ArticleCells2025
Targeted Inhibition of CHD1L by OTI-611 Reprograms Chemotherapy and Targeted Therapy-Induced Cell Cycle Arrest and Suppresses Proliferation to Produce Synergistic Antitumor Effects in Breast and Colorectal Cancer.
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Identification and Experimental Verification Reveal SLC2A3 Associated With Prognosis and Immune Infiltration in Colon Adenocarcinoma.Mediators of inflammation · 2026Article
- Targeting CHD1L suppresses prostate cancer progression via the FOXO3-PUMA axis.Journal of translational medicine · 2025Article
- Oncogenic Role and Drug Resistance Effect of CCDC6 in iCCA: Potential Strategies for Targeted Intervention.Journal of cellular and molecular medicine · 2025Article
- Chloroquine as a potential anticancer agent for triple-negative breast cancer: effects on MDA-MB-231 cells.Medical oncology (Northwood, London, England) · 2025Article
- CHD1L in cancer and beyond: structure, oncogenic functions, and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The second and third most frequently diagnosed cancers worldwide are breast (2.3 million new cases) and colorectal (1.9 million new cases), respectively. Although advances in cancer therapies and early detection have improved the overall survival of patients, patients still develop resistance or cancer recurrence. Thus, the development of novel therapies that can affect multiple mechanisms of drug resistance and cell survival is ideal for the treatment of advanced and metastatic cancers. CHD1L is a novel oncogenic protein involved in regulating chromatin remodeling, DNA damage repair, epithelial-mesenchymal transition (EMT), and programmed cell death via PARthanatos. Herein, we assess in real-time how the CHD1L inhibitor (CHD1Li) OTI-611 modulates cell cycle progression in Colo678, SUM149PT, and SW620 cell lines. By utilizing a cell cycle reporter, we tracked the real-time cell cycle progression of cancer cells treated with OTI-611 alone and in combination with standard-of-care (SOC) therapies. Our results indicate that OTI-611 causes G1 phase cell cycle arrest through a CHD1L-mediated mechanism that regulates Cyclin D1 expression and localization. As a result of this mechanism, OTI-611 can reprogram the cell cycle effects of other antitumor agents to modulate and arrest cells in G1 when used in combination, including agents commonly known to arrest cells in the G2/M phase. Therefore, we conclude that OTI-611-induced G1 arrest represents a critical component of its unique mechanism of action, contributing significantly to its anticancer activity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.