Evidence map›Paper›PMID 32409648›Full record

ArticleCell death & disease2020

A novel function of IMPA2, plays a tumor-promoting role in cervical cancer.

Kan Zhang, Lei Liu, Min Wang, Min Yang, Xianping Li, Xiaomeng Xia, Jingjing Tian, Shan Tan, Lingli Luo

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Predictive model for clear cell renal cell carcinoma: a novel model integrating sunitinib resistance and prognosis related genes and clinical factors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  3. Multi-omics analysis reveals that knockdown of IMPA2 induces apoptosis in cervical cancer cells through ROS/MYC/CDK1 signaling.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

9 authors at 1 institution in 1 country.

Kan Zhang *Department of Laboratory Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Lei Liu *Department of Laboratory Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Min WangDepartment of Laboratory Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China. wangmin0000@csu.edu.cn.ORCID http://orcid.org/0000-0002-3420-4031
Min YangDepartment of Laboratory Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xianping LiDepartment of Laboratory Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xiaomeng XiaDepartment of Obstetrics and Gynecology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jingjing TianDepartment of Laboratory Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Shan TanDepartment of Laboratory Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Lingli LuoDepartment of Laboratory Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Discovery of genes and molecular mechanism involved in cervical cancer development would promote the prevention and treatment. By comparing gene expression profiles of cervical carcinoma in situ (CCIS) and adjacent normal tissues, we identified a potential cancer-promoting gene, IMPA2. This study aimed to elucidate the role of IMPA2 and underlying molecular mechanisms in cervical cancer progression. To do this expression of IMPA2 was compared between human cervical cancer and corresponding adjacent normal cervical tissues firstly. CCK-8 assay, clone formation assay, wound healing assay, transwell assay, and tumor formation in nude mice were performed to demonstrate the effect of IMPA2 in cervical cancer proliferation and metastasis. Further proteomic profiling and western blotting explored the molecular pathway involved in the IMPA2-regulating process. The results showed that IMPA2 gene expression was upregulated in cervical cancer. Consistently, silencing of IMPA2 suppressed tumor formation in BALB/c nude mice. Short hairpin RNA (shRNA)-mediated IMPA2 silencing significantly inhibited proliferation and colony-forming abilities of cervical cancer cells, while IMPA2 overexpression had little impact. Also, IMPA2 silencing suppressed cellular migration, but overexpression promoted migration. Proteomics analysis revealed the involvement of mitogen-activated protein kinase (MAPK) pathway in tumor-promoting action of IMPA2. Significantly, the inhibition of IMPA2 activated ERK phosphorylation, and its inhibitory effects can be restored by using selective ERK inhibitor, FR180204. In conclusion, IMPA2 acts as an oncogene in the proliferation and migration of cervical cancer. IMPA2 downregulated ERK phosphorylation to promote cervical cancer. These findings identify a new mechanism underlying cervical cancer and suggest a regulating effect of IMPA2 in MAPK signaling pathway.

Indexed as

AdultCarcinogensCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMiddle AgedMitogen-Activated Protein KinasesPhosphoric Monoester HydrolasesUterine Cervical NeoplasmsCarcinogensMitogen-Activated Protein Kinasesmyo-inositol-1 (or 4)-monophosphatasePhosphoric Monoester Hydrolases

Identifiers

PMID32409648
PMCPMC7224180
OpenAlexW3025460502

What Socratic holds

Textmetadata
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 Socratic graph.