Evidence map›Paper›PMID 27220401›Full record

ArticleOncology reports2016

Regulation of cell apoptosis and proliferation in pancreatic cancer through PI3K/Akt pathway via Polo-like kinase 1.

Yonghuan Mao, Ling Xi, Quan Li, Zeling Cai, Yimei Lai, Xinhua Zhang, Chunzhao Yu

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

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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 3 institutions in 1 country.

Yonghuan MaoDepartment of General Surgery, The Second Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Ling XiDepartment of Gerontology, The First Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Quan LiDepartment of General Surgery, The Second Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Zeling CaiDepartment of General Surgery, The Second Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Yimei LaiDepartment of Pathology, The First Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Xinhua ZhangDepartment of Pediatric Medicine, Jiangsu Province Hospital, Nanjing, Jiangsu 210029, P.R. China.
Chunzhao YuDepartment of General Surgery, The Second Clinical Medical School of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Second Affiliated Hospital of Nanjing Medical University · CNNanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer has a poor prognosis. It is reported that the PI3K/Akt pathway is activated in many cancers, and inhibition of the PI3K/Akt pathway can induce cell apoptosis in most cancers. Polo-like kinase 1 (Plk1) is also overexpressed in most malignancies, and it controls multiple aspects of mitosis and apoptosis. Previous studies identified that PI3K/Akt-dependent phosphorylation of Plk1-Ser99 is required for metaphase-anaphase transition. In this study, we aimed to investigate the molecular mechanism of PI3K/Akt pathway regulating cell proliferation and apoptosis in pancreatic cancer cell lines (AsPC-1, BxPC-3, PANC-1). Immunohistochemistry (IHC) was used to assess Akt levels in human pancreatic tissues and pancreatic cancer tissues. MTT assay was used to detect cell proliferation. The mRNA was quantified by quantitative reverse transcription-PCR. Western blot analysis was used to detect the protein levels of p-Akt, Akt, Plk1, BAX, Bcl-2, XIAP, cleaved caspase-3 and caspase-3. Recombinant adenovirus vector containing Plk1-shRNA was constructed to inhibit Plk1 expression. Cell apoptosis was detected by flow cytometry and the apoptosis of tumor xenograft was assessed by TUNEL assay. The study showed that inhibition of PI3K/Akt pathway can induce cell apoptosis and reduce cell proliferation by downregulating Plk1 in vitro and in vivo. Additionally, Plk1 inhibition can lead to cancer cell apoptosis through inactivating XIAP, activating caspase-3, upregulating BAX and downregulating Bcl-2. Therefore, this study provided the molecular mechanism of PI3K/Akt pathway and Plk1 in the pancreatic cancer cell proliferation and apoptosis, which may benefit for the therapy of pancreatic cancer.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCaspase 3Cell Cycle ProteinsCell Line, TumorCell ProliferationChromonesFemaleHumansIn Situ Nick-End LabelingMiceMice, NudeMorpholinesPancreatic NeoplasmsPhosphatidylinositol 3-Kinases2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-onebcl-2-Associated X ProteinCaspase 3Cell Cycle ProteinsChromonesMorpholinesPhosphatidylinositol 3-KinasesPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRNA, Small InterferingXIAP protein, humanX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID27220401
PMCPMC4899032
OpenAlexW2405264636

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.