Evidence map›Paper›PMID 38757343›Full record

ArticleInternational journal of oncology2024

Daunorubicin induces GLI1‑dependent apoptosis in colorectal cancer cell lines.

Bo Ram Kim, Dae Yeong Kim, Na Ly Tran, Bu Gyeom Kim, Sun Il Lee, Sang Hee Kang, Byung Yook Min, Wooyoung Hur, Sang Cheul Oh

Abstract read
In one paragraph

Article in International journal of oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Bo Ram Kim *Division of Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University Guro Hospital, Seoul 08308, Republic of Korea.
Dae Yeong Kim *Division of Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University Guro Hospital, Seoul 08308, Republic of Korea.
Na Ly Tran *Division of Bio‑Medical Science & Technology, KIST School, University of Science and Technology (UST), Seoul 02792, Republic of Korea.
Bu Gyeom KimDivision of Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University Guro Hospital, Seoul 08308, Republic of Korea.
Sun Il LeeDepartment of Surgery, Korea University Guro Hospital, Korea University College of Medicine, Seoul 08308, Republic of Korea.
Sang Hee KangDepartment of Surgery, Korea University Guro Hospital, Korea University College of Medicine, Seoul 08308, Republic of Korea.
Byung Yook MinDepartment of Surgery, Korea University Guro Hospital, Korea University College of Medicine, Seoul 08308, Republic of Korea.
Wooyoung HurMedicinal Materials Research Center, Korea Institute of Science and Technology, Seoul 02792, Republic of Korea.
Sang Cheul OhDivision of Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University Guro Hospital, Seoul 08308, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Daunorubicin, also known as daunomycin, is a DNA‑targeting anticancer drug that is used as chemotherapy, mainly for patients with leukemia. It has also been shown to have anticancer effects in monotherapy or combination therapy in solid tumors, but at present it has not been adequately studied in colorectal cancer (CRC). In the present study, from a screening using an FDA‑approved drug library, it was found that daunorubicin suppresses GLI‑dependent luciferase reporter activity. Daunorubicin also increased p53 levels, which contributed to both GLI1 suppression and apoptosis. The current detailed investigation showed that daunorubicin promoted the β‑TrCP‑mediated ubiquitination and proteasomal degradation of GLI1. Moreover, a competition experiment using BODIPY‑cyclopamine, a well‑known Smo inhibitor, suggested that daunorubicin does not bind to Smo in HCT116 cells. Administration of daunorubicin (2 mg/kg, ip, qod, 15 days) into HCT116 xenograft mice profoundly suppressed tumor progress and the GLI1 level in tumor tissues. Taken together, the present results revealed that daunorubicin suppresses canonical Hedgehog pathways in CRC. Ultimately, the present study discloses a new mechanism of daunorubicin's anticancer effect and might provide a rationale for expanding the clinical application of daunorubicin.

Indexed as

ApoptosisColorectal NeoplasmsDaunorubicinZinc Finger Protein GLI1AnimalsAntibiotics, AntineoplasticCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHCT116 CellsHumansMiceSignal TransductionSmoothened ReceptorUbiquitinationXenograft Model Antitumor AssaysAntibiotics, AntineoplasticDaunorubicinGLI1 protein, humanSmoothened ReceptorZinc Finger Protein GLI1colorectal cancerdaunorubicinGLI1hedgehog signalingp53

Identifiers

PMID38757343
PMCPMC11095621

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Registered trials

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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.