Aberrantly expressed circulating microRNAs (miRNAs) have been demonstrated to have a crucial role in the diagnosis and prognostication of various cancers, including hepatocellular carcinoma (HCC). This research aimed to examine the role of specific miRNAs in predicting the outcomes for individuals with hepatitis B virus (HBV)-related HCC treated with transarterial chemoembolization (TACE). Stored serum specimens collected prior to the first TACE procedure were employed to determine the expression of serum miR-122, miR-221, and miR-224 using quantitative real-time PCR analysis. The study included 100 HCC patients (84% males, with an average age of 60 years) who were treated with TACE. Throughout the median follow-up spanning 18.5 months (within a range of 3 to 60 months), 42 (42.0%) patients met the criteria of TACE refractoriness. Through multivariate analysis, elevated expressed miR-221 (≥4.0 log10 copies) and advanced HCC staging were identified as independent factors related to TACE refractoriness and short overall survival. However, serum miR-122 and miR-224 levels were not linked to treatment response or overall survival. These findings underscored the potential of incorporating pretreatment levels of serum miR-221 into the established tumor staging to enhance the accurate assessment of TACE responsiveness and prognostic outcome of patients with HCC.

The Special Issue, entitled “From basic radiobiology to translational radiotherapy”, highlights recent advances in basic radiobiology and the potential to improve radiotherapy in translational research

This study aimed to establish a novel BRCA1 mutant cell line from Chinese hamster V79 cells and clarify the role of BRCA1 in the DNA damage response (DDR) by comparison with a BRCA2 mutant line, V-C8. Using CRISPR/Cas9 editing, we generated a hypomorphic BRCA1 mutant, designated B1-21, carrying a 27-bp in-frame deletion in exon 4. This mutation deletes nine amino acids within the RING domain. B1-21, V79, and V-C8 cells were analyzed for DDR phenotypes. Both mutants showed impaired RAD51 foci formation, defective homologous recombination repair, and increased sensitivity to DNA-damaging agents. B1-21 cells were particularly sensitive to camptothecin and the PARP inhibitor NU1025, whereas V-C8 cells showed higher sensitivity to etoposide, cisplatin, mitomycin C, and bleomycin. Although γH2AX and FANCD2 focus responses were similar between V79 and B1-21, RAD51 recruitment was only partially reduced in B1-21 and completely absent in V-C8. B1-21 also displayed chromosomal instability (19–20 chromosomes), while V79 and V-C8 maintained a stable karyotype. After gamma irradiation, V-C8 cells accumulated substantially more chromatid-type aberrations and retained unrepaired chromatin longer than B1-21. Neither mutant showed normal RAD51 foci formation, radiation-induced sister chromatid exchange or an effective G2/M checkpoint arrest, unlike wild-type cells. Mitotic index measurements further confirmed checkpoint failure: V79 cells suppressed mitotic entry after irradiation, while B1-21 and V-C8 continued to enter mitosis, with V-C8 showing the most complete checkpoint breakdown. These findings indicate that partial disruption of the BRCA1 RING domain results in a hypomorphic phenotype with impaired homologous recombination, defective checkpoint control, and enhanced genotoxic sensitivity. The isogenic BRCA1 and BRCA2 mutant V79 lines offer a valuable model for dissecting DDR pathway differences and developing mutation-specific therapeutic strategies targeting BRCA-mutant cancers.