Fig. 7: CENEXIN1 deficiency suppresses senescence induction.

a–d SA-β-gal staining (a), quantitation of SA-β-gal-positive cells (n = 3 independent experiments, 6-8fields per experiment, 200 cells per field) (b) in control or siCENEXIN1 RCTE cells with or without IR exposure. Western blot of senescence markers (c), and relative mRNA level of SASP genes (d) in control or shCENEXIN1 RCTE cells with or without IR exposure. For IR treatment, cells were collected at day 10 after irradiation. Scale bar, 100 μm. SA-β-gal staining (e) and quantitation of SA-β-gal-positive cells (n = 3 independent experiments, 6-8fields per experiment, 200–300 cells per field) (f), in control or CENEXIN1^-/-RCTE cells re-expressing CENEXIN1 or ODF2 (iso6) at day 10 after IR exposure. Scale bar, 100 μm. SA-β-gal staining (g), quantitation of SA-β-gal-positive cells (n = 3 independent experiments, 3-4fields per experiment, 200–500 cells per field) (h), and relative mRNA level of SASP genes (i) in IL-1β-treated (3 ng/ml for 5 days) control or shCENEXIN1 RCTE cells. Scale bar, 50 μm. j Proposed working model: Exposure to irreparable stresses triggers the reorganization of microtubules (MTs), leading to the nucleation of sinc-MTs in the proximity of the nuclear envelop towards the ciliary base. Concurrently, the minus-end-directed kinesin KIFC3 is recruited to the ciliary base. It subsequently facilitates the transportation of the CENEXIN1-FBF1 cargo complex along the sinc-MTs, directing it towards the nucleus. This process initiates cellular senescence in stressed human cells. All results from n = 3 independent experiments. Data are the mean ± SEM. Statistical significance was determined using one-way ANOVA. Three experiments were repeated independently with similar results (c). Source data are provided as a Source Data file.