Evidence map›Paper›PMID 40156610›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

B-AP15 inhibited colon cancer cell proliferation by decreasing CDK6, Cyclin A, Cyclin E, c-Myc, and VEGF gene expression.

Thanet Sophonnithiprasert, Sasiwan Konjanthet, Nattanicha Narinnork, Napat Prompat, Soottawat Benjakul, Jirakrit Saetang, Siriphorn Chimplee, Nadeeya Mad-Adam, Potchanapond Graidist, Thidarath Rattanaburee

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

10 authors.

Thanet SophonnithiprasertBiochemistry Unit, Department of Medical Sciences, Faculty of Science, Rangsit University, Pathum Thani, 12000, Thailand.
Sasiwan KonjanthetBiochemistry Unit, Department of Medical Sciences, Faculty of Science, Rangsit University, Pathum Thani, 12000, Thailand.
Nattanicha NarinnorkBiochemistry Unit, Department of Medical Sciences, Faculty of Science, Rangsit University, Pathum Thani, 12000, Thailand.
Napat PrompatFaculty of Medical Technology, Medical Technology Service Center, Prince of Songkla University, Songkhla, 90110, Thailand.
Soottawat BenjakulInternational Center of Excellence in Seafood Science and Innovation, Faculty of Agro-Industry, Prince of Songkla University, Hat Yai, Songkhla, 90110, Thailand.
Jirakrit SaetangInternational Center of Excellence in Seafood Science and Innovation, Faculty of Agro-Industry, Prince of Songkla University, Hat Yai, Songkhla, 90110, Thailand.
Siriphorn ChimpleeGeneral Education Department, School of Languages and General Education, Walailak University, Nakhon Si Thammarat, 80160, Thailand.
Nadeeya Mad-AdamDepartment of Biomedical Sciences and Biomedical Engineering, Faculty of Medicine, Prince of Songkla University, Songkhla, 90110, Thailand.
Potchanapond GraidistDepartment of Biomedical Sciences and Biomedical Engineering, Faculty of Medicine, Prince of Songkla University, Songkhla, 90110, Thailand.
Thidarath RattanabureeBiochemistry Unit, Department of Medical Sciences, Faculty of Science, Rangsit University, Pathum Thani, 12000, Thailand. Thidarath.r@rsu.ac.th.

Funding

This research funding was supported by the RSU Research Institute of Rangsit University, Thailand for the academic year 2023 Grant No. 8/2023
6 · The paper itself

Abstract

This study evaluated the screening of novel possible target proteins of B-AP15 (NSC687852) in silico. Through in vitro investigation, the anticancer activity of B-AP15 was examined with respect to gene expression and cell proliferation of SW620 cells (colon cancer cells). Twenty proteins associated with colon cancer were selected to screen possible target proteins of B-AP15 using molecular docking. The binding position of B-AP15 and the top five candidate proteins were investigated using the Discovery Studio 2021 software program. Cytotoxicity, colonization ability, and cell inhibition were evaluated in SW620 cells for 24, 48, and 72 h via MTT assay, colony formation assay, and trypan blue assay. The gene expression was estimated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) at 48 h. B-AP15 showed higher binding to E2F8 (- 10.88 kcal/mol), Ras (- 10.86 kcal/mol), GSK3B (- 10.77 kcal/mol), CDK6 (- 10.75 kcal/mol), and Raf (- 10.12 kcal/mol) than to USP14 (- 7.83 kcal/mol) as a target protein of B-AP15. Interestingly, Ras, GSK3B, and CDK6 shared the binding position between B-AP15 and known inhibitors. The IC

Indexed as

Antineoplastic AgentsColonic NeoplasmsCell Line, TumorCell ProliferationCyclin-Dependent Kinase 6Cyclin EGene Expression Regulation, NeoplasticHumansMolecular Docking SimulationOncogene ProteinsProto-Oncogene Proteins c-mycVascular Endothelial Growth Factor AAntineoplastic AgentsCCNE1 protein, humanCDK6 protein, humanCyclin-Dependent Kinase 6Cyclin EMYC protein, humanOncogene ProteinsProto-Oncogene Proteins c-mycVascular Endothelial Growth Factor AVEGFA protein, humanAnticancer activityAnti-cell proliferationB-AP15Colon cancer

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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.