Evidence map›Paper›PMID 36685674›Full record

ArticleBioMed research international2023

SPRR3 Contributes to Aggressiveness of Pancreatic Cancer Cells via NF-

Yuankang Xie, Heping Li, Baiyin Zhong, Xiansen Zhu, Rong Ye, Binhui Xie, Jianhong Zhang

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. 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

7 authors at 2 institutions in 1 country.

Yuankang XieDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, China.ORCID https://orcid.org/0000-0001-5374-4626
Heping LiDepartment of Medical Oncology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.ORCID https://orcid.org/0000-0002-4281-2475
Baiyin ZhongDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, China.ORCID https://orcid.org/0000-0001-6562-9000
Xiansen ZhuDepartment of Pathology, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, China.ORCID https://orcid.org/0000-0001-5523-0899
Rong YeDepartment of General Surgery III, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, China.ORCID https://orcid.org/0000-0002-7897-6009
Binhui XieDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, China.ORCID https://orcid.org/0000-0002-7324-9777
Jianhong ZhangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, China.ORCID https://orcid.org/0000-0002-0194-1334
First Affiliated Hospital of Gannan Medical University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer remains a deadly solid tumor with worst survival, and a better understanding of the mechanisms of carcinogenesis of pancreatic cancer is critical to promote the survival of patients with pancreatic cancer. qPCR and western blot assay were used to determine the expression of SPRR3 in pancreatic cancer. Anchorage-independent growth ability, BrdU labeling, Transwell assay, and in vivo experiment were used to examine the functions of SPRR3 in aggressiveness of pancreatic cancer. Luciferase reporter assay, nucleoplasmic-separation technique, qPCR, and western blot assay were used to investigate the mechanism of SPRR3 regulating aggressiveness of pancreatic cancer. Our results showed that SPRR3 was significantly increased in pancreatic cancer, which resulted in poor survival for patients with pancreatic cancer. Further analysis showed that overexpression of SPRR3 contributed to anchorage-independent growth ability, growth rate, and invasion ability of pancreatic cancer cells. While, knockdown of SPRR3 showed the reverse results. Mechanistically, overexpression of SPRR3 can promote the transcription of NF-

Indexed as

NF-kappa BPancreatic NeoplasmsCell Line, TumorCornified Envelope Proline-Rich ProteinsHumansSignal TransductionCornified Envelope Proline-Rich ProteinsNF-kappa BSPRR3 protein, human

Identifiers

PMID36685674
PMCPMC9859694
OpenAlexW4316036311

What OpenQuestion holds

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LicenceCC BY
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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.