Evidence map›Paper›PMID 36538983›Full record

ArticleCancer letters2023

Miz1 promotes KRAS-driven lung tumorigenesis by repressing the protocadherin Pcdh10.

Jing Yang, Changchun Hou, Huashan Wang, Edith A Perez, Hanh Chi Do-Umehara, Huali Dong, Vinothini Arunagiri, Fangjia Tong, Michelle Van Scoyk, Minsu Cho and 7 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer letters, 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
0.6field-weighted citation impact, top 35% 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, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The role of Pcdh10 in neurological disease and cancer.Journal of cancer research and clinical oncology · 2023
    Review
  5. 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

17 authors at 3 institutions in 1 country.

Jing YangDepartment of Surgery, College of Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Changchun HouDepartment of Surgery, College of Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Huashan WangDepartment of Surgery, College of Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Edith A PerezDepartment of Surgery, College of Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Hanh Chi Do-UmeharaDepartment of Surgery, College of Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Huali DongDepartment of Surgery, College of Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Vinothini ArunagiriDepartment of Surgery, College of Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Fangjia TongDepartment of Pharmacology and Regenerative Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, USA.
Michelle Van ScoykMassey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Minsu ChoDepartment of Pharmacology and Regenerative Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, USA.
Xinyi LiuDepartment of Pharmacology and Regenerative Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, USA.
Xiaodong GeDepartment of Pathology, University of Illinois at Chicago, 840 S. Wood St., Suite 130 CSN, MC 847, Chicago, IL, 60612, USA.
Robert A WinnMassey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Karen M RidgeDivision of Pulmonary and Critical Care Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Xiaowei WangDepartment of Pharmacology and Regenerative Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, USA.
Navdeep S ChandelDivision of Pulmonary and Critical Care Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Jing LiuDepartment of Surgery, College of Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL, 60612, USA. Electronic address: jinglius@uic.edu.
University of Illinois Chicago · USNorthwestern University · USVirginia Commonwealth University · US

Funding

The transcription factor Miz1-mediated mechanisms of lung agingR01HL141459 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LIU, JING · 2018 to 2021
$2.0M
NHLBI NIH HHS R01 HL141459
6 · The paper itself

Abstract

Targeting KRAS-mutated non-small-cell lung cancer (NSCLC) remains clinically challenging. Here we show that loss of function of Miz1 inhibits lung tumorigenesis in a mouse model of oncogenic KRAS-driven lung cancer. In vitro, knockout or silencing of Miz1 decreases cell proliferation, clonogenicity, migration, invasion, or anchorage-independent growth in mutant (MT) KRAS murine or human NSCLC cells but has unremarkable impact on non-tumorigenic cells or wild-type (WT) KRAS human NSCLC cells. RNA-sequencing reveals Protocadherin-10 (Pcdh10) as the top upregulated gene by Miz1 knockout in MT KRAS murine lung tumor cells. Chromatin immunoprecipitation shows Miz1 binding on the Pcdh10 promoter in MT KRAS lung tumor cells but not non-tumorigenic cells. Importantly, silencing of Pcdh10 rescues cell proliferation and clonogenicity in Miz1 knockout/knockdown MT KRAS murine or human tumor cells, and rescues allograft tumor growth of Miz1 knockout tumor cells in vivo. Miz1 is upregulated in MT KRAS lung tumor tissues compared with adjacent non-involved tissues in mice. Consistent with this, Miz1 is upregulated while Pcdh10 is downregulated in human lung adenocarcinomas (LUAD) compared with normal tissues, and high Miz1 levels or low Pcdh10 levels are associated with poor survival in lung cancer patients. Furthermore, the Miz1 signature is associated with worse survival in MT but not WT KRAS LUAD, and Pcdh10 is downregulated in MT compared to WT KRAS LUAD. Taken together, our studies implicate the Miz1/Pcdh10 axis in oncogenic KRAS-driven lung tumorigenesis.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsCarcinogenesisCell Line, TumorHumansKruppel-Like Transcription FactorsLungMiceProtein Inhibitors of Activated STATProtocadherinsProto-Oncogene Proteins p21(ras)Ubiquitin-Protein LigasesHras protein, mouseKRAS protein, humanKruppel-Like Transcription FactorsMiz1 protein, mousePCDH10 protein, humanPcdh10 protein, mouseProtein Inhibitors of Activated STATProtocadherinsProto-Oncogene Proteins p21(ras)Ubiquitin-Protein LigasesZBTB17 protein, humanGene regulationKRASMiz1Non-small cell lung cancerPcdh10

Identifiers

PMID36538983
PMCPMC9870713
OpenAlexW4312056260

What OpenQuestion holds

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Registered trials

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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.