Evidence map›Paper›PMID 32020231›Full record

ArticleOncology reports2020

Knockdown of SLCO4C1 inhibits cell proliferation and metastasis in endometrial cancer through inactivating the PI3K/Akt signaling pathway.

Xiang Hu, Tong Han, Yiding Bian, Huan Tong, Xiaoli Wen, Yiran Li, Xiaoping Wan

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  7. Endometrial Cancer Stem Cells: Where Do We Stand and Where Should We Go?International journal of molecular sciences · 2022
    Review
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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 1 institution in 1 country.

Xiang Hu *Department of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, P.R. China.
Tong Han *Department of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, P.R. China.
Yiding BianDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, P.R. China.
Huan TongDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, P.R. China.
Xiaoli WenDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, P.R. China.
Yiran LiDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, P.R. China.
Xiaoping WanDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, P.R. China.
Shanghai First Maternity and Infant Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometrial cancer (EC) is the second leading type of cancer among women, and its progression is dependent on several factors. The aim of the present study was to examine the effect of solute carrier organic anion transporter family member 4C1 (SLCO4C1) on human EC and determine the underlying molecular mechanism. A total of 57 differentially expressed genes associated with advanced stage and survival were identified in The Cancer Genome Atlas database. In addition, gene ontology analysis indicated that SLCO4C1 was highly expressed in cell differentiation and integral component of plasma membrane. High SLCO4C1 expression in EC tissues was verified by immunohistochemistry. The results demonstrated that the downregulation of SLCO4C1 could significantly suppress the viability, sphere formation, migration and invasion abilities of cells, but enhance apoptosis in EC cell lines. Furthermore, the present results demonstrated that SLCO4C1 had effects on the epithelial‑mesenchymal transition (EMT) phenotype in EC cells and regulated the expression of EMT‑related proteins. Mechanistically, the present study revealed that SLCO4C1 regulated the biological functions of EC cells by inactivating the PI3K/Akt signaling pathway. Collectively, it was demonstrated that the SLCO4C1/PI3K/Akt pathway may play an important role in EC progression and metastasis and serve as a potential biomarker and target for EC diagnosis and treatment.

Indexed as

ApoptosisBiomarkers, TumorCell Line, TumorCell ProliferationDisease ProgressionEndometrial NeoplasmsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansNeoplasm MetastasisOrganic Anion TransportersPhosphatidylinositol 3-KinasesPrognosisProto-Oncogene Proteins c-aktSignal TransductionBiomarkers, TumorOrganic Anion TransportersPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSLCO4C1 protein, humanapoptosisendometrial cancerinvasionmigrationPI3K/AktSLCO4C1

Identifiers

PMID32020231
PMCPMC7041124
OpenAlexW3002946578

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.