Evidence map›Paper›PMID 37540586›Full record

ArticleBiomolecules & biomedicine2024

CCNI2 promotes pancreatic cancer through PI3K/AKT signaling pathway.

Bingyang Hu, Wenzhi Zhang, Changsheng Zhang, Chonghui Li, Ning Zhang, Ke Pan, Xinlan Ge, Tao Wan

Open access · diamondAbstract read
In one paragraph

Article in Biomolecules & biomedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 32% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. 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

8 authors at 1 institution in 1 country.

Bingyang HuDepartment of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China.
Wenzhi ZhangDepartment of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China.
Changsheng ZhangDepartment of General Surgery, Kaifeng Central Hospital, Longting District, Kaifeng City, Henan Province, China.
Chonghui LiDepartment of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China.
Ning ZhangDepartment of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China.
Ke PanDepartment of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China.
Xinlan GeDepartment of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China.
Tao WanDepartment of Hepatobiliary Surgery, the First Medical Center, Chinese PLA General Hospital, Chinese PLA Medical School, Haidian District, Beijing City, China.
Chinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Globally, pancreatic cancer is recognized as one of the deadliest malignancies that lacks effective targeted therapies. This study aims to explore the role of cyclin I-like protein (CCNI2), a homolog of cyclin I (CCNI), in the progression of pancreatic cancer, thereby providing a theoretical basis for its treatment. Firstly, the expression of CCNI2 in pancreatic cancer tissues was determined through immunohistochemical staining. The biological role of CCNI2 in pancreatic cancer cells was further assessed using both in vitro and in vivo loss/gain-of-function assays. Our data revealed that CCNI2 expression was abnormally elevated in pancreatic cancer, and clinically, increased CCNI2 expression generally correlated with reduced overall survival. Functionally, CCNI2 contributed to the malignant progression of pancreatic cancer by promoting the proliferation and migration of tumor cells. Consistently, in vivo experiments verified that CCNI2 knockdown impaired the tumorigenic ability of pancreatic cancer cells. Moreover, the addition of phosphatidylinositol 3-kinase (PI3K) inhibitors could partially reverse the promoting effect of CCNI2 on the malignant phenotypes of pancreatic cancer cells. CCNI2 promoted pancreatic cancer through PI3K/protein kinase B (AKT) signaling pathway, indicating its potential as a prognostic marker and therapeutic target for pancreatic cancer.

Indexed as

Pancreatic NeoplasmsProto-Oncogene Proteins c-aktCell ProliferationCyclin IHumansPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesSignal TransductionCCNI protein, humanCyclin IPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID37540586
PMCPMC10950348
OpenAlexW4385460752

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.