Evidence map›Paper›PMID 41356425›Full record

ReviewCancer management and research2025

KRT17: A Key Driver of Cancer Therapy Resistance and Emerging Therapeutic Target.

Wei Hou

Abstract readReview
In one paragraph

Review in Cancer management and research, 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

1 author.

Wei HouTranslational Medicine Research Center, School of Clinical Medicine, Qilu Medical University, Zibo, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keratin 17 (KRT17), a type I intermediate filament protein normally restricted to basal epithelia and hair follicles, is aberrantly overexpressed across diverse aggressive malignancies where it correlates strongly with poor prognosis. Beyond driving core oncogenic processes like cell proliferation, migration, apoptosis evasion, and metabolic reprogramming, KRT17 is increasingly recognized as a pivotal regulator of cancer therapy resistance. Mechanistically, KRT17 induces chemoresistance in multiple cancers through distinct pathways: activating AKT/ERK signaling and epithelial-mesenchymal transition (EMT) in bladder cancer; modulating Wnt/β-catenin in triple-negative breast cancer; influencing the EMT/Snail2/E-cadherin axis in cervical cancer; and engaging FAK/SRC/ERK/CXCL8 immunosuppression in pancreatic cancer. It also contributes to resistance in gastric, thyroid, and skin cancers via EMT, AKT/mTOR, and immune evasion. While KRT17 predominantly drives therapy resistance and immunosuppression across various malignancies, it exhibits a contrasting, context-dependent role in colorectal cancer, where its expression is associated with enhanced T-cell infiltration and improved response to immunotherapy. Given its cancer-specific overexpression, multifaceted role in malignancy (including resistance), and promising preclinical evidence that targeting KRT17 can reverse resistance, KRT17 emerges as a significant diagnostic/prognostic biomarker and a compelling therapeutic target. This review critically synthesizes evidence for KRT17's role in drug resistance and evaluates its potential for overcoming this major barrier to successful cancer treatment.

Indexed as

cancerdrug resistanceKRT17therapeutic target

Identifiers

PMID41356425
PMCPMC12679929

What OpenQuestion holds

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LicenceCC BY-NC
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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.