative CSC biomarkers associated with aggressive behavior and a poor prognosis in LARC, offering opportunities for personalized targeted therapies.