Evidence map›Paper›PMID 35078507›Full record

ArticleBreast cancer research : BCR2022

KRT13 promotes stemness and drives metastasis in breast cancer through a plakoglobin/c-Myc signaling pathway.

Lijuan Yin, Qinlong Li, Stefan Mrdenovic, Gina Chia-Yi Chu, Boyang Jason Wu, Hong Bu, Peng Duan, Jayoung Kim, Sungyong You, Michael S Lewis and 4 more

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 52 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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  15. Junction Plakoglobin - A Dual-Role Player in Cancer Biology.International journal of surgery (London, England) · 2025
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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

14 authors at 4 institutions in 2 countries.

Lijuan YinDepartment of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Qinlong LiUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, 8750 Beverly Boulevard, Atrium 105, Los Angeles, CA, 90048, USA.
Stefan MrdenovicUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, 8750 Beverly Boulevard, Atrium 105, Los Angeles, CA, 90048, USA.
Gina Chia-Yi ChuUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, 8750 Beverly Boulevard, Atrium 105, Los Angeles, CA, 90048, USA.
Boyang Jason WuUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, 8750 Beverly Boulevard, Atrium 105, Los Angeles, CA, 90048, USA.
Hong BuDepartment of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Peng DuanUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, 8750 Beverly Boulevard, Atrium 105, Los Angeles, CA, 90048, USA.
Jayoung KimDivision of Cancer Biology and Therapeutics, Departments of Surgery and Biomedical Sciences, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Sungyong YouDivision of Cancer Biology and Therapeutics, Departments of Surgery and Biomedical Sciences, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Michael S LewisDepartment of Pathology, VA Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Gangning LiangDepartment of Urology, University of Southern California Keck School of Medicine, Los Angeles, CA, USA.
Ruoxiang WangUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, 8750 Beverly Boulevard, Atrium 105, Los Angeles, CA, 90048, USA. ruoxiang.wang@cshs.org.ORCID 0000-0003-2614-8292
Haiyen E ZhauUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, 8750 Beverly Boulevard, Atrium 105, Los Angeles, CA, 90048, USA.
Leland W K ChungUro-Oncology Research Program, Samuel Oschin Comprehensive Cancer Institute, Department of Medicine, Cedars-Sinai Medical Center, 8750 Beverly Boulevard, Atrium 105, Los Angeles, CA, 90048, USA.
Cedars-Sinai Medical Center · USSichuan University · CNUniversity of Southern California · USVA Greater Los Angeles Healthcare System · US

Funding

Prostate Cancer Bone Metastasis: Biology and TargetingP01CA098912 · NCI · EMORY UNIVERSITY · PI CHUNG, LELAND W.K. · 2003 to 2019
$24.0M
NCI NIH HHS P01 CA098912
6 · The paper itself

Abstract

backgroundKeratins (KRTs) are intermediate filament proteins that interact with multiple regulatory proteins to initiate signaling cascades. Keratin 13 (KRT13) plays an important role in breast cancer progression and metastasis. The objective of this study is to elucidate the mechanism by which KRT13 promotes breast cancer growth and metastasis.

methodsThe function and mechanisms of KRT13 in breast cancer progression and metastasis were assessed by overexpression and knockdown followed by examination of altered behaviors in breast cancer cells and in xenograft tumor formation in mouse mammary fat pad. Human breast cancer specimens were examined by immunohistochemistry and multiplexed quantum dot labeling analysis to correlate KRT13 expression to breast cancer progression and metastasis.

resultsKRT13-overexpressing MCF7 cells displayed increased proliferation, invasion, migration and in vivo tumor growth and metastasis to bone and lung. Conversely, KRT13 knockdown inhibited the aggressive behaviors of HCC1954 cells. At the molecular level, KRT13 directly interacted with plakoglobin (PG, γ-catenin) to form complexes with desmoplakin (DSP). This complex interfered with PG expression and nuclear translocation and abrogated PG-mediated suppression of c-Myc expression, while the KRT13/PG/c-Myc signaling pathway increased epithelial to mesenchymal transition and stem cell-like phenotype. KRT13 expression in 58 human breast cancer tissues was up-regulated especially at the invasive front and in metastatic specimens (12/18) (p < 0.05). KRT13 up-regulation in primary breast cancer was associated with decreased overall patient survival.

conclusionsThis study reveals that KRT13 promotes breast cancer cell growth and metastasis via a plakoglobin/c-Myc pathway. Our findings reveal a potential novel pathway for therapeutic targeting of breast cancer progression and metastasis.

Indexed as

Breast NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemalegamma CateninGene Expression Regulation, NeoplasticHumansKeratin-13MiceNeoplasm MetastasisProto-Oncogene Proteins c-mycSignal Transductiongamma CateninKeratin-13KRT13 protein, humanMYC protein, humanProto-Oncogene Proteins c-mycBreast cancerc-MycKRT13MetastasisPlakoglobinγ-Catenin

Identifiers

PMID35078507
PMCPMC8788068
OpenAlexW4206947542

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.