Evidence map›Paper›PMID 29636868›Full record

ArticleAmerican journal of translational research2018

Novasoy and genistein inhibit endometrial cancer cell proliferation through disruption of the AKT/mTOR and MAPK signaling pathways.

Kim M Malloy, Jiandong Wang, Leslie H Clark, Ziwei Fang, Wenchuan Sun, Yajie Yin, Weimin Kong, Chunxiao Zhou, Victoria L Bae-Jump

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 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

9 authors at 2 institutions in 2 countries.

Kim M MalloyVirginia Tech/Carilion Clinic, Department of Obstetrics and GynecologyBlacksburg, VA.
Jiandong WangDepartment of Gynecologic Oncology, Beijing Obstetrics and Gynecology Hospital, Capital Medical UniversityBeijing, P. R. China.
Leslie H ClarkDivision of Gynecologic Oncology, University of North Carolina at Chapel HillChapel Hill, NC. USA.
Ziwei FangDivision of Gynecologic Oncology, University of North Carolina at Chapel HillChapel Hill, NC. USA.
Wenchuan SunDivision of Gynecologic Oncology, University of North Carolina at Chapel HillChapel Hill, NC. USA.
Yajie YinDivision of Gynecologic Oncology, University of North Carolina at Chapel HillChapel Hill, NC. USA.
Weimin KongDepartment of Gynecologic Oncology, Beijing Obstetrics and Gynecology Hospital, Capital Medical UniversityBeijing, P. R. China.
Chunxiao ZhouDivision of Gynecologic Oncology, University of North Carolina at Chapel HillChapel Hill, NC. USA.
Victoria L Bae-JumpDivision of Gynecologic Oncology, University of North Carolina at Chapel HillChapel Hill, NC. USA.
University of North Carolina at Chapel Hill · USBeijing Obstetrics and Gynecology Hospital · CN

Funding

UNIV OF NORTH CAROLINA CLINICAL NUTRITION RESEARCH UNITP30DK056350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Ian Michael Carroll · 1999 to 2026
$31.6M
Metformin as a Novel Chemotheraeutic Strategy for the Treatment of Endometrial CaK23CA143154 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BAE-JUMP, VICTORIA LIN · 2010 to 2014
$854k
NCI NIH HHS K23 CA143154NIDDK NIH HHS P30 DK056350
6 · The paper itself

Abstract

objectivesExcess estrogen states, such as those generated by obesity, have long been associated with the development of type I endometrial cancers. Epidemiological studies have linked consumption of isoflavones with a decreased incidence of endometrial malignancy. Thus, our goal was to assess the effect of the isoflavones, novasoy and genistein, on cell proliferation, cell cycle, apoptosis, progesterone receptor (PR) and estrogen receptor-alpha (ERα) expression and the AKT/mTOR and MAPK pathways in endometrial cancer cells.

methodsThe endometrial cancer cell lines ECC-1 and RL-95-2 were used. Cell proliferation was assessed with MTT assay after exposure to novasoy and genistein at varying concentrations. Cell cycle progression was analyzed by flow cytometry. Apoptosis was assessed by flow cytometery for annexin V expression and ELISA for caspase-3 activity. Expression of ERα, PR and hTERT mRNA were evaluated using real time RT-PCR. Western immunoblotting was performed to evaluate the effects of novasoy and genistein on the AKT/mTOR and MAPK signaling pathways.

resultsNovasoy and genistein inhibited cell growth in a dose-dependent manner in both cell lines through induction of cell cycle G2 arrest and apoptosis. Treatment with novasoy and genistein decreased hTERT expression in a dose-dependent manner. Genistein decreased ERα mRNA expression while increasing PR expression. Genistein induced phosphorylation of p42/44 in a dose dependent manner in both cell lines but reduced phosphorylation of S6 in only the RL-95-2 cells.

conclusionsNovasoy and genistein inhibited cell proliferation through varying pathways in different cell lines but included decreased ERα expression and subsequent alteration in the expression of proteins upstream and downstream of the AKT/mTOR and MAPK pathways. Thus, isoflavones may be a promising therapeutic agent in the treatment and prevention of endometrial cancer.

Indexed as

Endometrial cancerestrogen receptorgenisteinMAPK pathwaymTOR pathwaynovasoy

Identifiers

PMID29636868
PMCPMC5883119
OpenAlexW2896854156

What OpenQuestion holds

Textmetadata
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.