Kuzuoglu-Ozturk et al. showcase a therapeutic approach, “translatome therapy,” to combat lethal prostate cancer. Zotatifin, a clinical molecule, targets the RNA-helicase eIF4A. Zotatifin decreases the select translation of key oncogenes, androgen receptor (AR), and HIF1α through remodeling their 5′ UTR RNA structure. Zotatifin enhances anti-androgen and radiotherapy sensitivity, highlighting a promising anti-cancer treatment.

Understanding the interactions between various mRNA features—such as RNA modifications, poly(A) tail length, and splicing—has been highly sought after but remains largely elusive. Here, Kim and Savill...

Translational control is emerging as a key regulator of cancer. The RNA-binding protein PABPC1 is shown to drive chronic myeloid leukaemia (CML) by enhancing the translation of pro-oncogenic mRNAs thr...

In Cancer Cell, two studies unveil mechanisms by which co-option of the protein synthesis machinery promotes cancer progression and potential therapeutic interventions. Kuzuoglu-Ozturk et al. show that eIF4A-mediated enhancement of oncogenic transcript translation initiation drives cancer progression, while Weller et al. demonstrate how aberrant transfer RNA (tRNA) modification disrupts translational fidelity to produce neoantigens.

Kuzuoglu-Ozturk et al. showcase a therapeutic approach, “translatome therapy,” to combat lethal prostate cancer. Zotatifin, a clinical molecule, targets the RNA-helicase eIF4A. Zotatifin decreases the select translation of key oncogenes, androgen receptor (AR), and HIF1α through remodeling their 5′ UTR RNA structure. Zotatifin enhances anti-androgen and radiotherapy sensitivity, highlighting a promising anti-cancer treatment.

Kuzuoglu-Ozturk et al. showcase a therapeutic approach, “translatome therapy,” to combat lethal prostate cancer. Zotatifin, a clinical molecule, targets the RNA-helicase eIF4A. Zotatifin decreases the select translation of key oncogenes, androgen receptor (AR), and HIF1α through remodeling their 5′ UTR RNA structure. Zotatifin enhances anti-androgen and radiotherapy sensitivity, highlighting a promising anti-cancer treatment.

UCSF scientists discover how cancer cells hijack the protein factory of the cell to churn out MYC protein, the driver of 70% of all cancers.