Recent Publications Harnessing the Power of Translatomics

Every week we provide a digest of a small number of recent interesting papers in the field of translatomics.

In this week’s Sunday papers,

  • Chen et al. find through polysome profiling that the circRNA, circTFRC, is protein coding and is upregulated in the lens epithelial cells of patients with age related cataracts promoting ferroptosis for cataract formation.
  • Elhamamsy et al. find through polysome profiling and RNA-seq that knockdown of TRMT112 in TNBC cells causes a reduction in translation in mRNAs that are associated with tumour survival and progression.
  • Ye et al. find through polysome profiling that SRSF2 mutations in AML cells increase THBS1 protein levels through translational regulation to cause resistance to daunorubicin.

A novel protein encoded by hsa_circ_0068626 contributes to age-related cataract via the p62/Keap1/Nrf2 signaling pathway-mediated ferroptosis

Experimental Eye Research, 2025

Chen, Y., Li, H., Wu, L., Zou, X., Zhang, Y., Huang, R. and Wang, Y.

Sunday Paper 1

Age related cataract (ARC) is the leading causative factor of blindness and visual impairment worldwide. This study investigated the contribution of the circular RNA (circRNA) called circTFRC in ferroptosis modulation in ATC. Through RNA-seq, it was first identified that circTFRC is upregulated in the lens epithelial cells of patients suffering from ARC. This finding led the researchers of this study to investigate whether this circRNA had a protein coding function rather than a regulatory function as was originally thought.

Polysome profiling using sucrose gradient ultracentrifugation was performed in 293T cells which were overexpressing circTFRC. From this, it was found that circTFRC was predominantly present in fractions with heavy and medium polysomes rather than light ones. This suggests that this circRNA is associated with translating ribosomes rather than existing as a non-coding transcript. As a control, the mRNA distribution of the housekeeping gene, GAPDH was unchanged showing that the experiment only reflected circTFRC translation rather than global translation.

The authors of this paper strengthened these findings by identifying an open reading frame and a functional internal ribosome entry site (IRES) showing that this translation of the circRNA is cap independent. Through, IRES reporter assays, flag-tagged constructs and a custom antibody detected circTFRC-236aa confirming that the circRNA produces a functional protein. This interacts with p62 to dysregulate the Keap1/Nrf2 pathway promoting ferroptosis for cataract formation. Through these various translatomic methods, a new potential therapeutic target for ARC has been identified and this may be utilised for future treatment of blindness.  

Learn more about EIRNABio’s polysome profiling services here.

TRMT112 drives a tumor growth and metastasis-promoting program in triple-negative breast cancer

Cell Death and Differentiation, 2026

Elhamamsy, A.R., Metge, B.J., Elbahoty, M.H., Papineni, B., Alsheikh, H.A.M., Chen, D., Samant, R.S. and Shevde, L.A.

Sunday Paper 2

TRMT112 is a ribosomal modifying protein, and the authors of this study were investigating its role in the development and progression of triple negative breast cancer (TNBC). The authors of this study used a multi-omics approach encompassing genomics, transcriptomics, translatomics, proteomics and functional genomics to investigate TRMT112 as a driver in TNBC.  Through multi-omics analysis it was revealed that TRMT112 was highly expressed in TNBC and metastatic breast and also identified that elevated expression is also associated with poor patient survival. The authors of this paper performed functional studies to demonstrate that TRMT112 promotes tumour growth migration, invasion and metastasis while knockdown reduced aggressive characteristics.

Polysome profiling analysis revealed that TRMT112 knockdown caused a reduction in global protein synthesis in TNBC cell lines. Upon reduction of TRMT112, there is decreased peaks of 40S, 60S, 80S and polysome peaks when compared to the wild type indicating that TRMT112 plays a role in global ribosome biogenesis, ribosome assembly and also the loading of ribosomes onto mRNA.

During polysome profiling, fractions were collected at various stages along the sucrose gradient. The RNA was then extracted from these fractions and RNA-seq was performed. RNA-seq showed downregulating TRMT112 reduces translation of mRNAs that encode proteins associated with the extracellular matrix, collagen organisation and metastasis. These findings show that TRMT112 promotes protein synthesis of factors that make TNBC more invasive and promote its survival causing poor patient outcomes. Therefore, downregulating TRMT112 may offer a potential therapeutic target to improve patient prognosis.

Learn more about EIRNABio’s polysome profiling and RNA-seq services here.

SRSF2 mutations drive daunorubicin resistance in acute myeloid leukemia via THBS1 stabilization

Journal of Experimental & Clinical Cancer Research, 2026

Ye, W., Wu, X., Tang, Y., Zhang, Y., Du, Y., Yang, K., Yang, Y. and Gong, Y.

Sunday Paper 3

This study focused on how mutations in the SRSF2 binding protein in acute myeloid leukaemia (AML) may lead to resistance to the therapeutic daunorubicin. The authors of this study found that AML cells with mutations in the SFSR2 gene had increased levels of the protein THSB1. However, the changes in mRNA levels of the THBS1 transcript did not increase to a level that could fully account for the much greater increase in the levels of protein suggesting post-transcriptional regulation.

Polysome profiling was used to further analyse the SRSF2 mutant AML cells to determine whether this mutation altered the efficiency of THBS1 translation. The polysome profiling data shows that the THBS1 mRNA was found in heavier polysome fractions in AML cells that had the SRSF2 mutation. This indicates that THSB1 mRNA is being translated more efficiently into protein in mutant cells as the heavier the polysomes, the more ribosomes that are associated with the mRNA.

This study found that SRSF2 mutations disrupt the interaction of SRSF2 with THBS1 mRNA therefore making it more stable. This increase in THBS1 protein caused by the SRSf2 mutation in AML cells shows evidence of daunorubicin resistance (DNR). Overall, this study used polysome profiling and functional assays to investigate the selective enhancement of THBS1 translation in AML cells that carry the SRSF2 mutation which has evolved to provide DNR to the cancer cells. These translatomic findings may be used to prevent the occurrence of DNR in AML patients.

Learn more about EIRNABio’s polysome profiling services here.