Evidence map›Paper›PMID 40660346›Full record

ReviewEuropean journal of medical research2025

NF-κB and apoptosis: colorectal cancer progression and novel strategies for treatment.

Sina Sadati, Amirreza Khalaji, Ali Bonyad, Sara Khoshdooz, Kosar Sadat Hosseini Kolbadi, Ashkan Bahrami, Mohammad Saeid Moeinfar, Mohammadmatin Morshedi, Amireza Ghamsaraian, Majid Eterafi and 3 more

Abstract readReview
In one paragraph

Review in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
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  4. Green-Synthesized Silver Nanoparticles fromAntioxidants (Basel, Switzerland) · 2026
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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

13 authors.

Sina SadatiStudent Research Committee, Kashan University of Medical Sciences, Kashan, Iran.
Amirreza KhalajiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Ali BonyadFaculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
Sara KhoshdoozFaculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
Kosar Sadat Hosseini KolbadiFaculty of Medicine, Lran University of Medical Sciences, Tehran, Iran.
Ashkan BahramiStudent Research Committee, Kashan University of Medical Sciences, Kashan, Iran.
Mohammad Saeid MoeinfarStudent Research Committee, Kashan University of Medical Sciences, Kashan, Iran.
Mohammadmatin MorshediDepartment of Exercise Physiology, Central Tehran Branch, Islamic Azad University, 14778-93855, Tehran, Iran.
Amireza GhamsaraianStudent Research Committee, Kashan University of Medical Sciences, Kashan, Iran.
Majid EterafiCancer Immunology and Immunotherapy Research Center, Ardabil University of Medical Sciences, Ardabil, Iran.
Reza EshraghiStudent Research Committee, Kashan University of Medical Sciences, Kashan, Iran. eshraghi.rza@gmail.com.
Mahmood Khaksary MahabadyAnatomical Sciences Research Center, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran. mkhaksarymahabady@gmail.com.
Hamed MirzaeiResearch Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran. h.mirzaei2002@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC), the third most prevalent cancer worldwide, presents a significant burden in terms of both mortality and morbidity. The development of CRC is a complex process, driven by a combination of genetic mutations and epigenetic alterations that disrupt normal cellular functions. These changes influence a range of cancer-regulating mechanisms, including metabolism, cell proliferation, invasion, metastasis, and apoptosis. Apoptosis, a crucial process in maintaining cellular homeostasis, plays a paradoxical role in CRC progression. While it helps eliminate damaged cells, the evasion of apoptosis allows cancer cells to thrive, gain nutrients, and avoid metabolic waste accumulation, thereby facilitating tumor growth. Additionally, the process of neovascularization, the formation of new blood vessels, is critical for tumor sustenance and expansion. The nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway is a key regulator involved in multiple physiological and pathological processes, including angiogenesis, tumor migration, cell proliferation, inflammation, apoptosis, and differentiation. Dysregulation of NF-κB activity is implicated in the progression of CRC. This review provides a comprehensive evaluation of the role of NF-κB signaling in CRC, particularly its involvement in apoptosis. Moreover, it explores the therapeutic potential of targeting the NF-κB pathway with natural and synthetic compounds, highlighting their ability to modulate CRC progression and improve patient outcomes. These insights underscore the potential of NF-κB inhibition as a novel therapeutic strategy in CRC management.

Indexed as

ApoptosisColorectal NeoplasmsNF-kappa BAnimalsAntineoplastic AgentsDisease ProgressionHumansSignal TransductionAntineoplastic AgentsNF-kappa BApoptosisColorectal cancerNF-κB

Identifiers

PMID40660346
PMCPMC12261797

What OpenQuestion holds

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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 OpenQuestion graph.