Evidence map›Paper›PMID 40261446›Full record

ReviewMolecular biology reports2025

Understanding the role of Hedgehog signaling pathway and gut dysbiosis in fueling liver cancer.

Naz Fatima, Hooriya Fatima, Sadia Ahmad, Muhammad Abu Talha Safdar Hashmi, Nadeem Sheikh

Abstract readReview
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In one paragraph

Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Naz FatimaDepartment of Zoology, Faculty of Science and Technology, University of Central Punjab, Lahore, Pakistan. nazfatima.pu@gmail.com.
Hooriya FatimaInstitute of Zoology, University of Punjab (Quaid-i-Azam Campus), Lahore, 54590, Pakistan.
Sadia AhmadInstitute of Zoology, University of Punjab (Quaid-i-Azam Campus), Lahore, 54590, Pakistan.
Muhammad Abu Talha Safdar HashmiDepartment of Zoology, Faculty of Science and Technology, University of Central Punjab, Lahore, Pakistan.
Nadeem SheikhInstitute of Zoology, University of Punjab (Quaid-i-Azam Campus), Lahore, 54590, Pakistan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver cancer is one of the most prevalent types of cancer worldwide with less than 20% of patients surviving in the past half a decade. Several molecular pathways have been uncovered that may lead to the development of liver cancer but more recently the Hedgehog pathway (HH) and its interactions with the gut microbiota has emerged as an underlying cause of the development of liver cancer. Gut-liver axis is vital to maintaining homeostasis. The HH pathway controls cellular differentiation, proliferation, and apoptosis evasions, its abnormal activation can lead to uncontrolled proliferation of liver cancer stem cells. Additionally, the intricate interplay between HH signaling and the gut microbiota introduces a novel dimension. Recent investigations suggest that potential modulation of HH activity by gut microbiota influence HCC progression. This review explores a crosstalk between HH signaling and the gut microbiota, uncovering intricate mechanisms by which it fuels liver cancer development. This interplay provides insights into gut dysbiosis, HCC etiology and potential therapeutic avenues, highlighting the cooperative role of HH signaling and gut microbiota in shaping the overall HCC landscape.

Indexed as

Carcinoma, HepatocellularDysbiosisGastrointestinal MicrobiomeHedgehog ProteinsLiver NeoplasmsAnimalsCell ProliferationHumansSignal TransductionHedgehog ProteinsGut dysbiosisGut metabolitesGut microbiomeHedgehog inhibitorsHedgehog signaling pathwayToll like receptors

Identifiers

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.