Evidence map›Paper›PMID 26084985›Full record

ArticleClinical and experimental medicine2016

Par3 regulates invasion of pancreatic cancer cells via interaction with Tiam1.

Xingjun Guo, Min Wang, Yan Zhao, Xin Wang, Ming Shen, Feng Zhu, Chengjian Shi, Meng Xu, Xu Li, Feng Peng and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical and experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Loss of TDP43 inhibits progression of triple-negative breast cancer in coordination with SRSF3.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. Altered methylation of specific DNA loci in the liver ofFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  15. Review
  16. Claudin proteins, outside-in signaling, and carcinogenesis.Pflugers Archiv : European journal of physiology · 2017
    Review
  17. 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

20 authors at 4 institutions in 1 country.

Xingjun GuoDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Min WangDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Yan ZhaoDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Xin WangDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Ming ShenDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Feng ZhuDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Chengjian ShiDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Meng XuDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Xu LiDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Feng PengDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Hang ZhangDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Yechen FengDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Yu XieDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Xiaodong XuDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Wei JiaDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Ruizhi HeDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China.
Jianxin JiangDepartment of Hepatic-Biliary-Pancreatic Surgery, Hubei Cancer Hospital, Wuhan City, People's Republic of China.
Jun HuDepartment of Colon Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, People's Republic of China.
Rui TianDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China. jinguxiong@gmail.com.
Renyi QinDepartment of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave, Wuhan City, 430030, Hubei Province, People's Republic of China. ryqin@tjh.tjmu.edu.cn.
Tongji Hospital · CNHuazhong University of Science and Technology · CNHubei Cancer Hospital · CNTianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The conserved polarity complex, which comprises partitioning-defective proteins Par3, Par6, and the atypical protein kinase C, affects various cell-polarization events, including assembly of tight junctions. Control of tight junction assembly is closely related to invasion and migration potential. However, as the importance of conserved polarity complexes in regulating pancreatic cancer invasion and metastasis is unclear, we investigated their role and mechanism in pancreatic cancers. We first detect that the key protein of the conserved polarity complex finds that only Par3 is down-regulated in pancreatic cancer tissues while Par6 and aPKC show no difference. What is more, Par3 tissues level was significantly and positively associated with patient overall survival. Knocking-down Par3 promotes pancreatic cancer cells invasion and migration. And Par3 requires interaction with Tiam1 to affect tight junction assembly, and then affect invasion and migration of pancreatic cancer cells. Then, we find that tight junction marker protein ZO-1 and claudin-1 are down-regulated in pancreatic cancer tissues. And the relationship of the expression of Par3 and ZO-1 in pancreatic cancer tissue is linear correlation. We establish liver metastasis model of human pancreatic cancer cells in Balb/c nude mice and find that knocking down Par3 promotes invasion and metastasis and disturbs tight junction assembly in vivo. Taken together, these results suggest that the Par3 regulates invasion and metastasis in pancreatic cancers by controlling tight junction assembly.

Indexed as

Neoplasm InvasivenessAdultAgedAnimalsCarrier ProteinsDisease Models, AnimalFemaleGene Knockdown TechniquesGuanine Nucleotide Exchange FactorsHumansMaleMembrane ProteinsMice, Inbred BALB CMiddle AgedNeoplasm MetastasisPancreatic NeoplasmsCarrier ProteinsGuanine Nucleotide Exchange FactorsMembrane ProteinsPARD3B protein, humanTIAM1 protein, humanT-Lymphoma Invasion and Metastasis-inducing Protein 1InvasionPancreatic cancerPar3Tiam1Tight junction

Identifiers

PMID26084985
OpenAlexW2132317285

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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.