RPL5 (Ribosomal Protein L5)

Ile and Val are glycogenic branched-chain amino acids (BCAAs) that regulate fundamental cell processes by affecting mTOR activation through BCAA metabolism. In conclusion, RPL5 depletion-induced ribosomal stress disrupted stemness maintenance by affecting BCAA metabolism in AML, specifically inhibiting the PI3K-Akt-mTOR signaling pathway, which resulted in LSC eradication.

Further, RBPs like RPS8, RPL5, RPS3A, EEF1A1, and EIF4E1B were found to be strongly correlated with patients' overall survival. Taken together, our analyses identified several candidate RBPs which might serve as potential targets for oncological measures against gliomas.

We then evaluated the response of these mutant cells to a panel of compounds targeting protein synthesis at various levels-including an MNK1 inhibitor, metformin, silvestrol, homoharringtonine, anisomycin, resveratrol, and hygromycin B-as well as cytarabine, a chemotherapeutic agent commonly used in T-ALL treatment. Our results showed that the RPL5-I60V mutation confers increased sensitivity to most of these compounds, with the exception of hygromycin B. This study advances our understanding of how oncoribosomes contribute to cancer pathogenesis and highlights the therapeutic potential of directly or indirectly targeting altered ribosomes, offering insights for the development of personalized treatment strategies.

This study elucidates the malignant evolution of epithelial cells, along with changes in metabolic pathway activity and key regulators, jointly promote CRC development. This research provides new insights into early CRC detection from the perspective of metabolic reprogramming, while nominating candidate targets worthy of further investigation for precise treatment strategies.

Moreover, MRPL51 may promote the malignant biological behaviors of LUAD cells through neurotensin (NTS) and its downstream EGFR/PI3K/AKT signaling axis. MRPL51 is upregulated in LUAD and associated with poor prognosis, potentially driving progression via the downstream molecule NTS.

These findings suggest that RPL5 plays a critical role in mediating cellular senescence and chemotherapy response in AML, providing insights into novel therapeutic strategies for overcoming chemotherapy resistance and preventing disease relapse. Future studies may explore RPL5-targeted therapies and assess their clinical applicability in AML.

Studies using mouse xenograft models revealed that silencing Skiv2l2 (the homologue of human hMTR4) in mouse hepatoma cells inhibited xenograft development, and tumor growth was suppressed by intratumoral injection of antisense oligonucleotides (ASO) targeting Skiv2l2. These data suggest the significance of hMTR4 overexpression in promoting tumor growth and its potential as a therapeutic target.

In conclusion, the data here show that p53 level and activity are differentially controlled in malignant and benign thyroid cells through miR-7-5P/IPO7-mediated regulation of RP-MDM2-p53 nucleocytoplasmic trafficking. In PTC, downregulation of miR-7-5p with consequent overexpression of IPO7 might be a protective mechanism used by cancer cells to evade p53 growth suppression during carcinogenesis.

Additionally, when co-administered with the standard chemotherapeutic agents doxorubicin and 5-fluorouracil, CS&Z demonstrated synergistic effects, thereby further emphasizing its potential efficacy as a therapeutic option for the treatment of colorectal cancer. Moreover, the constituents of CS&Z, detected through liquid chromatography-mass spectrometry analysis, reportedly exhibit anticancer activities. Taken together, our findings suggest that CS&Z holds promise as a natural product capable of modulating oncogenic signaling in colorectal cancer and may serve as a complementary agent in future therapeutic strategies.

Furthermore, we used machine learning methods to perform feature selection and reduction, which generated a clinically applicable scoring system consisting of the seven hub genes for predicting clinical outcomes in BC patients. This novel IR-based prognostic signature offers a valuable tool for stratifying BC patients by risk and tailoring personalized therapeutic strategies, thus enhancing precision oncology in breast cancer care.

RPL22's effect on MDM4 and other mRNA splicing events is a striking example. A better understanding of the mechanisms involved could guide the development of improved cancer treatments.

As proof of concept the same experiments were conducted in vitro to validate the computational findings, confirming the potential of RPL5 in transcriptional regulation in cancer. This seminal study provides a foundation for future investigations into the multifaceted roles of RPs in the regulation of gene expression in physiological and pathological contexts.