Evidence map›Paper›PMID 30497511›Full record

ArticleBiological research2018

Overexpression of PIK3R1 promotes hepatocellular carcinoma progression.

Xuejun Ai, Lei Xiang, Zhi Huang, Shi Zhou, Shuai Zhang, Tao Zhang, Tianpeng Jiang

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 87 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.

Xuejun AiThe Key Laboratory of Medical Molecular Biology, Guizhou Medical University, Guiyang, 550002, China.
Lei XiangDepartment of Interventional Radiology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550002, China.
Zhi HuangThe Key Laboratory of Medical Molecular Biology, Guizhou Medical University, Guiyang, 550002, China.
Shi ZhouDepartment of Interventional Radiology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550002, China.
Shuai ZhangDepartment of Interventional Radiology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550002, China.
Tao ZhangThe Key Laboratory of Medical Molecular Biology, Guizhou Medical University, Guiyang, 550002, China. zhangtaodoctor@163.com.
Tianpeng JiangThe Key Laboratory of Medical Molecular Biology, Guizhou Medical University, Guiyang, 550002, China. 26900988@qq.com.
Affiliated Hospital of Guizhou Medical University · CNGuiyang Medical University · CNThe First People's Hospital of Guiyang · CN

Funding

National Natural Science Foundation of China 81560297Scientific Cooperation in Guizhou Province LH2016[7405]
6 · The paper itself

Abstract

backgroundPhosphoinositide-3-kinase, regulatory subunit 1 (PIK3R1) could regulate cancer cell proliferation important for cancer cell proliferation; however, its role in Hepatocellular carcinoma (HCC) remains largely unknown. Here, we investigated the role of PIK3R1 in HCC and examined the underlying molecular mechanisms.

methodsThe expression of PIK3R1 was evaluated by immunohistochemistry and qRT-PCR in a series of HCC tissues. The mRNA and protein expression of PIK3R1 was used by qRT-PCR and western blot assays in a series of human HCC cell lines, and then we choose MHCC97H and HCCLM3 cells as a model to investigate the effect of PIK3R1 on HCC progression. The effects of PIK3R1 knowdown on cell proliferation, migration, apoptosis of HCC were assessed by the MTT assay, clonogenic assays, wound healing assay and flow cytometry in vitro. Western blot assay was performed to assess the expression changes of PI3K/AKT/mTOR signaling pathway.

resultsOur results found that PIK3R1 was highly expressed in HCC tissues compared with adjacent normal tissues. Knockdown of PIK3R1 inhibited the proliferation, migration and promoted apoptosis of HCC cell lines. In addition, we proved that knockdown of PIK3R1 downregulated p-PI3K, p-AKT, and p-mTOR expressions in MHCC97H and HCCLM3 cells.

conclusionsIn conclusion, PIK3R1 providing potential novel targets for the treatment of HCC.

Indexed as

ApoptosisBlotting, WesternCarcinoma, HepatocellularCell Line, TumorCell ProliferationClass Ia Phosphatidylinositol 3-KinaseDisease ProgressionGene Expression Regulation, NeoplasticHumansImmunohistochemistryLiver NeoplasmsPhosphatidylinositol 3-KinasesReal-Time Polymerase Chain ReactionClass Ia Phosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesPIK3R1 protein, humanApoptosisHepatocellular carcinomaPIK3R1Targeted therapy

Identifiers

PMID30497511
PMCPMC6264640
OpenAlexW2903508110

What OpenQuestion holds

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LicenceCC BY
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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.