Evidence map›Paper›PMID 38474202›Full record

ArticleInternational journal of molecular sciences2024

Regulation of Cell Cycle Progression through RB Phosphorylation by Nilotinib and AT-9283 in Human Melanoma A375P Cells.

Trang Minh Pham, Mahmoud Ahmed, Trang Huyen Lai, Md Entaz Bahar, Jin Seok Hwang, Rizi Firman Maulidi, Quang Nhat Ngo, Deok Ryong Kim

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
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  4. Article
  5. 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

8 authors at 1 institution in 1 country.

Trang Minh PhamDepartment of Biochemistry and Convergence Medical Science, Institute of Medical Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea.ORCID 0000-0003-1862-464X
Mahmoud AhmedDepartment of Biochemistry and Convergence Medical Science, Institute of Medical Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea.ORCID 0000-0002-4377-6541
Trang Huyen LaiDepartment of Biochemistry and Convergence Medical Science, Institute of Medical Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea.ORCID 0000-0003-4619-6558
Md Entaz BaharDepartment of Biochemistry and Convergence Medical Science, Institute of Medical Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea.ORCID 0000-0001-7106-0578
Jin Seok HwangDepartment of Biochemistry and Convergence Medical Science, Institute of Medical Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea.ORCID 0000-0002-2051-504X
Rizi Firman MaulidiDepartment of Biochemistry and Convergence Medical Science, Institute of Medical Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea.
Quang Nhat NgoDepartment of Biochemistry and Convergence Medical Science, Institute of Medical Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea.ORCID 0009-0009-4128-0372
Deok Ryong KimDepartment of Biochemistry and Convergence Medical Science, Institute of Medical Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea.ORCID 0000-0002-3288-8257
Gyeongsang National University · KR

Funding

National Research Foundation of Korea RS-2023-00219399 and RS-2023-00274727
6 · The paper itself

Abstract

BCR-ABL tyrosine kinase inhibitors are commonly employed for the treatment of chronic myeloid leukemia, yet their impact on human malignant melanoma remains uncertain. In this study, we delved into the underlying mechanisms of specific BCR-ABL tyrosine kinase inhibitors (imatinib, nilotinib, ZM-306416, and AT-9283) in human melanoma A375P cells. We first evaluated the influence of these inhibitors on cell growth using cell proliferation and wound-healing assays. Subsequently, we scrutinized cell cycle regulation in drug-treated A375P cells using flow cytometry and Western blot assays. Notably, imatinib, nilotinib, ZM-306416, and AT-9283 significantly reduced cell proliferation and migration in A375P cells. In particular, nilotinib and AT-9283 impeded the G1/S transition of the cell cycle by down-regulating cell cycle-associated proteins, including cyclin E, cyclin A, and CDK2. Moreover, these inhibitors reduced RB phosphorylation, subsequently inhibiting E2F transcriptional activity. Consequently, the expression of the E2F target genes (

Indexed as

BenzimidazolesMelanomaCell DivisionFusion Proteins, bcr-ablHumansImatinib MesylatePhosphorylationProtein Kinase InhibitorsPyrimidinesTyrosine Kinase InhibitorsUrea1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)ureaBenzimidazolesFusion Proteins, bcr-ablImatinib MesylateProtein Kinase InhibitorsPyrimidinesTyrosine Kinase InhibitorsUreaBcr-Abl tyrosine kinase inhibitorcell cycleE2F1melanomaRb1

Identifiers

PMID38474202
PMCPMC10932151
OpenAlexW4392376558

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.