Evidence map›Paper›PMID 36610719›Full record

ArticleJournal of radiation research2023

KRT13 is upregulated in pancreatic cancer stem-like cells and associated with radioresistance.

Wataru Takenaka, Yuhki Yokoyama, Katsuya Ikehata, Shihori Kouda, Haruka Hirose, Kazumasa Minami, Yoshinosuke Hamada, Seiji Mori, Masahiko Koizumi, Hirofumi Yamamoto

Open access · goldFull text read
In one paragraph

Article in Journal of radiation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. KRT13 Drives Pancreatic Cancer Malignancy Via the PI3K/AKT-PPARG Axis While Enhancing Sensitivity to Navitoclax.Medical science monitor : international medical journal of experimental and clinical research · 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

10 authors at 4 institutions in 1 country.

Wataru TakenakaDepartment of Medical Physics and Engineering, Division of Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita city, Osaka, 565-0871, Japan.
Yuhki YokoyamaDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita city, Osaka, 565-0871, Japan.
Katsuya IkehataDepartment of Medical Physics and Engineering, Division of Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita city, Osaka, 565-0871, Japan.
Shihori KoudaDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita city, Osaka, 565-0871, Japan.
Haruka HiroseDepartment of Systems Biology, Graduate School of Medicine, Nagoya University, 65 Tsurumai-cho, Showa-ku, Nagoya city, Nagoya, 466-8550, Japan.
Kazumasa MinamiDepartment of Medical Physics and Engineering, Division of Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita city, Osaka, 565-0871, Japan.
Yoshinosuke HamadaDepartment of Health Economics and Management, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita city, Osaka, 565-0871, Japan.
Seiji MoriDepartment of Medical Technology, Faculty of Health Sciences, Morinomiya University of Medical Sciences, 1-26-16 Nankokita, Suminoe-ku, Osaka city, Osaka, 559-8611, Japan.
Masahiko KoizumiDepartment of Medical Physics and Engineering, Division of Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita city, Osaka, 565-0871, Japan.
Hirofumi YamamotoDepartment of Molecular Pathology, Division of Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita city, Osaka, 565-0871, Japan.
Osaka University · JPMorinomiya University of Medical Sciences · JPNagoya University · JPOsaka Dental University · JP

Funding

Kagoshima Shinsangyo Sousei Investment Limited Partnership
6 · The paper itself

Abstract

Pancreatic cancer is one of the most aggressive cancers and the seventh leading cause of cancer-associated death in the world. Radiation is performed as an adjuvant therapy as well as anti-cancer drugs. Because cancer stem-like cells (CSCs) are considered to be radioresistant and cause recurrence and metastasis, understanding their properties is required for the development of novel therapeutic strategies. To investigate the CSC properties of pancreatic cancer cells, we used a pancreatic CSC model, degron (++) cells, which have low proteasome activity. Degron (++) cells displayed radioresistance in comparison with control cells. Using Ribonucleic acid (RNA) sequencing, we successfully identified KRT13 as a candidate gene responsible for radioresistance. Knockdown of KRT13 sensitized the degron (++) cells to radiation. Furthermore, a database search revealed that KRT13 is upregulated in pancreatic cancer cell lines and that high expression of KRT13 is associated with poorer prognosis. These results indicate that a combination therapy of KRT13 knockdown and radiation could hold therapeutic promise in pancreatic cancer.

Indexed as

Pancreatic NeoplasmsRadiation ToleranceCell Line, TumorHumansKeratin-13Neoplastic Stem CellsPancreasKeratin-13KRT13 protein, humancancer stem-like cell (CSC)KRT13pancreatic cancerradioresistance

Identifiers

PMID36610719
PMCPMC10036105
OpenAlexW4313702931

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read25
Read underepoch 390

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.