Evidence map›Paper›PMID 41522355›Full record

ReviewInternational journal of biological sciences2026

The Role of Hedgehog Signaling in Non-small Cell Lung Cancer: Targeting Tumor Invasion, Therapy Resistance and Novel Therapeutic Strategies.

Yu Kang, Hongmei Zheng, Qiuyuan Wen, Songqing Fan

Abstract readReview
In one paragraph

Review in International journal of biological sciences, 2026. 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

4 authors.

Yu KangDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Hongmei ZhengDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Qiuyuan WenDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Songqing FanDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although essential for normal development and tissue homeostasis, aberrant activation of the Hedgehog (Hh) signaling pathway is implicated in non-small cell lung cancer (NSCLC) progression and treatment resistance. This review details the contribution of Hh signaling to NSCLC, focusing on its promotion of tumor invasion and therapeutic resistance, and establishes a rationale for disrupting this pathway to improve treatment efficacy. Malignant phenotypes in NSCLC are driven by dysregulated Hh pathway activity, often via autocrine or paracrine loops. We specifically assess how Hh pathway activation enables tumor invasion, metastasis, and the development of drug resistance. The review elucidates key resistance mechanisms against diverse therapies-encompassing chemotherapy, targeted therapy and immunotherapy-with a focus on epithelial-mesenchymal transition (EMT), cancer stem cell maintenance, and multidrug resistance (MDR). Therefore, combining Hh pathway inhibitors with standard therapies represents a promising approach for managing treatment-resistant NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungHedgehog ProteinsLung NeoplasmsAnimalsDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHumansNeoplasm InvasivenessNeoplastic Stem CellsSignal TransductionHedgehog Proteinscancer stem cells (CSCs)drug resistanceepithelial-mesenchymal transition (EMT)Hedgehog pathwaynon-small cell lung cancer

Identifiers

PMID41522355
PMCPMC12781077

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.