Evidence map›Paper›PMID 36333284›Full record

ArticleCell death & disease2022

MACC1 promotes pancreatic cancer metastasis by interacting with the EMT regulator SNAI1.

Xianglian Zhang, Ya Luo, Yu Cen, Xin Qiu, Jing Li, Mengmeng Jie, Shiming Yang, Shanyu Qin

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  5. Review
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  8. EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025
    Review
  9. Article
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  11. Article
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  14. Review
  15. The Role of Redox Environment in Tumors.Current medicinal chemistry · 2025
    Review
  16. Article
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  19. Review
  20. Review
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

8 authors at 2 institutions in 1 country.

Xianglian Zhang *Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China.
Ya Luo *Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Yu CenDepartment of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China.
Xin QiuDepartment of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China.
Jing LiDepartment of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Mengmeng JieDepartment of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Shiming YangDepartment of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China. 13228686589@163.com.
Shanyu QinDepartment of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China. qinshanyu@gxmu.edu.cn.ORCID 0000-0002-8906-964X
Army Medical University · CNGuangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is the dominant cause of cancer-related mortality. Metastasis-associated with colon cancer protein 1 (MACC1) has been proven to play a critical role in cancer metastasis. However, the prometastatic role of MACC1 in regulating the pancreatic cancer (PC) metastatic phenotype remains elusive. Here, we report that MACC1 is highly expressed in The Cancer Genome Atlas (TCGA) and tissue microarray (TMA) and identified as a good indicator for poor prognosis. Overexpression or knockdown of MACC1 in PC cells correspondingly promoted or inhibited pancreatic cancer cell migration and invasion in a MET proto-oncogene receptor tyrosine kinase (MET)-independent manner. Notably, knockdown of MACC1 in PC cells markedly decreased the liver metastatic lesions in a liver metastasis model. Mechanistically, MACC1 binds to the epithelial-mesenchymal transition (EMT) regulator snail family transcriptional repressor 1 (SNAI1) to drive EMT via upregulating the transcriptional activity of SNAI1, leading to the transactivation of fibronectin 1 (FN1) and the trans-repression of cadherin 1 (CDH1). Collectively, our results unveil a new mechanism by which MACC1 drives pancreatic cancer cell metastasis and suggest that the MACC1-SNAI1 complex-mediated mesenchymal transition may be a therapeutic target in pancreatic cancer.

Indexed as

Colonic NeoplasmsPancreatic NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansNeoplasm MetastasisProto-Oncogene Proteins c-metSnail Family Transcription FactorsTrans-ActivatorsMACC1 protein, humanProto-Oncogene Proteins c-metSNAI1 protein, humanSnail Family Transcription FactorsTrans-Activators

Identifiers

PMID36333284
PMCPMC9636131
OpenAlexW4308298185

What OpenQuestion holds

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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.