Evidence map›Paper›PMID 40595789›Full record

ArticleScientific reports2025

MO-2097 inhibits EMT and angiogenesis in colorectal cancer by targeting RAF/MEK/ERK signaling.

Sumin Kim, Ho Jin Han, Junyeol Han, Yerim Choi, In-Ja Ryoo, Aneesh Sivaraman, Kyeong Lee, Bo Yeon Kim, Eun-Yi Moon, Nak-Kyun Soung

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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. Review
  2. 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.

Sumin Kim *Chemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, 28116, Republic of Korea.
Ho Jin Han *Chemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, 28116, Republic of Korea.
Junyeol HanChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, 28116, Republic of Korea.
Yerim ChoiChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, 28116, Republic of Korea.
In-Ja RyooChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, 28116, Republic of Korea.
Aneesh SivaramanCollege of Pharmacy, Dongguk University-Seoul, Goyang, 10326, Republic of Korea.
Kyeong LeeCollege of Pharmacy, Dongguk University-Seoul, Goyang, 10326, Republic of Korea.
Bo Yeon KimChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, 28116, Republic of Korea.
Eun-Yi MoonDepartment of Bioscience and Biotechnology, Sejong University, Seoul, 05006, Republic of Korea.
Nak-Kyun SoungChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, 28116, Republic of Korea. soungnak@kribb.re.kr.

Funding

Korea Research Institute of Bioscience and Biotechnology KGM1272511National Research Council of Science and Technology CAP21021-200National Research Foundation of Korea RS-2020-NR049557National Research Foundation of Korea RS-2023-00244570National Research Foundation of Korea RS-2024-00437524
6 · The paper itself

Abstract

Colorectal cancer is a leading cause of cancer-related deaths, with metastasis being the primary contributor to its poor prognosis. Despite the development of various therapeutic strategies, metastatic colorectal cancer prognosis still needs improvement. MO-2097, a novel therapeutic compound, was evaluated for its potential to inhibit metastasis by targeting critical processes such as cancer cell migration and invasion. The ability of MO-2097 to inhibit cancer cell migration was confirmed through wound healing and trans-well migration assays. Further investigation using western blot analysis revealed that MO-2097 inhibited the RAF/MEK/ERK signaling pathway by destabilizing RAF-1, a key regulator of cancer progression and metastasis. Moreover, MO-2097 treatment led to the downregulation of mesenchymal markers N-cadherin and Vimentin while reducing the expression of EMT-related transcription factors such as Snail, Slug, and ZEB1. In a 3D spheroid invasion model, MO-2097 significantly inhibited cancer cell invasion by reducing their ability to penetrate the extracellular matrix. Furthermore, MO-2097 disrupted the vascular network formation in HUVECs, indicating its impact on angiogenesis, a process essential for tumor growth and metastasis. These findings demonstrate MO-2097's promise as both an anti-metastatic and anti-angiogenic agent, offering a novel therapeutic approach for treating metastatic colorectal cancer and emphasizing its potential for future clinical applications.

Indexed as

Colorectal NeoplasmsEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemNeovascularization, PathologicProto-Oncogene Proteins c-rafAngiogenesisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansHuman Umbilical Vein Endothelial Cellsraf KinasesProto-Oncogene Proteins c-rafRaf1 protein, humanraf Kinases3D spheroid invasionAnti-angiogenesisAnti-metastasis agentEpithelial-Mesenchymal transition (EMT)RAF-1 inhibitor

Identifiers

PMID40595789
PMCPMC12216171

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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.