Cyclin D1 binding protein 1 (CCNDBP1) is considered a tumor suppressor, and when expressed in tumor cells, CCNDBP1 can contribute to the viability of cancer cells by rescuing these cells from chemotherapy-induced DNA damage. Therefore, this study focused on investigating the function of CCNDBP1, which is directly related to the survival of cancer cells by escaping DNA damage and chemoresistance. Hepatocellular carcinoma (HCC) cells and tissues obtained from Ccndbp1 knockout mice were used for the in vitro and in vivo examination of the molecular mechanisms of CCNDBP1 associated with the recovery of cells from DNA damage. Subsequently, gene and protein expression changes associated with the upregulation, downregulation, and irradiation of CCNDBP1 were assessed. The overexpression of CCNDBP1 in HCC cells stimulated cell growth and showed resistance to X-ray-induced DNA damage. Gene expression analysis of CCNDBP1-overexpressed cells and Ccndbp1 knockout mice revealed that Ccndbp1 activated the Atm–Chk2 pathway through the inhibition of Ezh2 expression, accounting for resistance to DNA damage. Our study demonstrated that by inhibiting EZH2, CCNDBP1 contributed to the activation of the ATM–CHK2 pathway to alleviate DNA damage, leading to chemoresistance.

The dextran sodium sulfate (DSS)-induced colitis mouse model has been widely utilized for human colitis research. While its mechanism involves a response to double-strand deoxyribonucleic acid (DNA) damage, ataxia telangiectasia mutated (Atm)–checkpoint kinase 2 (Chk2) pathway activation related to such response remains unreported. Recently, we reported that cyclin D1-binding protein 1 (Ccndbp1) activates the pathway reflecting DNA damage in its knockout mice. Thus, this study aimed to examine the contribution of Ccndbp1 and the Atm–Chk2 pathway in DSS-induced colitis. We assessed the effect of DSS-induced colitis on colon length, disease activity index, and histological score and on the Atm–Chk2 pathway and the subsequent apoptosis in Ccndbp1-knockout mice. DSS-induced colitis showed distal colon-dominant Atm and Chk2 phosphorylation, increase in TdT-mediated dUTP-biotin nick end labeling and cleaved caspase 3-positive cells, and histological score increase, causing disease activity index elevation and colon length shortening. These changes were significantly ameliorated in Ccndbp1-knockout mice. In conclusion, Ccndbp1 contributed to Atm–Chk2 pathway activation in the DSS-induced colitis mouse model, causing inflammation and apoptosis of mucosal cells in the colon.

There was an error in Dis. Model. Mech. (2021) 14, dmm048922 (doi:10.1242/dmm.048922).An incorrect image was used for Sham+HFD (8W) in Fig. 2B. The original and corrected versions are shown below.The online full text and PDF versions of the paper have been corrected. The authors apologise to readers for this error, which does not impact the results or conclusions of the paper.

Background and study aims Endoscopic management of colonic diverticular bleeding remains challenging. Endoscopic coagulation with clipping (ECC) has been performed at our institution, but real-world outcome data remain limited. We aimed to describe the clinical outcomes and safety of ECC. Patients and methods We conducted a single-center retrospective case series of consecutive patients with colonic diverticular bleeding who underwent ECC for endoscopically confirmed diverticular bleeding between January 2017 and December 2025. Rebleeding was defined as clinically significant recurrent hematochezia within 30 days after initial hemostasis. Rebleeding rates and procedure-related adverse events were evaluated. Results Among 256 patients presenting with hematochezia and clinically suspected diverticular bleeding, 238 underwent colonoscopy. Of these, 83 patients who underwent ECC for endoscopically confirmed diverticular bleeding were included in the analysis. Rebleeding within 30 days occurred in 7 patients (8.4%), including 6 cases within 7 days. Among the 83 patients treated with ECC, stigmata of recent hemorrhage were identified in 81 patients. Among these, rebleeding occurred in 3 of 54 patients (5.6%) with active bleeding and in 4 of 27 patients (14.8%) with nonbleeding visible vessels or adherent clots. Procedure-related adverse events were observed in 3 patients (3.6%), all managed conservatively. Conclusions In this single-center case series, ECC was associated with a low rebleeding rate in this cohort. ECC may represent a practical hemostatic option when the bleeding diverticulum is clearly identified.