Evidence map›Paper›PMID 26239324›Full record

ArticleJournal of experimental & clinical cancer research : CR2015

Overexpression of TMEM158 contributes to ovarian carcinogenesis.

Zhongping Cheng, Jing Guo, Li Chen, Ning Luo, Weihong Yang, Xiaoyan Qu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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  12. Oncogenic transmembrane protein 158 drives the PI3K/Akt signaling pathway to accelerate gastric cancer cell growth.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023
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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

6 authors at 1 institution in 1 country.

Zhongping ChengDepartment of Obstetrics and Gynecology, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, China. mdcheng18@263.net.
Jing GuoDepartment of Obstetrics and Gynecology, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, China. Jingguojr@163.com.
Li ChenDepartment of Obstetrics and Gynecology, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, China. Lichenjr@163.com.
Ning LuoDepartment of Obstetrics and Gynecology, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, China. Ningluojr@163.com.
Weihong YangDepartment of Obstetrics and Gynecology, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, China. Weihongyangjr@163.com.
Xiaoyan QuDepartment of Obstetrics and Gynecology, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, China. Xiaoyanqujr@163.com.
Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTransmembrane protein 158 (TMEM158) is a recently identified upregulated gene during Ras-induced senescence. Its association with various cancers has been recently reported. However, the expression and biological function of TMEM158 in ovarian cancer is still unclear. This study was aimed to elucidate the roles of TMEM158 in cell proliferation, adhesion and cell invasion of ovarian cancer cells.

methodsWe analyzed TMEM158 mRNA level in ovarian cancer tissues and adjacent no-tumorous tissues by real-time PCR. We then suppressed TMEM158 expression of ovarian cancer cells by RNA interference and examined the effects of TMEM158 knockdown on cancerous transformation of ovarian cancer cells.

resultsThe RNA-sequencing data of the ovarian cancer cohort from The Cancer Genome Atlas project (TCGA) and our real-time PCR data showed that TMEM158 was overexpressed in ovarian cancer. Knockdown of TMEM158 by RNA interference in ovarian cancer cells significantly inhibited cell proliferation, which may be due to the increase of G1-phase arrest. Silencing of TMEM158 also inhibited cell adhesion, cell invasion as well as tumorigenicity in nude mice. Moreover, knockdown of TMEM158 notably repressed cell adhesion via down-regulating the expression intercellular adhesion molecule1 (ICAM1) and vascular cell adhesion molecule1 (VCAM1). Transforming Growth Factor-β (TGF-β) signaling pathway was also remarkably impaired by TMEM158 silencing.

conclusionsOur data suggests that TMEM158 may work as an oncogene for ovarian cancer and that inhibition of TMEM158 may be a therapeutic strategy for ovarian cancer.

Indexed as

AnimalsCarcinogenesisCell AdhesionCell Line, TumorCell MovementCell ProliferationFemaleHumansMaleMembrane ProteinsMiceMice, Inbred BALB CMice, NudeOvarian NeoplasmsTransfectionTumor Suppressor ProteinsMembrane ProteinsTMEM158 protein, humanTumor Suppressor Proteins

Identifiers

PMID26239324
PMCPMC4524016
OpenAlexW1936583519

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.